What the blood results are actually telling you
Biochemistry is taught as pathways to be memorised and forgotten, and then every day of a nurse's career a result comes back and somebody has to know what it means. A sodium that has fallen, a potassium that has risen, a glucose that will not settle, a liver test nobody has explained, a kidney function that has drifted over three days. These are not laboratory curiosities; each one describes something happening inside a patient that will shortly show itself at the bedside, and frequently the nurse sees the number before anybody else does. This manual is written backwards from that moment — not the chemistry for its own sake, but enough of it that a result stops being a value to transcribe and becomes information about a person.
A reference range describes where most results from a healthy population fall, which means a small proportion of perfectly well people sit outside it by definition. It is not a boundary between health and disease. Ranges also differ between laboratories, between measurement methods, with age, and in pregnancy, which is why the range printed beside the result is the only one that applies to that result.
A creatinine at the top of the range in somebody whose usual value is at the bottom represents a substantial change, while a result slightly outside the range that has sat there for years usually represents nothing. Looking back at previous results before reacting to a current one is the single most useful habit in this subject and takes a few seconds.
A sample haemolysed by difficult venepuncture raises potassium falsely, a sample taken from an arm receiving fluid is diluted, a delayed sample changes, and a mislabelled sample belongs to somebody else entirely. A result that does not fit the patient should prompt a look at the patient and a question about the sample, not an intervention.
Look at the patient, check when and how the sample was taken, compare with previous results, and escalate with the specific value, the trend and what the patient looks like. Passing on a number without the clinical picture wastes the call, and passing on the picture without the number wastes it equally.
The sodium concentration in blood is largely a statement about how much water the sodium is dissolved in rather than about how much sodium there is. A low sodium usually means too much water relative to salt, and a high sodium usually means too little water. Understanding this reverses most students' intuition and makes the whole topic tractable.
Water follows sodium, so when the concentration outside cells falls, water moves into them — including brain cells inside a skull that cannot expand. This produces confusion, headache, nausea, drowsiness, seizures and, if the fall is rapid, death. The speed of change matters as much as the level, which is why a slowly developed low sodium may be almost silent.
Cells adapt to a low sodium over days, and raising it quickly pulls water back out of them abruptly, causing severe and sometimes irreversible injury. This is one of the clearest situations in medicine where the speed of treatment is the hazard, and it is why correction is deliberately slow, monitored, and never something to be enthusiastic about.
A person with access to water and a working thirst mechanism does not usually become hypernatraemic, so a high sodium points at somebody who could not drink — the very young, the very old, the confused, the immobile, the intubated. It is frequently a statement about care and access rather than about the kidney, which makes it a nursing finding as much as a laboratory one.
Potassium sits mostly inside cells, and the difference across the cell membrane is what allows nerve and muscle to fire. Because the heart is muscle, modest changes in the potassium outside cells disturb its rhythm, which is why both high and low values are treated urgently and why the measurement is repeated so often.
Kidney failure, tissue breakdown from crush injury or burns, acidosis shifting potassium out of cells, and several medicines. A rapidly rising potassium in a patient with failing kidneys is among the more immediately lethal abnormalities in this manual and produces very little warning before the rhythm changes.
Vomiting, diarrhoea, certain diuretics, poor intake, and shifts into cells. Low potassium causes weakness, cramps, constipation and rhythm disturbance, and it frequently occurs alongside a low magnesium, which is why potassium that will not correct despite replacement is a recognised sign that something else needs measuring.
A haemolysed sample releases potassium from the red cells inside the tube, producing a high result in a patient whose potassium is normal. Difficult venepuncture, a small needle, prolonged tourniquet and vigorous shaking all cause it, which makes the technique of taking the sample part of the accuracy of the result.
Blood acidity is held within very narrow limits because enzymes stop working outside them. Chemical buffers act instantly, the lungs adjust within minutes by changing how much carbon dioxide is exhaled, and the kidneys adjust over hours and days. Fast lungs, slow kidneys — that pairing explains most of what this topic contains.
Either acid accumulates in the body, from poor tissue perfusion, uncontrolled diabetes, kidney failure or severe infection, or carbon dioxide is retained because the patient is not moving enough air. The first is usually a whole-body problem and the second is a breathing problem, and distinguishing them determines almost everything about the response.
When acid accumulates, the lungs compensate by blowing off carbon dioxide, producing deep, rapid breathing in a patient whose chest is clear and whose oxygen saturation is normal. Recognising this pattern as compensation for a problem elsewhere is one of the most useful inferences available at a bedside without any equipment.
A patient compensating well can look stable while the underlying problem worsens, and when the compensation fails the deterioration is abrupt. This is why the effort a patient is making is recorded rather than only the result they are achieving, and why a tiring patient is an emergency even when the numbers still look acceptable.
Blood glucose is held within a narrow range by hormones that move it into cells and hormones that release it from stores. Illness, injury, pain and stress all raise it even in people without diabetes, because the body is mobilising fuel, which is why glucose is monitored in acutely unwell patients generally rather than only in those with a diagnosis.
Above a certain level glucose is lost in urine and drags water with it, so the patient passes large volumes and becomes thirsty and dehydrated. Meanwhile cells cannot use glucose, so fat and muscle are broken down for fuel and the person loses weight while eating. Thirst, polyuria and weight loss are one mechanism rather than three symptoms.
Without enough insulin, fat is broken down rapidly and the products are acidic, producing profound dehydration, deep rapid breathing, vomiting, abdominal pain and a characteristic smell on the breath. This is a fluid emergency as much as a glucose one, and the dehydration is frequently what kills.
Glucose falling too low threatens the brain directly and produces sweating, tremor, hunger, confusion, aggression and eventually unconsciousness. It is frequently caused by treatment rather than by disease, it is the metabolic emergency a nurse is most likely to encounter, and it is the one they are most able to reverse immediately.
A measure reflecting average glucose over the preceding weeks exists because a single reading describes one moment. It is not useful for immediate decisions, is unreliable where red cell survival is abnormal such as in some anaemias, and is used for reviewing control rather than for managing a patient in front of you.
A finger-prick meter is accurate enough for routine decisions and less accurate at the extremes, which is precisely where decisions matter most, so a very high or very low reading in an unwell patient is confirmed on a laboratory or blood gas sample rather than acted on alone. Readings are also distorted by poor perfusion, by a cold or oedematous hand, by squeezing the finger hard enough to dilute the drop with tissue fluid, and by sugar left on unwashed skin, which produces a falsely reassuring or a falsely alarming number for entirely mechanical reasons.
Kidney function is estimated from waste products that accumulate when filtration falls, principally creatinine, together with a calculated estimate of filtration rate. These are indirect measures, they lag behind the actual event by a day or more, and a rising creatinine therefore describes damage that has already happened rather than damage occurring now.
Creatinine comes from muscle, so a frail person with little muscle can have severely impaired kidneys and a creatinine that still looks acceptable, while a large muscular person can sit above the range while being entirely well. This is why the calculated estimate adjusts for age and sex and why it is still a poor guide at the extremes of body size.
Urea rises with reduced kidney function and also with dehydration, with bleeding into the gut, and with a high protein intake, and it falls in liver disease. A urea rising out of proportion to creatinine therefore points towards volume depletion or gut bleeding, which is a genuinely useful piece of bedside reasoning.
Both measures lag, and urine output does not. A falling hourly output is the earliest available sign that the kidneys are underperfused, it requires no laboratory, and it is entirely within nursing's control to measure and to total. This is why it is watched so closely in acutely unwell patients.
Impairment arises from inadequate blood reaching the kidney, from damage within it, or from obstruction to urine leaving it, and the first and third are frequently reversible while the second often is not. This matters at the bedside because an obstructed patient can be transformed by drainage, which means a patient whose kidney function is deteriorating should always prompt the question of whether they are passing urine at all rather than only a repeat blood test.
Liver tests answer two separate questions that are frequently confused: is liver tissue being damaged, and is the liver still doing its work. Enzymes released from injured cells answer the first; clotting, albumin and bilirubin answer the second. A patient can have dramatically abnormal enzymes and a liver that is functioning, and the reverse.
One group of enzymes rises mainly when liver cells are injured and another rises mainly when the flow of bile is obstructed. Which group is raised therefore points towards hepatitis of some kind or towards a blockage, and it is one of the few patterns in this manual that genuinely narrows the possibilities on its own.
The liver makes most clotting factors, and they have a short life, so clotting becomes abnormal quickly when synthetic function fails. This makes a clotting test one of the most sensitive indicators of how the liver is actually performing, and it is why it is measured in liver disease rather than only before procedures.
Albumin is made in the liver and falls in liver disease, and it also falls in malnutrition, in inflammation, in kidney disease where it is lost in urine, and with dilution from fluid. A low albumin is therefore a signal to look further rather than a diagnosis, and it explains the swelling seen in several unrelated conditions.
Calcium influences how readily nerve and muscle fire, so a low level produces tingling, cramps, twitching and at the extreme spasm of the airway, while a high level produces thirst, constipation, confusion, stones and bone pain. It is controlled by hormones acting on gut, kidney and bone, which is why disorders of those glands and of the kidney disturb it.
Much of the calcium in blood is bound to albumin and only the unbound portion is active, so a patient with low albumin can have a low total calcium and an entirely normal active level. This is why laboratories report an adjusted value, and why acting on the total figure alone leads to treating something that is not there.
Magnesium is required for many enzyme reactions and for maintaining potassium inside cells, and it is depleted by diarrhoea, poor intake, alcohol and several medicines. A potassium that will not correct despite adequate replacement is the classic sign of an unmeasured low magnesium, and it is a genuinely common and easily missed situation.
When somebody who has eaten very little for a prolonged period begins to eat again, the shift back to using carbohydrate drives phosphate, potassium and magnesium rapidly from blood into cells, and the resulting falls can cause heart failure, seizures and death. This is why feeding after starvation is slow, supervised and monitored with blood tests.
Carbohydrate is the immediate fuel, fat is the store, and protein is building material that the body will burn if nothing else is available. This last point is the clinically important one: a patient not eating enough energy breaks down their own muscle to supply it, which is why they lose strength so quickly during illness.
Enzymes, antibodies, clotting factors, transport molecules, hormones and structural tissue are all proteins, which is why a shortage produces poor healing, poor immunity, easy bleeding and swelling simultaneously. Requirements rise substantially with wounds, burns, infection and surgery, at exactly the time intake usually falls.
Fat supplies more than twice the energy of the other two per gram, carries the vitamins that dissolve in it, and forms part of every cell membrane. Cholesterol is both made by the body and eaten, it is essential rather than simply harmful, and its clinical importance lies in how it is transported rather than in its presence.
Fever, infection, injury, burns and surgery all raise energy and protein requirements substantially, at the same time as appetite falls and patients are repeatedly fasted for procedures. That mismatch is the basic mechanism by which hospital patients become malnourished, and it operates regardless of how well nourished they were on admission.
Iron is required to make haemoglobin, and the amount of oxygen blood can carry depends far more on how much haemoglobin there is than on anything else. A severely anaemic patient can show a perfectly normal oxygen saturation while their tissues are short of oxygen, because saturation measures the proportion of haemoglobin carrying oxygen rather than the quantity present.
Iron is measured in several ways that answer different questions: how much is circulating, how much is stored, and how much capacity remains to carry more. Stores fall before the haemoglobin does, which means deficiency can be identified before anaemia appears, and a normal haemoglobin does not establish that iron is adequate.
The measure of iron stores also rises during inflammation regardless of how much iron is present, so a normal or high value in an unwell patient does not exclude deficiency. This is one of the more common interpretive traps in routine practice and is the reason these results are read alongside markers of inflammation.
Iron from plant sources is absorbed less readily than from meat, is improved by vitamin C taken at the same meal, and is reduced by tea taken with food. Advice naming a nutrient without its partners frequently fails, and this is one of the most commonly missing pieces of information in what patients have been told.
Markers of inflammation rise in infection, in tissue injury, after surgery, in autoimmune disease and in some cancers, which makes them useless for identifying what is wrong and useful for establishing whether something is and whether it is changing. Treating a raised value as evidence of infection specifically is a very common error.
Several enzymes normally live inside particular cells and appear in blood when those cells are damaged, which is why particular patterns point to heart, liver, muscle or pancreas. The timing matters as much as the value, since each rises and falls on its own schedule and a result is interpreted against how long ago the event occurred.
When muscle is crushed or deprived of blood, its contents enter the circulation and damage the kidneys while raising potassium sharply. This is why a patient found on the floor after many hours is not simply dehydrated, and why the period immediately after rescue can be more dangerous than the period before it.
A single inflammatory marker says little; a series over days says whether a patient is improving, static or deteriorating, and frequently does so before the clinical picture changes clearly. This is another instance of the general rule that in this subject the direction of travel outperforms any individual value.
A urine dipstick requires no laboratory, costs almost nothing, and answers several useful questions about glucose, protein, blood, infection and acidity. In settings without a laboratory it is frequently the only biochemistry available, and knowing what each pad can and cannot establish is disproportionately valuable.
Protein in urine indicates that the kidney's filter is leaking, and persistent protein is one of the earliest signs of kidney damage in diabetes and hypertension. A single positive result can follow fever, exercise or infection, so it is repeated rather than acted on, and its persistence is what carries the meaning.
Glucose appears in urine once blood levels exceed what the kidney can reclaim, which makes it a crude indicator of a level already substantially raised. Ketones indicate that fat is being broken down for fuel, which occurs in uncontrolled diabetes and also in prolonged fasting and vomiting.
Dark, scant, concentrated urine in somebody not otherwise unwell is usually a statement about their fluid intake, and it is a statement a nurse can act on directly. In an acutely unwell patient the same finding is a sign that the kidneys are conserving water because perfusion is inadequate, which is a considerably more urgent interpretation.
A sample intended to identify infection is collected so that it is not contaminated on the way out, which means cleaning first and catching the middle of the stream rather than the beginning. A sample drawn from a catheter bag has been sitting at room temperature growing organisms for hours and describes the bag rather than the bladder. Where a full day's collection is required, missing a single void invalidates the whole thing, and explaining that clearly to the patient beforehand is what determines whether the result means anything at all.
A blood gas measures oxygen, carbon dioxide, acidity and, on most machines, several electrolytes and lactate within minutes. Its value is speed: it answers questions about oxygenation, ventilation and acid-base at the bedside while a laboratory sample is still in transit, which is why it is taken in exactly the situations where waiting is not safe.
An arterial sample gives reliable information about oxygenation; a venous one does not, because the oxygen has already been used by tissue. A venous sample remains useful for acidity, carbon dioxide trends, electrolytes and lactate, and it is far less painful to obtain, so knowing which question you are asking determines which sample is appropriate.
Lactate rises when tissue is not receiving enough oxygen for its needs and switches to a less efficient way of making energy. A rising lactate in an unwell patient is therefore a signal that perfusion is inadequate somewhere, and a lactate that falls with treatment is one of the more reassuring things available in an acute situation.
Look at the acidity first to see whether the patient is acidotic or alkalotic, then at carbon dioxide to see whether the lungs explain it, then at the bicarbonate to see whether the kidneys are involved, then at oxygen separately. Taking the numbers in a fixed order prevents the common outcome of staring at four values and concluding nothing.
Most hormone systems are controlled by feedback, so a hormone is interpreted alongside the signal that drives it. A gland can be underactive while the signal pushing it is very high, and that combination says something quite different from both being low. This is why thyroid results come as at least two numbers and why one alone is close to meaningless.
Several hormones follow a daily rhythm or fluctuate with the menstrual cycle, with food, with stress and with illness, which means a sample taken at the wrong moment produces a result that cannot be interpreted. Acute illness disturbs several systems substantially, which is why testing during a critical illness frequently produces figures that mislead.
Thyroid hormone sets the pace at which the body works, so excess produces weight loss, heat intolerance, tremor, fast heart rate and anxiety, and deficiency produces the reverse — weight gain, cold intolerance, slowing, low mood and constipation. Because the symptoms are so general, both are frequently attributed to something else for a long time.
Injury, illness, pain and fear trigger a coordinated hormonal response that raises glucose, retains fluid, increases heart rate and blood pressure, and suppresses some immune function. Much of what is seen in a deteriorating patient is this response rather than the disease itself, and it explains why biochemical results in acutely unwell people are disturbed in predictable directions.
For several common poisonings the decision about treatment depends on the interval since ingestion rather than on how unwell the person currently looks, because the damage develops hours later while the patient still appears well. Establishing when, not only what, is therefore the critical piece of information, and it is usually obtained by whoever is talking to the patient or the family.
Some of the most dangerous overdoses produce almost no symptoms in the first hours. A patient who looks entirely fine may already have taken a lethal amount, and treating apparent wellbeing as reassurance is the error that recurs in every review of such deaths. This is a situation where the history outweighs the examination.
Certain poisonings are detected biochemically by an unexplained acidosis, or by a difference between the measured components of the blood and what the known substances account for. A nurse is not expected to calculate this, but knowing that an unexplained severe acidosis in somebody who may have ingested something is a specific and urgent pattern is worth having.
Many presentations follow deliberate self-harm, and the person will be assessed psychiatrically as well as medically. How they are spoken to during the physical treatment affects whether they engage with the rest, and hostility at this point is both common and known to reduce the likelihood of seeking help next time.
A glucose meter, a urine dipstick, a haemoglobin meter, a pregnancy test and increasingly rapid tests for several infections can be used anywhere with no power and little training. In much of the world these are the whole of available biochemistry, and a nurse who understands their limits can extract a great deal from very little.
Meters drift, strips expire, heat and humidity degrade reagents, and a device that has never been checked against a known sample may be confidently wrong for months. Recording lot numbers, storing strips as specified and running whatever control the manufacturer provides are not bureaucracy; they are the only thing standing between a device and a wrong decision.
A negative rapid test has a different meaning from a negative laboratory test, because rapid tests trade accuracy for speed and portability. Knowing roughly how often a particular test misses a case determines whether a negative can be trusted in a patient who looks unwell, and the answer is frequently that it cannot.
Where testing is limited, assessment, history and observation do more of the work, and a nurse's description of a patient becomes the principal evidence. This is not a lesser form of practice; it is the situation most of the world's nursing is conducted in, and being good at it is a skill rather than a compromise.
The majority of laboratory errors occur in the steps around the test rather than in the analysis: the wrong patient, the wrong tube, an inadequate volume, contamination from a drip, delay in transport, and incorrect storage. The analytical stage is the most controlled part of the process and the least likely to be responsible for a wrong result.
Blood taken from an arm receiving intravenous fluid is diluted by that fluid and may contain enormous amounts of whatever is being infused, producing results that look like a metabolic catastrophe. Taking the sample from the other arm, and recording which arm was used, prevents a specific and entirely avoidable category of alarm.
Tubes contain different additives, they are filled in a defined order to prevent carry-over between them, they require a specified volume to keep the ratio of blood to additive correct, and they need gentle inversion rather than shaking. An underfilled clotting tube produces a wrong result reliably, and it is one of the most frequent reasons samples are rejected.
Every year samples are discarded unlabelled or mislabelled, and each one is a patient sampled again or treated on somebody else's result. Labelling at the bedside from the patient's own stated identity, immediately after taking the sample, is the whole defence, and it fails whenever tubes are carried to a desk to be labelled there.
Intravenous fluids differ in what they contain and therefore in where they go. A fluid whose dissolved content matches the body's stays mainly in the circulation and the spaces between cells; one that is effectively water once the sugar in it is used distributes through the whole body including into cells. This single difference determines whether a litre given expands the circulation usefully or mostly ends up somewhere it was not wanted.
Giving large volumes of a fluid that behaves like water lowers the sodium concentration and can cause exactly the brain swelling described earlier in this manual, particularly in children and after surgery when the body is already retaining water. Giving large volumes of a salt-rich fluid loads sodium and chloride and can produce its own acid disturbance. Neither is a neutral act.
Fluids are given for three different reasons: to cover ordinary daily losses in somebody not drinking, to replace what is being lost abnormally through vomiting, diarrhoea, drains or fever, and to restore circulating volume in somebody who is shocked. The volume, the speed and the composition differ for each, and confusing the three is the commonest prescribing error in this area.
Fluid is prescribed once and administered over many hours by somebody watching the patient throughout. Rising breathlessness, new crackles, swelling, a falling saturation, a rising weight or an output that does not match the input are all seen at the bedside long before anyone reviews the prescription, and saying so is the intervention.
A fluid balance chart that is filled in but never added up is a record of nothing, and an untotalled chart is one of the most widespread failures in hospital nursing. Totalling during the shift rather than reconstructing at the end, and reading the running balance as a trend, is what turns the paperwork into information.
A single abnormal result is frequently uninterpretable; a pattern across several usually is not. A raised urea with a normal creatinine, concentrated urine and a fast pulse describes volume depletion. A low sodium with low potassium in somebody vomiting describes gut losses. Learning to read two or three results together is what converts this subject from memorisation into reasoning.
The first test of any result is whether it matches the person in front of you. A potassium incompatible with life in somebody sitting up eating breakfast is a sample problem until proved otherwise, and a normal set of results in somebody who looks seriously unwell is a reason to keep looking rather than to be reassured.
A patient with long-standing kidney disease has their own baseline, and a value that would be alarming in somebody else may be unchanged for them. Checking what this person's results usually look like before reacting is the same habit as checking the trend, and it prevents both unnecessary alarm and missing a real change.
A useful handover of a result gives the value, the trend, when the sample was taken, what the patient looks like, and what has been done. A number passed on alone generates a question rather than a decision, and a decision made without the clinical picture is made on incomplete information that somebody had and did not pass on.
Almost every chemical reaction in the body would proceed far too slowly to sustain life without an enzyme to speed it up, and each enzyme works within a narrow range of temperature and acidity. This is the underlying reason the body defends its temperature and its acidity so tightly, and why a patient who becomes very cold or very acidotic deteriorates across every system at once rather than in one.
Most vitamins act as partners to enzymes rather than as fuel or building material, which is why they are needed in tiny amounts and why their absence produces dramatic illness in somebody eating plenty of food. It also explains why deficiency and adequate calorie intake coexist routinely, and why a well-fed-looking patient can be seriously deficient.
Vitamins that dissolve in fat are stored, so deficiency takes months to appear and excess can accumulate to harmful levels. Those that dissolve in water are barely stored and are lost in urine, so deficiency can develop within weeks in somebody not eating and excess is usually excreted. This distinction explains both why some deficiencies appear quickly in hospital and why some supplements can be taken to excess.
One water-soluble vitamin is depleted rapidly in heavy alcohol use and in prolonged poor intake, and its deficiency can cause sudden, permanent brain injury. The clinically important point for a nurse is that this is preventable, that the risk rises when carbohydrate is given to a depleted person, and that the order in which things are given therefore matters.
Students resent memorising metabolic pathways and largely forget them, which is reasonable. What survives usefully is the shape: that fuel is converted through a small number of common routes, that the routes require oxygen at the end, and that when oxygen is short the body switches to a less efficient path that produces acid. That single fact explains lactate, explains shock, and is worth more than any diagram.
Sodium and its effect on the brain, potassium and the heart, the acid-base pattern of a deteriorating patient, glucose emergencies in both directions, and the meaning of a rising creatinine. All of it is interpretation attached to a short clinical scenario rather than chemistry for its own sake.
Treating a reference range as a boundary between health and disease; reading a normal saturation as adequate oxygen delivery in anaemia; reacting to a potassium from a haemolysed sample; assuming a raised inflammatory marker means infection; correcting a low sodium quickly because it is very low.
Take each common result and write one sentence on what raises it, one on what lowers it, and one on what the patient looks like in each case. That produces a page you can actually use on a ward, which memorising pathways does not.
Look at the previous results before reacting to this one. Look at the patient before believing a number that does not fit. Total the fluid chart. Ask how the sample was taken when the potassium is surprising. These four take almost no time and prevent most of the errors in this subject.