Theory of the dependence in the critically ill patient (1)

Theory of the dependence in the critical care patient (1)

Theme 1. Fluids state

One of the most complex problems in the management of critically ill patients is to know the state electrolyte, vascular control and cardiovascular responses to physiological stress. Is vast amount of information that we need to manage patients est0s theoretically, but on the other hand with a simple understanding of the physiology of the cardiovascular circuit applied to these patients, can manage in an optimum way.

The critically ill patient is to be understood, as no ordinary patient. The physiological functions of many organs are affected after a state of chock, regardless of the shock to occur. In addition, such patients require mechanical or pharmacological media for sustaining life, such as mechanical ventilation, continuous renal clearance techniques (dialysis and ultrafiltration), complex systems of monitoring catheters and lines that give extensive details of information added.


Any patient admitted under shock (any type) and survives the same for at least seven days, keeping some type of life support, your vital status is independent of the cause which admitted to the ICU and a clearly “dependencies” are defined. This theory was called, “THE LAW OF DEPENDENCE IN THE CRITICAL ILL PATIENT.” It is an unwritten personal theory above is an observational law, based on fluid changes in the venous compartment most of them by an albumin oncotic changes related to the initial shock in hemodynamic changes (hyperdynamic moderate) reflecting a sustained vasodilation relatively little expression in neurohormonal changes (influenced after the collision prior corticosteroid), metabolic changes (changes in plasma and urinary Na) and a moderate dysfunction of renal function. Driving conditions in these patients often are similar in certain sections and include special needs.

1. – Why this dependency happened?

Normally under the following conditions:

  • Hemodynamic STATE OR MAINTAINS turn to hyperdynamic state

A. – STATE OF FLUIDS. This chapter is for talking about, how changes in circulating volume and vascular compartments, determines the state of cardiocirculatory Unit.

Vessels and lymphatic capillaries:

The circulatory system is composed of the heart as a pump and the source of a network of hundreds of thousands of tubes (arteries, veins and capillaries) of different sizes (from several centimeters to millimeters and microns).
This vast network, which originates from the heart to the body (blood system) and through the capillaries returns to the heart (venous system) to the lungs (lower circuit) and oxygenated blood is returned immediately to the organs .

The so-called contact area between the arterial and venous system is called arteriolar and venular system and is a huge mesh of fine arteries and veins in all organs of the body (called capillaries).

Types of capillaries

  •      Capillary blood (red), to carry oxygenated blood to different tissues and organs (60,000 million cells in the body).
  •      Capillary venous (blue), responsible for carrying oxygen-poor blood to the heart through venules where the veins to pump then this what the different parts of the body.

Really when you look through a microscope is a “tissue” composed of a layer of extremely flattened endothelial cells, a basal lamina and a small network of reticular fibers. What is important is that these capillaries are a series of pores through which a passage of substances produced by two mechanisms:

Intercellular clefts: passage of small substances.
Vesicles and ducts pinocíticos: transport of large molecules or solid particles.

Thus capillaries in some territories we can find certain features to encourage the passage of some molecules, nutrients, …

IE to prevent the passage of substances or foreign bodies into the cerebrospinal fluid.

In the liver if required to pass and therefore find substances larger pores. In hepatocytes can spend even plasma proteins. At the kidney there is also known as fenestrae specific grooves which will allow passage of a large n ° are substances. It has to allow the passage of some substances from the blood.

They will be very important because they are exchanged water and substances which may be dissolved or in the interstitial spaces. We speak of the territory or capillary bed, consisting of a series of small vessels, with a specific function that will lead to the role of various vessels.

Will always start at the end of an arteriole and the beginning of the bed, where the diameter decreases, it becomes metaarteriolas, which have a discontinuous muscle layer. From this form capillaries in the muscle layer that does not exist, only a muscle endothelium, thus neither shrink nor swell. Then go to the heart and lead to venules where again displayed a muscular layer.

Importantly, the presence of capillary sphincters are governing you have more or less blood to flow into these capillaries.


Made from very thin wall pipes and which are formed from the lymphatic capillaries, which are found in all animal tissues. They will join these capillaries forming a larger capillaries that flow into the jugular and subclavian veins.

Lets pick up liquid and bring to the bloodstream. Excess fluid collects and recovers proteins that can escape from the capillaries. These proteins have to be a through vessels, increasing the oncotic pressure and increases the filtration process which would have an excess of fluid in tissues.

The liquid flowing through them is the lymph (interstitial fluid is identical). The lymphatic vessels pass through lymph nodes will have the filtration function. Lymph flow through vessels is similar to the blood in the veins. The lymph moves through muscle contractions and by contractions of the walls themselves. These vessels will also help for a system like the venous valves that prevent the retreat of the lymph.

Another important factor is the progressive entry of fluid into the lymphatic capillaries, which depends on the hydrostatic pressure of interstitial fluid (PIF). Increasing the pressure favors the liquid flow.


Therefore the severe fall in blood pressure, can be started from the HEART (cardiogenic shock) from the circuit or circuit LUNG veins of lower (obstructive shock as pulmonary embolism) and from within the ductwork due to changes in endothelial cells in arteries, veins and capillaries (distributive shock as in sepsis, anaphylaxis or disorders of the spinal cord).

In the graph you can see how from the heart chambers, some back and forth the pulmonary circuit (left atrium and right ventricle) and from the left ventricle into the aorta, blood is ejected into other organs (heart, brain, intestine, liver, kidneys and organs of the pelvis and legs). This blood returns by the venous system from each body before the right atrium and the process begins with each heartbeat. The total mobilized blood is 4.5 to 5 liters per minute (this is called cardiac output).

Obviously this figure is only illustrative of a schematic manner, since the total area of ducts in the body is enormous.

If you read my article on SHOCK (Shock, that terrible word about the danger of dying!) You can learn in detail how HAPPENS (Spanish language).

But after any shock and after a period of about 7 days if the patient still survives and remains seriously ill, this is balanced ductwork and reaches a state of “UNIT” which is nothing but a state where processes converge to a situation of “bad circulation distribution” very similar to that produced by sepsis in a stable patient. The patient is serious, you need mechanical ventilation or other media of both mechanical and life-sustaining drugs.

The process leading to the stabilization does not mean that conditions improved, but it allows management more standardized, which at the beginning of shock.

Consider the cardiovascular system, such as a hydraulic closed circuit that includes the heart, arteries, arterioles, capillaries and veins (1).

The venous side of this system is conceptually divided into two compartments, each plays a different role for inherent differences in anatomic volume, flow resistance and compliance (WARNING NOT INCLUDE THE PULMONARY CIRCUIT):

  • The peripheral venous compartment
  • The vena cava and right atrium or central venous compartment

Now if we look at the components of the arteriovenous circuit, we have the following characteristics (2):

OBSERVE: the left ventricle in diastole (end-diastolic) has a high compliance (ml / mmHg), which makes it very sensitive to small changes in cardiac filling pressures (CVP).

The difference between the 3.5-liter volume of the complete circuit corresponding to the cardiac output (4.5 liters) is 1 liter and this in the system corresponds to a compliance of 7.1 ml / mmHg (1000/140). This pressure, is called mean pressure circulatory filling (is that the system is observed when flow is absent, for example after a cardiac arrest, SO IS A MEASURE THEORY). The variables affecting this medial pressure are:

  • Circulating blood volume
  • Vessel tone peripheral venous

Cardiocirculatory DEPENDENCE occurs when, after a shock process, which the patient has survived after 7 days in keeping all media, the adaptation of compartments to any process is the same. Usually feature is the presence of edema as the cause of the maldistribution of the liquid. These edemas occur by several mechanisms:

Resuscitation with fluids after a very intense shock. habituation, lly are needed in any kind of shock a large initial volume (between 1 liter and 6-7 liter septic shock), the patient finds it hardly handle even with normal renal function (usually renal dysfunction in shock is the standard).
Vasoplegia in septic shock, conditions a loss of fluid into the interstitial space, which is difficult to extraeer, since the morphological changes of renal function (the tendency to tubular necrosis, causes retention of Na and H2O). Even the need for vasoactive agents (noradrenaline) does not produce the reintroduction of the interstitial fluid, because there are more mechanisms involved (endothelial dysfunction, adrenal insufficiency, pituitary insufficiency, presence of inflammatory mediators, etc.).
Plasma albumin level (hypoalbuminemia after acute systemic inflammatory response syndrome)
Venous return (venous resistance) from the blood to the heart. The peripheral venous compartment, has a very altered tone and the effect of pressure inside the chest in patients with mechanical ventilatory support.
The fall of intravascular volume, conditions Na and H2O retention.

When we act on the shock of onset, recovery of bodies is not immediate. The intent is to prevent cell death (hyperlactataemia due to the poor presence of oxygen in tissues). Always in shock (regardless of type) is a relative hipovemia (1000 ml minimum pressure corresponding to half fill circulatory). Fluid management is a priority before initiating supportive measures (vasoactive pressor drugs), except imminent death due to very low blood pressure. When we got to stabilize the blood pressure usually exists organ dysfunction, maldistribution of liquid and acidosis, which is not corrected immediately, the norm is for a period of days. If the case continues and is in brackets, pass the dependency circulation, in this case in need of correction fluid and the rational use of diuretics and maintaining a support with albumin to maintain a tone of plasma oncotic circulation and promote the reabsorption of fluid from the interstitium.

The influence of central venous pressure (CVP) on venous return. One of the most important mechanisms are altered in critically ill patients to maintain cardiac output (liters / minute of blood leaving the heart). The peripheral venous compartment under normal conditions usually found close to the average pressure circulatory filling.

The flow of blood between the peripheral venous compartment and the central venous compartment is governed by the basic flow equation:

(Q = Flow or Delta P / R) Delta P is the pressure between the peripheral and central venous compartment and R is the resistance associated with the peripheral veins.

If we assume for example 7 mmHg Ppv (peripheral venous compartment pressure) and the PVC is also 7 mmHg, —–> no venous return (since then intrathoracic pressure will be “0”).
If we assume that the PPV is 10 mmHg and CVP is 7 mm Hg, venous return here will increase significantly given the pressure difference arises between the peripheral compartment and the thorax. The venous return is for only when the central venous pressure is raised to 10 mmHg.

In normal conditions the half intrathoracic pressure during the respiratory cycle is negative. This facilitates venous return to the heart, especially during inspiration, when the pressure becomes more negative. All situations that increase intrathoracic pressure impede venous return and decrease intrathoracic blood volume and ventricular volume and, thus, stroke volume and ejection fraction and ventricular work.

Pressures in the thorax can be raised in various causes:

  • Cough,
  • The Valsalva maneuver
  • Tension pneumothorax
  • Mechanical ventilation with positive pressure levels at the end of expiration than 2-3 mmHg
  • Pulmonary embolism
  • Cardiac tamponade
  • Other … as DVT (deep vein thrombosis), portal thrombosis, hyperdynamic states (cirrhosis with ascites), postoperative abdominal, etc.

The initial impact is the drop in circulating volume by decreasing the central venous pressure and therefore the preload (atrial filling).
The following result is leakage from that volume to the interstitium (third space) appearing edema or swelling.

The influence of peripheral venous pressure on venous return. As mentioned before, the difference between central venous compartment and the peripheral is what determines venous return.

Therefore, an increase in peripheral venous pressure can be as effective in increasing venous return as a decrease in central venous pressure (CVP).

Veins are elastic vessels, changes in blood volume contained within the peripheral veins, peripheral venous pressure alters. Moreover, because the veins are much more accommodating than any other segment vascular changes in the circulating blood volume, can produce large changes in the volume of blood in the veins. For example after a hemorrhage, or loss of large amounts of liquid and after a great sweating, vomiting or severe diarrhea, could decrease the volume of circulating blood and significantly reduces the volume of blood in the veins, descending subsequently in the compartment peripheral vein. Conversely, by increasing the circulating volume, is achieved by increasing the peripheral venous compartment shifting the curve to the right venous function.

By a similar logic, if the peripheral venous pressure is caused by loss of blood or sympathetic vasoconstriction in peripheral veins, moves the venous function curve to the left.

The influence of plasma albumin on peripheral venous pressure.

Albumin is a protein produced by the liver. Is a protein found in high proportions in the blood plasma, the main blood protein and one of the most abundant. The serum albumin test measures the amount of this protein in the clear liquid portion of blood.

Albumin is essential for the maintenance of osmotic pressure necessary for the correct distribution of body fluids between the intravascular compartment and extravascular located between tissues.


  • Oncotic pressure maintenance.
  • Transport of thyroid hormones.
  • Transport of soluble hormones.
  • Transport of free fatty acids. (That is, non-esterified)
  • Transport of unconjugated bilirubin.
  • Transport of many drugs and drugs.
  • Competitive binding with calcium ions.
  • PH control.
  • Regulator of extracellular fluid, Donnan effect.

As shown, the albumin is participating in a large number of processes, virtually all related to the complimentary of the blood, but the most important role is to maintain a suitable oncotic pressure which is the osmotic pressure due to plasma protein that appears between vascular and interstitial compartment. Blood capillaries being less permeable to high molecular weight compounds, such as proteins, they tend to accumulate in the blood plasma, resulting less abundant in the interstitial fluid. This concentration gradient between the inside of the capillary and interstitial space arises a tendency of water to compensate for this difference capillary blood returning to a certain pressure, capillary oncotic pressure. Similarly, proteins that are part of the interstitial fluid, interstitial generate an oncotic pressure in normal oncotic pressure less than the capillary.

The blood vessels of this protein required to maintain the balance between vascular and interstitial spaces. Otherwise, the difference between a space more or less osmotic hypertonic conditions the water passage between them, generating the differences between both compartments.

Starling’s equation (4):

Formulated in 1896 by the British physiologist Ernest Starling, the Starling equation illustrates the role of hydrostatic and oncotic forces (also called Starling forces) in the movement of flow through the capillary membranes. Predicts the net filtration pressure for a given liquid in the capillaries.

According to the Starling equation, fluid motion depends on six variables:

  • Capillary hydrostatic pressure (Pc)
  • Interstitial hydrostatic pressure (Pi)
  • Reflection coefficient (R), an index value that is the effectiveness of the capillary wall to prevent passage of proteins and that, under normal conditions is admitted that is equal to 1, which means that it is totally impermeable to the thereof and in pathological situations less than 1, until the value 0 when it can be pierced by them without difficulty.
  • Capillary oncotic pressure (πc)
  • Interstitial oncotic pressure (πi)
  • Filter coefficient (Kf), expresses the capillary wall permeability to fluids

All pressures are measured in millimeters of mercury (mm Hg), and the filter coefficient is measured in milliliters per minute per millimeter of mercury (mL · min-1 · mm Hg-1). Starling’s equation described in the following manner:

\ Q = K_f ( [P_c - P_i] - R [\pi_c - \pi_i] )

For example:

  • -Arteriolar hydrostatic pressure (Pc arteriolar) = 37 mmHg
  • -Venular hydrostatic pressure (Pc venular) = 17 mmHg

According to the equation, P (Q) arteriolar = (37-1) + (0-25) = 11 and P (Q) venular = (17-0) + (0-25) = -9. Filtration is therefore greater than resorption. The difference is recovered to the bloodstream through the lymphatic system.

The solution to equation is the flow of water from the capillaries into the gap (Q). If positive, the flow will tend to leave the capillary (filtration). SI is negative, the flow will tend to enter the capillary (absorption).

The Gibbs-Donnan equilibrium

Due to the nature of semi-permeable capillary endothelium, plasma proteins are retained in the vascular compartment and its influence on the osmotic activity is central to the movement of fluids between the capillary and interstitial compartments. The Gibbs-Donnan equilibrium across the epithelium established the existence of diffusible proteins adds a small but significant increase in the osmotic activity. Plasma proteins originate an osmotic pressure of about 20 mm Hg and caused by the charged particles produced in the Gibbs-Donnan equilibrium is about 6-7 mm Hg. The sum of both is the oncotic pressure that is the pull exerted by the water plasma proteins.

The appearance of oedema:

In general, the amount of interstitial fluid is defined by the balance of body fluids through the mechanism of homeostasis.

Fluids intravascular and extravascular compartments are easily exchanged to maintain the right balance. Intravascular fluid out of blood vessels (primarily through the capillaries) and enters the interstitial space (5). This is the process fluid filtration. It is estimated that in a typical body, about 1% plasma seeps into the interstitial space. Under normal conditions, so that the body is in equilibrium, the same fluid from blood vessels into the interstitial space must return to the vasculature. There are two ways in which the fluid returns to the blood:

most of the fluid is absorbed in the final segment of the capillary venules or below, however, the rate of fluid absorption is less than the filtration rate, so it takes a second mechanism that collects excess filtering fluid into the interstitial fluid;
The second mechanism involves the lymph vessels, which collect excess interstitial fluid and pour it into the venous system at the level of the subclavian veins.

The edema is formed when an excessive secretion of fluid into the interstitial space, or when he does not recover properly, due to problems of absorption or lymphatic problems.

The appearance of generalized edema in critically ill patients is the classic feature. Also called systemic edema, which causes severe when diffuse swelling of all tissues and organs, especially the subcutaneous tissue, then called anasarca.

In heart failure, there is an increase in hydrostatic pressure, whereas in nephrotic syndrome and hepatic failure occurs an oncotic pressure drop. It is considered that these conditions explain the occurrence of edema, although this may be more complex (6).

In these cases, it may cause edema in multiple organs and peripheral members. For example, a major heart failure can cause pulmonary edema, pleural effusion, ascites and peripheral edema (7).

Conclusion: The protein albumin is perhaps the central axis of the vascular compartments. The proper management of it, along with the infusion of fluids (liquids), it will be optimal recovery of the gap and altered intravascular volume, helped by diuretics in the management of renal dysfunction that accompanies.

Theme 2. – HEMODYNAMICS: MODERATE hyperdynamic.

In Spanish language


1.- Cardiovascular Physiology (Lange Physiology Series 2006). Central Venous Pressure. An indicator of Circulatory Hemodynamics, Chapter 8. Page: 146-153. ISBN: 0-07-146561-8

2.- Shock, esa terrible palabra acerca el peligro de morir!

3.- Funciones de la Albúmina.

4.- Ecuación de Starling.

5.- Klabunde, R.E. (2005). «Ch.8 Exchange function of the microcirculation.». Cardiovascular physiology concepts. Lippincott Williams & Wilkins.

6.- Renkin EM. (1994) Cellular aspects of transvascular exchange: a 40-year perspective. Microcirculation 1(3):157–67.

7.- Cho S, Atwood J (2002). «Peripheral oedema». Am J Med 113 (7):  pp. 580–6.


Santiago Herrero. “Theory of the dependence in the critical care patient (1)”. Pearls in Intensive Care Medicine. April 2012 Vol. 54

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