Normal and Abnormal Fluid Distribution and Function

nerve endThe reflections on the broad role of fluid in health and disease in this blog post considers the chapters ‘Fluid and Electrolyte Balance’, ‘Oedema’, ‘Hyperaemia and Congestion’, ‘Haemorrhage’, ‘Shock’, ‘Thrombosis and Embolism’, and ‘Ischaemia and Infarction’ in the prescribed textbook General Pathology by J.J. Rippey. This post explores the role of fluid in health and disease, the concept that mechanisms of human disease are the same as the mechanisms of physiological homeostasis, and further examples of the body constantly striving to survive.

I believe the role of fluid in health and disease can be partly summed up by the golden rule of normal and abnormal fluid distribution and function that is in our notes and was discussed in class: ‘a fluid that is meant to move in the body, that does not move, will make the patient susceptible to infection and/or fibrosis’. (Leisegang, 2012) It is a place for me to start with this large subject matter! I think this rule is particularly true for the pathological concept of congestion where there is reduced venous drainage – blood flow is slowed (the fluid that is meant to move in the body) and there is a build up of deoxygenated haemoglobin. As a chronic or severe condition this can lead to oedema because of an increase in hydrostatic pressure, or haemorrhage because of increased permeability of the vessel wall due to anoxia – both of these are also examples of abnormal fluid distribution that will be looked at further. (Rippey, 1994) In researching congestion I found the truly excellent video below, it describes how congestive heart failure affects the rest of the body and beautifully illustrates what I was reflecting on above.

 

nutmeg liver cardiac cirrhosisWith chronic congestion, eventually the organs will show anoxic degeneration, particularly the liver, spleen and lungs. To the left is a macroscopic image of what is called ‘nutmeg liver’ where on the cut surface of the liver the central veins appear red and are surrounded by uncongested liver, yellowish-brown in colour and may show fatty change. (Rippey, 1994) To the right is a microscopic image of a liver with diffuse fibrosis called ‘cardiac cirrhosis’, this is a progression from ‘nutmeg liver’ and shows how chronic hindered blood flow can lead to fibrosis.

pulmonary oedemaIn considering the golden rule mentioned above I thought that it could also be true that when fluid moves in the body, into areas it shouldn’t move into or in volumes it shouldn’t move in, it will also make the patient susceptible to infection and/or fibrosis. The pathological concept of oedema is an example of this, the excessive accumulation of extracellular fluid in the interstitial tissue spaces. (Rippey, 1994) The mechanisms of fluid movement in oedema are physiologically normal but the amount of fluid that moves is pathological. It is natural that extracellular fluid can move into and out of the interstitial and intravascular compartments through the strictly controlled balance of hydrostatic pressure and colloid osmotic pressure – it is a fluid in the body that moves – but when it moves too much oedema will develop. (Rippey, 1994) For example, due to a pathological aetiology such as left-sided heart failure there is peripheral vasoconstriction and a shift of blood to the lungs leading to increased hydrostatic pressure in the pulmonary vessels and the pushing of fluid into the alveolar wall. When lymph drainage fails the fluid is pushed further, into the alveolar space causing transudate oedema. (Rippey, 1994) Soon, the alveolar capillaries become hypoxic leading to increased capillary permeability allowing proteins to escape with the fluid and causing exudate oedema. In this state the lungs are very prone to infection. (Rippey, 1994) And yet the body had to push the fluid out of the vascular system and into the lungs because the hydrostatic pressure in the lung vessels had increased so much. The image above is of “a piece of lung tissue where the alveoli are partly full of oedematous fluid, which is seen as pink staining. There are also red blood cells and some macrophages can be seen. The capillaries of the alveolar septums are dilated and congestive. Also, some typical features of pneumonia can be seen. 40x magnification, HE-staining.” (Solunetti, 2006)

shock Cardiogenic Shock Complicating Acute Myocardial InfarctionI have understood the concept that mechanisms of human disease are the same as the mechanisms of physiological homeostasis to mean that it is possible that when faced with an imbalance in homeostasis the body’s physiological tools/mechanisms for correcting the imbalance may cause a, or worsen the already present, pathological circumstance. I started to understand the implications of this concept when I was studying the pathological concept of shock. A specific example of this is cardiogenic shock with the aetiology of extensive myocardial infarction, or even massive pulmonary embolism, leading to low cardiac output and stroke volume with peripheral pooling of blood. The resulting poor perfusion causes metabolic acidosis and the body’s normal physiological mechanism to deal with metabolic acidosis is dilatation of small vessels to increase blood flow to the area – there is loss of tone and arteriolar vasoconstriction. Unfortunately, this has the effect of causing inadequate venous return and loss of effective circulating volume thus worsening the shock state! (Rippey, 1994) The diagram above shows the aetiologies and consequences of shock. The diagram below that outlines how cardiogenic shock complicates acute myocardial infarction.

I thought that another example of this concept is the formation of a thrombus and/or embolus. Normal thrombus formation is vital to maintain haemostasis if a vessel becomes damaged. The normal physiological mechanisms used in this process can also cause a pathological thrombus if the body is unable to fibrinolyse it and it prevents blood flow within the vessel it is trying to repair, or if it separates from the vessel wall entering circulation as an embolus to impact somewhere else in the circulation, causing a blockage and leading to ischaemia and infarction if it is not dissolved by fibrinolysis fast enough. (Rippey, 1994) Below is a video describing the process of deep vein thrombus formation.

 

blood loss mechanismsThe body always strives to survive, is always actively trying to maintain homeostasis and survival even in the most challenging circumstances. While tackling this subject matter this became clear to me again, particularly when studying the pathological concept of haemorrhage. I found it amazing how much blood can be lost by the body and it will still recover! Importantly, this depends on the amount of blood lost, the speed with which it is lost and the site of haemorrhage (it is far more serious in the brain than if from peripheral circulation). (Rippey, 1994) However, a sudden loss of 20% of blood can be coped with by the body’s compensatory mechanisms! A sudden loss of about 40% will result in death, but if this same amount is lost over 24 hours or so the body will also be able to compensate. The reasons for this are the body’s different mechanisms that it can use in response to blood loss and these are outlined in the diagram above. (Rippey, 1994:91) Another example of the body striving to survive, that I find incredible, is when the body recovers from an infarct. An infarct is caused by complete ischaemia leading to ischaemic necrosis and depending on its severity and site of occurrence infarction is often fatal. But if the infarction does not lead to a major heart attack or stroke then the body is able to recover – it reacts to infarction as it does to any large area of necrotic tissue. (Rippey, 1994) It is remarkable to me how the body can cope with a relatively large area of an organ becoming necrotic, how it can heal, given time, and continue to function. The diagrams below show this process. (Rippey, 1994:119-120)

infarction 1infarction 2

infarction 3

In conclusion, my experience of reading the chapters mentioned at the beginning of the post has been very interesting for me – seeing how the concept that mechanisms of human disease are the same as the mechanisms of physiological homoeostasis  and yet more amazing examples of the body’s ability to survive.  Absorbing and engaging with the subject matter not as separate bits of knowledge to be learned but as a larger concept of fluid in health and disease has been a process and a challenge, as each of these blog posts has been so far, and rewarding in that at the end I realise the information contained here is now firmly in my mind, has been thought about and actively tackled with rather than passively memorised.

 

References

ASKVisualScience, 2010. 3D Medical Animation Congestive Heart Failure. Available at: <http://www.youtube.com/watch?feature=player_embedded&v=3YddwXPWVSc> [Accessed 21 March 2013].

BupaHealth, 2008. How deep vein thrombosis (DVT) forms. Available at: <http://www.youtube.com/watch?feature=player_embedded&v=CETfozL0cQg> [Accessed 21 March 2013].

Leisegang, K., 2012. Hyperaemia and Congestion, NAT311 General Pathology. University of the Western Cape, unpublished.

Rippey, J.J., 1994. General Pathology. Johannesburg: Witwatersrand University Press.

Solunetti, 2006. Pulmonary Edema (OEDEMA Pulmonum) 40x. [online] Available at: <http://www.solunetti.fi/en/patologia/keuhkoodeema_40x/&gt; [Accessed 21 March 2013].

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One thought on “Normal and Abnormal Fluid Distribution and Function

  1. A real good introduction actually – simple, basic, descriptive and to the point!

    Well written and designed. You did look closely at the concepts required. Maybe a little more focus on the physiology/pathology mechanisms relationships.

    Too long unfortunately! Possibly too much on heart failure-congestion-stasis etc.

    In the paragraph on congestion as an example for stasis – you need to link to infection and/or fibrosis, as that example is of my golden rule! You did not illustrate this actually, but rather an example of one mechanism of oedema really….opps, I see one small refernece as the blog continues, but still maybe not enough in light of the start of the paragraph. Is congestion the only concept that could lead to chronic stasis of fluid?

    ‘The mechanisms of fluid movement in oedema are physiologically normal but the amount of fluid that moves is pathological.’ – excellent, yes, but also the lack of fluid moving, as with lymphatics or congestion…. ‘The mechanisms of fluid movement in oedema are physiologically normal but the amount of fluid that moves is pathological’ – again, if it moves too much away from tissue (e.g. dehydration), then what? Not oedema is it?

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