Flashcards in Anaesthetics - Fluid management Deck (69):
How much is total body water?
Total body water is approximately 60% of body weight
In who is total body water largest?
TBW is highest in newborns and adult males and lowest in adult females and in adults with a large amount of adipose tissue
What are the body fluid compartments?
TBW is divided into intracellular fluid (ICF) and extracellular fluid (ECF).
ICF is two thirds of TBW or 40% of body weight.
ECF is one third of TBW or 20% of body weight, and is composed of interstitial fluid and plasma.
How is the extracellular fluid further divided?
ECF is further divided into interstitial fluid (3/4 ECF) and plasma (1/4).
The composition of the interstitial fluid is the same as that of plasma, except that it has less protein. Thus interstitial fluid is an ultrafiltrate of plasma.
The major plasma proteins are albumin and globulins.
What are the major cations and anions of the ECF and ICF?
ECF - Na+, Cl- and bicarbonate
ICF - K+, Mg+, protein and organic phosphate
What is the 60-40-20 rule?
This helps to remember the relative sizes of each fluid compartment relative to body weight.
TBW is 60% of total body weight.
ICF is 40% of total body weight
ECF is 20% of total body weight (3/4 interstitial, 1/4 plasma)
What is osmosis?
Osmosis is the passive movement of solvent (water) across a semi-permeable membrane to a region of higher concentration of solute.
The ECF and ICF have different solute of import. Osmosis is the process by which fluid equilibrates between the body fluid compartments.
The rate of solvent movement depends on the number of particles of solute rather than the molecular mass.
What is effective osmotic pressure?
Osmotic pressure is the hydrostatic pressure that must be applied to the solution of greater concentration to prevent water movement across a semi-permeable membrane separating the two aqueous solutions of unequal concentration.
So, the movement of solvent by osmosis can be considered as moving down an osmotic pressure gradient.
What is the difference between osmolaRity and osmolaLity?
Osmolarity = the number of osmoles per litre
Osmolality = the number of osmoles per Kg
These two terms are often used interchangeably because 1L of water weighs 1Kg. However, they do not mean the same thing when discussing solvents other than water.
Osmotic activity is expressed in osmoles - 1 osmole of solute dissolved in 1Kg of solvent has an osmolality of 1 osmol/L
How is plasma osmolality calculated? What is a normal value? Why is it important?
Plasma osmolality = 2Na + Glucose + Urea = 290 mosmol/Kg
At a steady state, ECF osmolality = ICF osmolality. To achieve this, water moves by osmosis between the ECF and ICF compartments. It is assumed that solutes such as NaCl and mannitol do not cross cell membranes and are confined to the ECF.
Notice that protein concentration does not determine plasma osmolality. That is because we are interested in osmotic pressure not colloid oncotic pressure.
What is tonicity?
Tonicity refers to the osmolality of a solution relative to plasma. There are 3 different solutions under this definition.
1) Hypotonic - e.g. distilled water
- lower osmolality compared to plasma
- water moves from plasma into cells (causing red cell lysis)
2) Hypertonic - e.g. twice normal saline
- causes red cells to shrink
3) Isotonic - e.g. 0.9% normal saline
- identical osmolality to plasma so no fluid shift
What are isotonic fluid disorders?
Disorders where there is isotonic loss or addition of fluid.
1) Isotonic fluid loss:
= net isotonic loss of Na+ and water
- POsm and serum Na+ are normal (hypovolaemic normonatraemia)
- No osmotic gradient or fluid shift exists between compartments; ECF volume contracts, ICF unchanged
- signs of volume depletion are present
- e.g. adult diarrhoea, secretory type
- Rx: infusion of normal saline
2) Isotonic fluid gain
= net isotonic gain of Na+ and water
- POsm and serum Na+ are normal (hypervolaemic normonatraemia)
- No osmotic gradient or fluid shift; ECF volume expands, ICF unchanged
- pitting oedema and body cavity effusions may be present
- e.g. excess infusion of normal saline
What are hypotonic fluid disorders?
These are disorders where the underlying pathology makes the plasma hypotonic (decreased osmolarity). As a result, an osmotic gradient is present so fluid shifts into the ICF compartment (expands). HYPOnatraemia is always present:
- hypertonic loss of sodium (more sodium is lost relative to water so osmolarity decreases)
- gain of pure water
- hypotonic gain of sodium (more water is gained relative to sodium)
What causes a hypertonic loss of sodium?
This is net loss of sodium in excess of water (more sodium is lost than water) - i.e. a hypotonic fluid disorder
POsm and serum Na+ are decreased (hypovolaemic hyponatraemia)
ECF volume cotracts; ICF volume expands
Signs of volume depletion are present
e.g. thiazide diuretics, Addison's disease, 21 hydroxylase deficiency (loss of mineralocorticoids)
Rx: infuse normal saline
What is central pontine myelinolysis?
In an alcoholic, rapid i.v. correction of hyponatraemia with saline may result in central pontine myelinolysis, an irreversible demyelinating disorder. However, as a general rule, all i.v. replacement of sodium containing fluids should be given slowly over the first 24 hours regardless of the underlying cause.
What causes gain of pure water?
This is a net gain in water.
POsm and serum Na+ are decreased (euvolaemic hyponatraemia)
Expansion of both ICF and ECF compartments
Normal skin turgor, because total body Na+ is normal
e.g. SIADH, psychogenic polydipsia
Rx: water restriction
What causes hypotonic gain of sodium?
This is a net gain of water in excess of sodium (more water is gained than sodium)
POsm and serum Na+ decrease (hypervolaemic hyponatraemia)
Expansion of both compartments
This type of fluid gain produces pitting oedema and body effusions associated with Starling force alteration, e.g.
- RHF with an increase in venous hydrostatic pressure
- Cirrhosis and nephrotic syndrome with a decrease in plasma oncotic pressure
Rx: restrict water and sodium, diuretics
What are hypertonic fluid disorders?
An increase in POsm is most often due to hypernatraemia or hyperglycaemia. In these disorders and osmotic gradient exists so water shifts from the ICF to the ECF compartment causing expansion. Hypernatraemia is always a feature.
What causes a hypotonic loss of sodium?
Definition - net loss of water in excess of Na+ (more water is lost than Na+)
Both POsm and serum Na+ increase (hypovolaemic hypernatraemia)
Both compartments contract
Signs of volume depletion are present
e.g. sweating, osmotic diuresis (e.g. glucose, mannitol), diarrhoea (osmotic type - laxatives), diuretics and vomiting
Rx: isotonic saline if hypotension is present and then switch to oral replacement or more hypotonic Na+ containing i.v. fluids
What causes loss of pure water?
There is net loss of water.
Both POsm and serum Na+ are increased (euvolaemic hypernatraemia)
Both compartments are contracted
- ECF contraction is mild because there is no loss of Na+
e.g. diabetes insipidus (loss of ADH or refractory ADH), insensible water loss (e.g. fever)
What is hypertonic gain of sodium?
Definition - net gain of Na+ in excess of water (most sodium is gained than water)
Both POsm and serum Na+ increase (hypervolaemic hypernatraemia)
ECF compartment expands; ICF contracts
Pitting oedema and body cavity effusions may be present
e.g. infusion of sodium bicarbonate or Na+ containing antibiotics
What are the normal maintenance fluid requirements of a nil by mouth patient?
Depends on the patients weight...
Water = 1.5ml/kg/hour
Na+ = 1-2mmol/kg/24 hour
K+ = 0.5-1mmol/kg/24 hour
Urine output should be >0.5ml/kg/hour
These values are important to know in order to work out what a patient needs for maintenance and how much of the available fluids to give to match this.
Overall requirements = MAINTENANCE + REPLACEMENT
What is Hartmann's solution? When is it best used?
Hartmann's solution is the most physiological (i.e. similar to plasma) meaning it is very good for replacing plasma loss e.g. during surgery or GI losses. However, this does not mean that it is good for maintenance fluids, as 3L of Hartmann's solution over 24 hours would give 3 times too much Na+ (1L contains 131mmol Na+) and not enough K+ (1L contains only 5mmol when the 24 hour requirement is 35-70mmol).
What is the composition of normal saline?
Saline is much more physiological than dextrose as it contains salts, but not as physiological as Hartmann's solution. Also be warned, too much chlorine will give a hyperchloraemic acidosis and also cause renal vascoconstriction. 0.9% NaCl contains 154mmol of Na and Cl.
What is 5% dextrose?
5% dextrose contains no salt but 50g of glucose. It is given instead of pure water (the glucose is used up) to maintain osmolarity. The glucose content plays no role whatsoever. It is used for maintenance to give water when needed with no electrolytes. It has to place for replacing plasma/ blood loss because it is not physiological. Too much too quickly can cause hyponatraemia.
What id dextrose-saline?
This contains some dextrose and some sodium chloride. It is a good solution for maintenance fluids because, given at the correct rate for the patients weight, it contains approximately the correct requirements of sodium. But it should not be used to replace plasma/ blood loss because it is not physiological.
How should hydration be assessed?
Hydration status should always be assessed prior to prescribing fluids. It is important to assess blood pressure, capillary refill time, fluid balance charts, skin turgor and weight.
How does 0.9% NaCl distribute between the body fluid compartments?
The fluid distributes between the intravascular and extravascular compartments according to the ratio of their relative concentrations in the extravascular fluid:
- 25% of the volume will go to the intravascular compartment
- 75% will go to the interstitial compartment
If a patient lost 1L of blood, what is the equivalent volume of normal saline that would be required to replace it?
As only 25% of administered normal saline enters the vascular compartment 4L will be required to expand the plasma sufficiently to replace the fluid lost.
How does 5% dextrose distribute between the body fluid compartments?
Dextrose is rapidly metabolised by the liver to produce pure water. It is isotonic with plasma. As such 2/3 goes to the intracellular fluid, 1/3 goes to the extracellular fluid, and of this 1/3 approximately 80ml (of a 1000 given) will stay in the vascular compartment.
What are colloids?
Colloids contain large molecules that cannot easily pass across the capillary membrane. Colloids exert and osmotic force across the capillary membrane drawing fluid from the interstitial to the intravascular compartment.
Human albumin solution
Drawbacks of colloids include cost and risk of allergy and anaphylaxis.
What is the effect of colloid administration?
When colloids are administered, all of the fluid remains in the intravascular compartment (i.e. 1L of colloid expands the vascular compartment by 1L). An important point is that although crystalloid solutions eventually redistribute, initially when they are rapidly infused they do cause expansion of the plasma volume. So in an emergency with a volume depleted patient, DO NOT wait until the ideal fluid becomes available give whatever is available for haemodynamic stability.
What are the sources of fluid gain in a patient?
Water released from metabolism (about 400ml per day)
In a healthy adult male with no insensible losses, maintenance requirements are about 2 to 2.5L per day (e.g. 1.5L in urine and 500-800ml insensible losses).
What are physiological sources of fluid loss?
- healthy person will pass approximately 1ml/kg/hr. This roughly equates to 1700ml per day in a 70kg adult.
- in fluid replacement you should aim for a minimum urine output of 0.5ml/kg/hr
- losses are normally minor
- form part of the insensible losses (along with skin and lungs) that equates to 0.5L per day
- but these losses can be substantial in patients with diarrhoea, vomiting and skin lesions or drains, fistulae and stomata
- you should quantify and document theses losses
- e.g. bleeding, burns
If a patient is sweating, febrile or tachypnoeic then insensible losses should be doubled
What electrolytes are lost in sweating?
Sweat contains a large amount of sodium and chloride ions, so sweating can result in sodium loss.
What is the composition of ileal and colonic fluid?
Ileal fluid contains:
- Na+ = 140mmol
- K+ = 5mmol
- Cl- = 105mmol
- bicarb = 60mmol
Colonic fluid contains
- Na+ = 140mmol
- K+ = 5mmol
- Cl- = 85mmol
- bicarb = 60mmol
This is important because diarrhoea/ increased stoma output can be a cause of sodium, potassium and bicarb loss. These can be difficult to measure because of the different types of fistula/ stoma types.
What is the composition of gastric fluid?
Gastric juice contains a large amount of sodium, chloride and potassium. Vomiting can therefore cause a depletion in sodium, chloride and hydrogen ions (and thus leads to the picture of hypochloraemic metabolic alkalosis, sometimes accompanied by mild hypokalaemia).
What features would point towards hypovolaemia on a volume assessment?
Decreased skin turgor
Dry mucous membranes
Prolonged cap refill
Tachycardia (may not be evident in patients taking beta blockers)
What are the signs of hypervolaemia on a volume assessment?
Cough +/- white frothy sputum
Fluid accumulation within serosal cavities
Pulmonary oedema, dyspnoea
S3/S4 heart sounds
What is shock?
Shock can be defined as organ hypoperfusion that results in impaired oxygenation. There are many different types of shock and management differs from one type to the other.
What is distributive shock?
This results in a relative hypovolaemia. Causes include sepsis, anaphylaxis, and neurogenic shock.
What is hypovolaemic shock?
Shock is due to excessive loss of sodium containing fluid (e.g. blood, sweat) causing hypotension and multiorgan failure.
Massive blood loss is MCC, loss of >20% of ECF can result in shock.
There is NO initial drop in haemoglobin and haematocrit because there is an equal loss of RBCs and plasma. Plasma is replaced first with fluid fro the interstitial space, this uncovers the RBC deficit within hours to days and produces a dilutional anaemia. Infusion of 0.9% saline immediately uncovers the deficit. An increase in peripheral blood reticulocytes (indicators of effective bone marrow erythropoiesis) begins in 5 to 7 days.
What is the pathophysiology of hypovolaemic shock?
1) Decreased cardiac output
- due to decreased volume of blood
2) Decreased left ventricular end-diastolic pressure (LVEDP)
- loss of blood volume entering the left ventricle decreases LVEDP
3) Increased peripheral vascular resistance
- due to vasoconstriction of arterioles from cetecholamines, ADH, and angiotensin II, which are released in response to decreased CO
4) Decreased mixed venous oxygen content
- measured in the right heart by a Swan-Ganz catheter
- MVO2 indicates the degree of extraction of O2 from the blood delivered to tissue
- in hypovolaemic shock, decreased blood flow through the microcirculation leads to increased extraction of O2 from the blood and decreased MVO2
What are the grades of hypovolaemic shock?
Grade I - 15% of blood loss
- Mild resting tachycardia, slightly delayed cap refill at 3 seconds
Grade II - 15-30% blood loss
- cool peripheries, tachycardia, decreased pulse pressure, delayed cap refill
- may have a catecholamine driven increase in diastolic BP
Grade III - 30-40%
- marked tachycardia and tachypnoea, decreased systolic BP
- very narrow pulse pressure, oliguria, low volume pulse, postural drop of 20-30mmHg, confusion/ agitation
Grade IV - 40-50%
- low GCS or unconscious, minimal or no urine output
- thready pulse, very tachycardic, very low or immeasurable BP, cold skin
What type of acid base disturbance can occur in hypovolaemic shock?
Increased anion gap type of metabolic acidosis due to lactic acidosis from anaerobic glycolysis
What is cardiogenic shock?
This is a relative or absolute reduction in cardiac output due to a primary cardiac disorder. MCC AMI - other causes include myocarditis, acute valvular dysfunction (e.g. infective endocarditis) and cardiomyopathy
What is the pathophysiology of cardiogenic shock?
1) Decreased CO
- due to decreased force of contraction in the infarcted left ventricle
2) Increased LVEDP
- because CO is decreased, blood accumulate in the left ventricle causing an increase in pressure and volume
3) Increased PVR
- same mechanism as hypovolaemic shock
4) Decreased MVO2
- same mechanism as hypovolaemic shock
Patients with cardiogenic shock may have raised JVP or cardiac arrhythmias.
What is obstructive shock?
Obstructive shock occurs when there is physical impedance to blood flow. Causes include massive PE and cardiac tamponade. The aim is to remove obstruction quickly (pericardiocentesis/ anticoagulation).
What is septic shock?
Microbes invade the bloodstream (septicaemia)
Most common site of infection leading to sepsis is the lungs, then blood, abdomen, urinary tract and skin.
What microbial pathogens are responsible for septic shock?
Gram positive organisms - 65% of cases, coagulase negative Staph and Staph aureus most common
Gram negative organisms - 25% of cases, E.coli most common
Systemic fungi - 9% of cases, Candida species most common
What is the pathogenesis of septic shock?
Lipoteichoic acid in gram positive pathogens cause the release of tumour necrosis factor (TNF) and interleukin (IL-1).
Endotoxins (lipopolysaccharide) are released by gram negative bacteria. They activate macrophages causing release of IL-1 and TNF. IL-1 produces fever, TNF damages endothelial cells causing them to release vasodilators such as NO and prostaglandin. Endotoxins activate the alternate complement pathway. Anaphylotoxins (C3a and C5a) are produced, which stimulate mast cell release of histamine (vasodilator). Endotoxins damage tissue, causing the release of tissue thromboplastin. It activates the extrinsic coagulation system producing DIC. Endotoxins activate neutrophil adhesion molecules causing the circulating pool to become a marginating pool (produces neutropenia).
What is the pathophysiology of septic shock?
1) Initial increase in CO
- due to rapid blood flow through dilated PVR arterioles causing increased venous return of blood to the right heart
2) Decreased LVEDP
- decreased compliance of the left ventricle (stiff ventricle)
3) Decreased PVR
- vasodilation of PVR arterioles
4) Increased MVO2
- tissues are unable to extract oxygen, because of increased blood flow through the microcirculation related to dilated PVR arterioles
Do all forms of shock respond well to fluids?
No. Hypovolaemic and distributive shock respond well to fluids because the pain pathology is loss of effective circulating volume.
Cardiogenic and obstructive shock respond poorly. The heart cannot deal with the increased fluid load and this exacerbates the decreased cardiac output. In cardiogenic shock the extra fluid leads to pulmonary oedema (if the left ventricle is involved).
How should you assess a patient who is in shock but the aetiology is unknown?
Perform A to E assessment:
- Airway: patent? adjuncts?
- Breathing: resp rate, saturation, ABG (gives instant U&E values as well as checking oxygenation), VBG, CXR, give oxygen if sats low
- Circulation: ECG, check cap refill, HR, BP, cardiovascular examination, bloods (FBC, U&E, CRP, renal function), take cultures if pyrexial (2 sites), fluids might be needed if the capillary refill time is elevated or the patient is hypovolaemic
- Disability: GCS? Intubation required?
- Exposure: look at dressings, sources of bleeding, abdominal examination
How is base deficit useful in the shocked patient?
Base deficit is a way of measuring fluid response to resuscitation. This is essentially a surrogate marker of organ perfusion. It is important to remember that large volumes of 0.9% sodium chloride, may result in hyperchloraemic metabolic acidosis; this may paradoxically worsen the base deficit when resuscitating a shocked patient.
What are the complications of fluid overload?
1) Dilutional hyponatraemia - treat with appropriate fluid restriction
2) Pulmonary oedema - think about getting ITU support for patients with cardiogenic pulmonary oedema
What medical therapies can be used to treat fluid overload?
1) Stop i.v. fluids - essential to avoid further deterioration. Fuorsemide can be given as a bolus or infusion. It causes diuresis and vasodilatation
2) Sublingual nitrates - causes a reduction in preload, the effects of which can be seen in 5 minutes
3) i.v. nitrate - provides excellent and titratable pre and afterload reduction. BP monitoring is essential as hypotension is an indication for stopping the infusion
4) CPAP - improves gas exchange whilst reducing pre and afterload
How should fluids be prescribed in post operative patients?
K+ is intracellular and levels can increase due to cell lysis during surgery. Hence, if K+ is >4.5mmol/L, omit it for 24 hours. If K+ is normal/ low you can give a smaller amount - e.g. 40mmol/24 hours.
Some centres advise against using normal saline immediately after surgery because of the sodium retention mechanisms triggered by surgery and sodium containing substances used in theatre. Too much NaCl can result in oedema, hyperchloraemic acidosis, increased kidney load, increased post operative complications and GI problems. These centres advise dextrose saline.
How should fluid be replaced is sepsis?
Sepsis causes intravascular depletion due to plasma loss by leaky capillaries and vasodilatation. Replace fluid with crystalloid - e.g. Hartmann's - but avoid too much sodium and chloride. The patient may need inotropes and ITU support.
How should fluids be replaced in heart failure?
HF patients are prone to pulmonary oedema so there fluid needs to be monitored carefully. Requirements are usually no more than 2L/24 hours. If overload develops then restrict fluids, give furosemide and do daily weights. BUT, if a patient as low SBP and a low urine output who is at risk of LVF you MUST examine them as there are 2 opposite causes for this clinical picture:
1) dehydration - they may just be fluid deplete (give fluids)
2) LVF and overload - they may be in LVF which causes a low SBP and hence low urine output. Check for signs of fluid overload and give diuretics.
How should fluids be replaced in alcoholics?
MUST give Pabrinex before giving any 5% dextrose (even if hypoglycaemic). It can precipitate Korsakoff syndrome.
What is red cell concentrate?
Used to increase red blood cell mass in patients with anaemia and in acute blood loss. ABO compatability with the patient is essential.
Used to treat and prevent bleeding due to thrombocytopaenia.
= Fresh Frozen Plasma
Used to replace coagulation factors
Obtained from plasma and contains proteins including fibrinogen, factor VIII and vWF. It is used to replace fibrinogen.
Outline a fluid strategy you can use to give a patient their daily requirement of electrolytes
The traditional method is to give "one salty, two sweet"
This could be 2L of 5% dextrose + 20mmol K+ (each bag over 8 hours) + 1L 0.9% NaCl (over 8 hours).
Note. This is only acceptable for a large patient, because it gives more water and more sodium than normally required. For an average person it is better to give:
1L 5% dextrose + 20mmol K+ (over 10 hours)
1L 5% dextrose + 20mmol K+ (over 10 hours)
500ml dextrose-saline (over 4 hours)
Remember that this is for maintenance fluids and does not include any losses.
What is red cell incompatibility?
There are 4 different ABO groups, determined by whether or not an individuals red blood cells express A or B antigens. Healthy individuals have antibodies directed against the A or B antigens that are not expressed on their own cells. If red cells of an incompatible ABO group are transfused, the patients antibodies bind to the transfused cells, leading to red cell haemolysis. This is the main cause of an acute transfusion reaction and can give rise to DIC, renal failure and death.
What is rhesus compatibility?
About 15% of Caucasians lack the Rhesus D red cell antigen ("Rhesus negative"). IgG antibodies to RhD positive red cells are produced if such cells enter the circulation of an RhD negative individual via fetomaternal haemorrhage during pregnancy. During a subsequent pregnancy with RhD positive fetus, these antibodies can cross the placenta and cause haemolytic disease of the newborn and severe neurological disease. Administration of anti-RhD immunoglobulin (anti-D) after delivery blocks the immune response to the RhD antigen and prevents development of Rhesus antibodies in RhD negative women.