BLOOD GAS ANALYSIS

DR SRINIVAS SMD, DNB, FRCP, FNB (CCM), EDIC

CONSULTANT AND HEADDEPARTMENT OF CRITICAL CARE

CARE HOSPITALSBANJARA HILLS

BASIC MECHANISMS

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RESPIRATORY COMPENSATORY MECHANISMS• Works within minutes to control pH; maximal in 12-24

hours• Only about 50-75% effective in returning pH to normal• Excess CO2 & H+ in the blood act directly on respiratory

centers in the brain• CO2 readily crosses blood-brain barrier reacting w/ H2O to

form H2CO3

• H2CO3 splits into H+ & HCO3- & the H+ stimulates an increase

or decrease in respirations

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RENAL COMPENSATORY MECHANISMS

• Don’t work as fast as the respiratory system; function for days to restore pH to, or close to, normal

• Regulate pH through excreting acidic or alkaline urine; excreting excess H+ & regenerating or reabsorbing HCO3

-

• Excreting acidic urine decreases acid in the EC fluid & excreting alkaline urine removes base

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H+ elimination & HCO3-

conservation

TERMINOLOGY OF ACID-BASE DISORDERS

• The definitions of the terms used here to describe acid-base disorders are those suggested by the Ad-Hoc Committee of the New York Academy of Sciences in 1965.

• Though this is over 45 years ago, the definitions and discussion remain valid today.

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BASIC DEFINITIONS• Acidosis - an abnormal process or condition which would lower arterial pH

if there were no secondary changes in response to the primary aetiological factor.

• Alkalosis - an abnormal process or condition which would raise arterial pH if there were no secondary changes in response to the primary aetiological factor.

• Simple (Acid-Base) Disorders are those in which there is a single primary aetiological acid-base disorder.

• Mixed (acid-Base) Disorders are those in which two or more primary aetiological disorders are present simultaneously.

• Acidaemia - Arterial pH < 7.36 (ie [H+] > 44 nM )

• Alkalaemia - Arterial pH > 7.44 (ie [H+] < 36 nM )ABG 2013

THE DISORDERS• The 4 simple acid base disorders are:

• Respiratory acidosis

• Respiratory alkalosis

• Metabolic acidosis

• Metabolic alkalosis.

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METABOLIC ACIDOSIS

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RESPIRATORY ACIDOSIS

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RESPIRATORY ALKALOSIS

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SUMMARY OF COMPENSATORY MECHANISMS

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THE ANION GAP

• The term anion gap (AG) represents the concentration of all the unmeasured anions in the plasma.

• AG is calculated from the following formula:

Anion gap = [Na+] - [Cl-] - [HCO3-]

• Reference range is 8 to 16 mmol/l.

• The [K+] is low relative to the other three ions and it typically does not change much so omitting it from the equation doesn’t have much clinical significance.

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MAJOR CLINICAL USES OF THE ANION GAP

• To signal the presence of a metabolic acidosis and confirm other findings

• Help differentiate between causes of a metabolic acidosis: high anion gap versus normal anion gap metabolic acidosis.

• In an inorganic metabolic acidosis (eg due HCl infusion), the infused Cl- replaces HCO3 and the anion gap remains normal.

• In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not normally measured. This means that the AG is increased.

• To assist in assessing the biochemical severity of the acidosis and follow the response to treatment

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HYPOALBUMINAEMIA CAUSES A LOW ANION GAP

• Albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. Every one gram decrease in albumin will decrease anion gap by 2.5 to 3 mmoles.

• A normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis.

• This is particularly relevant in Intensive Care patients where lower albumin levels are common. A lactic acidosis in a hypoalbuminaemic ICU patient will commonly be associated with a normal anion gap.

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THE DELTA RATIO

• This Delta Ratio is sometimes useful in the assessment of metabolic acidosis.

• The Delta Ratio is defined as: Delta ratio = (Increase in Anion Gap / Decrease in bicarbonate)

• The delta ratio quantifies the relationship between the changes in the Anion Gap and the bicarbonate levels.

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THE DELTA RATIO

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THE URINARY ANION GAP

• The cations normally present in urine are Na K+, K+, NH4+, Ca++ and Mg++.

• The anions normally present are Cl-, HCO3-, sulphate, phosphate and some organic anions.

• Only Na+, K+ and Cl- are commonly measured in urine so the other charged species are the unmeasured anions (UA) and cations (UC).

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THE URINARY ANION GAP

• Urinary Anion Gap = ( UA - UC ) = [Na+]+ [K+] - [Cl-]

• The urinary anion gap can help to differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.

• If the acidosis is due to loss of base via the bowel then the kidneys can response appropriately by increasing ammonium excretion to cause a net loss of H+ from the body.

• The UAG would tend to be decreased, That is: increased NH4+ (with presumably increased Cl-) => increased UC =>decreased UAG.

• If the acidosis is due to loss of base via the kidney, then as the problem is with the kidney it is not able to increase ammonium excretion and the UAG will not be increased.

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OSMOLAR GAP

• Calculated osmolarity = (1.86 x [Na+]) + [glucose] + [urea] + 9

• Calculated osmolarity = (1.86 x [Na+]) + glucose/18 + BUN/2.8 + 9

• Calculated osmolarity = ( 2 x [Na+] ) + glucose/18 + BUN/2.8 + ethanol/4.6

• Osmolar gap = Osmolality - Osmolarity

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ARE THE VALUES CONSISTENT

• [H+]= 24 x Pa CO2 / HCO3-

• Subtract calculated [H + ] from 80; this gives the last two digits of a pH beginning with 7 – example: calculated [H + ] of 24 converts to pH of (80-24)~7.56 – example: calculated [H + ] of 53 converts to pH of (80-53)~7.27

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CORRELATION BETWEEN H+ AND PH

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• The Six Steps of Systematic Acid-Base Evaluation

• 1. pH: Assess the net deviation of pH from normal •• 2. Pattern: Check the pattern of bicarbonate & pCO2 results •• 3. Clues: Check for additional clues in other investigations •• 4. Compensation: Assess the appropriateness of the compensatory

response •• 5. Formulation: Bring the information together and make the acid base

diagnosis •• 6. Confimation: Consider if any additional tests to check or support the

diagnosis are necessary or available & revise the diagnosis if necessary

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1. pH: Check arterial pH

Principle: The net deviation in pH will indicate whether an acidosis or an alkalosis is present (but will not indicate mixed disorders)

Guidelines: IF an acidaemia is present THEN an acidosis must be present

IF an alkalaemia is present THEN an alkalosis must be present

IF pH is normal pH THEN Either (no acid-base disorder is present) or (Compensating disorders are present ie a mixed disorder with an acidosis and an alkalosis)

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2. PATTERN: Look for suggestive pattern in pCO2 & [HCO3] Principle:Each of the simple disorders produces predictable changes in [HCO3] & pCO2.

Guidelines: IF Both [HCO3] & pCO2 are low THEN Suggests presence of either a Metabolic Acidosis or a Respiratory Alkalosis (but a mixed disorder cannot be excluded)

IF Both [HC)3 & pCO2 are high THEN Suggests presence of either a Metabolic

Alkalosis or a Respiratory Acidosis (but a mixed disorder cannot be excluded)

IF [HCO3] & pCO2 move in opposite directions THEN a mixed disorder MUST be present

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3. CLUES: Check for clues in the other biochemistry results

Principle: Certain disorders are associated with predictable changes in other biochemistry results

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4. COMPENSATION: Assess the Compensatory Response

Principle: The 6 Bedside Rules are used to assess the appropriateness of the compensatory response.

Guidelines: If the expected & actual values match => no evidence of mixed disorder If the expected & actual values differ => a mixed disorder is present

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5. FORMULATION: Formulate the Acid-Base Diagnosis

Consider all the evidence from the history, examination & investigations and try to formulate a complete acid-base diagnosis

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6. CONFIRMATION: Check for specific biochemical evidence of particular disorders for confirmation

Principle: In some cases, further biochemical evidence can confirm the presence of particular disorders. Changes in these results may be useful in assessing the magnitude of the disorder or the response to therapy. Examples:Lactate, urinary ketones, salicylate level, aldosterone level, various tests for renal tubular acidosis

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SIMPLE ACID-BASE DISORDERS

PH & PCO2 RELATIONSHIP IN RESPIRATORY DISORDERS

H+ < 0.3 - Chronic

PaCO2

>0.8–acute

0.3–0.8–acute on chronic

BEDSIDE RULES FOR ASSESSMENT OF COMPENSATION

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Know the clinical details of the patient

Find the cause of the acid-base disorder

The snapshot problem: Are the results 'current'?

Determine the major primary process then select the correct rule

RULES FOR RESPIRATORY ACID-BASE DISORDERS

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Rule 1 : The 1 for 10 Rule for Acute Respiratory Acidosis The [HCO3] will increase by 1 mmol/l for every 10 mmHg elevation in pCO2 above 40 mmHg.

The increase in CO2 shifts the equilibrium between CO2 and HCO3 to result in an acute increase in HCO3. This is a simple physicochemical event and occurs almost immediately.

EXAMPLE

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A patient with an acute respiratory acidosis (pCO2 60mmHg) has an actual [HCO3] of 31mmol/l.

The expected [HCO3] for this acute elevation of pCO2 is 24 + 2 =26mmol/l.

The actual measured value is higher than this indicating that a metabolicalkalosis must also be present.

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The 4 for 10 Rule for Chronic Respiratory Acidosis

The [HCO3] will increase by 4 mmol/l for every 10 mmHg elevation in pCO2 above 40mmHg.

With chronic acidosis, the kidneys respond by retaining HCO3, that is, renal compensation occurs. This takes a few days to reach its maximal value.

EXAMPLE

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A patient with a chronic respiratory acidosis (pCO2 60mmHg) has an actual [HCO3] of 31mmol/l.

The expected [HCO3] for this chronic elevation of pCO2 is 24 + 8 = 32mmol/l.

The actual measured value is extremely close to this so renalcompensation is maximal and there is no evidence indicating a second acid-base disorder.

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Rule 3 : The 2 for 10 Rule for Acute Respiratory Alkalosis

The [HCO3] will decrease by 2 mmol/l for every 10 mmHg decrease in pCO2 below 40 mmHg.

In practice, this acute physicochemical change rarely results in a [HCO3] of less than about 18 mmol/s.

So a [HCO3] of less than 18 mmol/l indicates acoexisting metabolic acidosis.

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Rule 4 : The 5 for 10 Rule for a Chronic Respiratory Alkalosis

The [HCO3] will decrease by 5 mmol/l for every 10 mmHg decrease inpCO2 below 40 mmHg.

It takes 2 to 3 days to reach maximal renal compensation

The limit of compensation is a [HCO3] of about 12 to 15 mmol/l

RULES FOR METABOLIC ACID-BASE DISORDERS

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Rule 5 : The One & a Half plus 8 Rule - for a Metabolic Acidosis

The expected pCO2 (in mmHg) is calculated from the following formula

Maximal compensation may take 12-24 hours to reach

The limit of compensation is a pCO2 of about 10 mmHg

Hypoxia can increase the amount of peripheral chemoreceptor stimulation

EXAMPLE

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A patient with a metabolic acidosis ([HCO3] 14mmol/l) has an actual pCO2 of 30mmHg.

The expected pCO2 is (1.5 x 14 + 8) which is 29mmHg.

This basically matches the actual value of 30 so compensation is maximal and there is no evidence of a respiratory acid-base disorder (provided that sufficient time has passed for thecompensation to have reached this maximal value).

If the actual pCO2 was 45mmHg and the expected was 29mmHg, then this difference (45-29) would indicate thepresence of a respiratory acidosis and indicate its magnitude.

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Rule 6 : The Point Seven plus Twenty Rule - for a Metabolic Alkalosis

The expected pCO2(in mmHg) is calculated from the following formula

Remember that only primary processes are called acidosis or alkalosis.

The compensatory processes are just that - compensation. Phrases such as ‘secondary respiratory alkalosis’ shouldnot be used.

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MIXED ACID-BASE DISORDERS

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A mixed acid-base disorder is present when two or more primary disorders are present simultaneously.

A double disorder is present when any two primary acid-base disorders occur together, but not all combinations of disorders are possible.

The particular exclusion here is that a mixed respiratory disorder can never occur as carbon dioxide can never be both over- and under-excreted by the lungs at the same time!

A triple disorder is present when a respiratory acid-base disorder occurs in association with a double metabolic disorder.

SUMMARY

• ABG is a clinical sign

• Step wise approach is best

• Don’t judge by single numbers

• Mixed disorders not uncommon in ICU

• Practice makes you perfect

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CASE HISTORY 1*

• Man after a Postoperative Cardiac Arrest

• Surgery for orbital mucormycosis

• Hypertensive on ACEI

• VT – VF arrest intraoperatively

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Biochemistry Results): Na+ 138, K+ 4.7, Cl- 103, urea 64 & creatinine 2.3

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• Ph < 7.35 Acidemia

• CO2 High – respiratory acidosis

• Compensation – 1 for 10 rule

• = 24 + 1 ( 55.4-40/10)

• = 24 + 1 x 1.4 = 25.4

• Measured CO2 ~ Calculated CO2

• Acute respiratory acidosis

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CASE 2*

• A sick diabetic patient

• A 19 year old pregnant insulin dependent diabetic patient was admitted with a history of polyuria and thirst.

• There was a history of poor compliance with medical therapy.

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Biochemistry on admission: Na+ 136, K+ 4.8, Cl- 101, 'total CO2' 10, glucose 334urea 81and creatinine 0.9

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• Ph < 7.35 – acidemia

• CO2 < 30 – not respiratory acidosis

• HCO3 < 20 – Metabolic acidosis

• Anion gap - 136 – ( 101 +7) = 136 – 108

• High anion gap

• Compensation – 1.5 (hco3) + 8

• = 1.5 (7) + 8 = 10 + 8 = 18

• Measured CO2 ~ Expected CO2

• High Anion Gap Metabolic Acidosis

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CASE 3 : A WEAK OLD LADY*

• An elderly woman from a nursing home was transferred to hospital because of profound weakness and areflexia. Her oral intake had been poor for a few days.

• Current medication was a sleeping tablet which was administered as needed.

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CASE 3 : A WEAK OLD LADY

Admission biochemistry (in mmol/l): Na+ 145, K+ 1.9, Cl- 86, bicarbonate 45, anion gap 14 and a spot urine chloride 74 mmols/l.

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• Ph > 7.45 - Alkalemia

• CO2 > 30 – Not respiratory alkalosis

• HCO3 > 24 – Metabolic alkalosis

• Compensation = 0.7 (HCO3) + 20

• 0.7 ( 44.4) +20

• = 31.1 + 20 = 51

• Measured CO2 ~ Expected CO2

• Primary Metabolic Alkalosis

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CASE 4 : A CASE OF PNEUMONIA*

• A 60 year old woman was admitted with lobar pneumonia. She was on a thiazide diuretic for 9 months following a previous admission with congestive cardiac failure.

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CASE 4 : A CASE OF PNEUMONIA

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• Ph > 7.45 – Alkalemia

• CO2 > 30 – may be not respiratory alkalosis

• HCO3 > 24 – probably metabolic alkalosis

• Compensation – 0.7 (HCO3) + 20

• = 0.7 ( 33) + 20

• = 23.3 + 20

• Expected CO2 =43

• Measured CO2 < Expected CO2

• Primary metabolic alkalosis and Primary Respiratory Alkalosis

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CASE 5 : AN OLD LADY FROM A MOTOR VEHICLE CRASH

• An 80 year old lady (wt 40 kgs) was admitted to the Intensive Care Unit following a motor vehicle accident

• Injuries were a left anterior flail segment, a fractured left patella and facial bruising. She was haemodynamically stable but had respiratory distress with paradoxical movement of her left anterior chest wall.

• Only significant past history was of hypertension for which she took propranolol 120 mgs/day.

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CASE 5 : AN OLD LADY FROM A MOTOR VEHICLE CRASH

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CASE 6 : A COAD PATIENT WITH ACUTE ABDOMINAL PAIN

• A 54 year old obese woman presented at night with a history of sudden onset of left upper quadrant and epigastric pain. Past history included ‘moderate chronic obstructive airways disease’ and polymyositis.

• She had an exercise tolerance of about 10 meters because of breathlessness.

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CASE 6 : A COAD PATIENT WITH ACUTE ABDOMINAL PAIN

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CASE HISTORY 7: A MAN WITH DIARRHOEA AND DEHYDRATION

• A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhoea.

• Electrolyte results (in mmol/l): Na+ 134, K+ 2.9, Cl- 113, HCO3- 16, urea 12.3, creatinine 1.1 mg/dl.

• Anion gap 8.

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CASE HISTORY 7: A MAN WITH DIARRHOEA AND DEHYDRATION

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CASE 8 : AN ILL DIABETIC PATIENT WITH VOMITING AND POLYURIA

• A 23 year old 53kg female was admitted with persistent vomiting, polyuria and thirst. She had been ill for about 16 hours.

• She had been an insulin dependent diabetic for 11 years but her health was usually excellent.

• • There was no dysuria and no evidence of chest, pelvic or skin

infection.

• She had omitted several doses of insulin in the previous 3 days.

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CASE 8 : AN ILL DIABETIC PATIENT WITH VOMITING AND POLYURIA

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CASE 9 : A MAN WITH A POST-OPERATIVE CARDIAC ARREST

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CASE 10 : A SEMI-COMATOSE DIABETIC ON DIURETICS

• A 55 year old insulin dependent diabetic woman was brought to Casualty by ambulance.

• She was semi comatose and had been ill for several days. • Past history of left ventricular failure.

• Current medication was digoxin and a thiazide diuretic.

• Results include: K+ 2.7, glucose 450mg/dl , anion gap 34 mmol/l

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CASE 10 : A SEMI-COMATOSE DIABETIC ON DIURETICS

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CASE HISTORY 11: A MAN WITH CCF & VOMITING

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A 70 year old man was admitted with severe congestive cardiac failure. He has been unwell for about a week and has been vomiting for the previous 5 days. He was on no medication. He was hyperventilating and was very distressed.. He was on high concentration oxygen by mask.

Biochemistry results: Na+ 127, K+ 5.2, Cl- 79, HCO3- 20, urea 50.5, creatinine 2.4 & glucose 180 mg/dl. Anion gap 33 mmols/l

CASE HISTORY 11: A MAN WITH CCF & VOMITING

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CASE 12 : A WEAK PATIENT AFTER A WEEK OF DIARRHOEA

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A 68 year old woman was admitted with a one week history of severe diarrhoea. She was now weak and clinically dehydrated. Blood pressure was 100/60 (lying) and 70/40 (sitting). She was admitted and treated with IV fluids and potassium supplementation to repair her volume and electrolyte deficits. Urine output improved with fluid repletion. Electrolytes and arterial blood gases were collected on admission and the next day.

CASE 12 : A WEAK PATIENT AFTER A WEEK OF DIARRHOEA

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CASE HISTORY 13: A WOMAN WITH A POSTOP MORPHINE INFUSION

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A 28 year old woman was admitted electively to a HDU (high dependency unit) following a caesarian section.

A diagnosis of 'fatty liver of pregnancy' had been made preoperatively.

She was commenced on a continuous morphine infusion at 5 mg/hr and received oxygen by mask.

This was continued overnight and she was noted to be quite drowsy the next day

CASE HISTORY 13: A WOMAN WITH A POSTOP MORPHINE INFUSION

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CASE HISTORY 15 : AN OLD MAN WITH ABDOMINAL PAIN & SHOCK

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An 85 year old man was admitted with severe abdominal pain and shock.

The abdominal pain started about 1500hrs and quickly became quite severe. There was no radiation to the back.

The patient was known to have an abdominal aortic aneurysm (AAA). On arrival at hospital, the patientwas shocked with peripheral circulatory failure and hypotension (BP 70-80 systolic). The abdomen was guarded and quite tender. He was distressed but able to talk and could understand instructions.

Past history was of hypertension (on metoprolol and prazosin) and angina..

CASE HISTORY 15 : AN OLD MAN WITH ABDOMINAL PAIN & SHOCK

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Biochemistry at 1520hrs was Na+ 138, K+ 4.9, Cl- 107, Total CO2 20, Glucose 200, Urea 68 creatinine 0.9. Anion gap was 11.

A ruptured AAA was diagnosed clinically and he was transferred to theatre for emergency laparotomy. On arrival in theatre BP was 120 systolic. The patient was talking but distressed by pain with rapid respirations at a rate of 30/min. It was noted that neck veins were very distended. An external jugular triple lumen central line and a brachial arterial line were placed before the surgical team had arrived in theatre. CVP was +40 mmHg.

CASE HISTORY 15 : AN OLD MAN WITH ABDOMINAL PAIN & SHOCK

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CASE HISTORY 16 : A WOMAN WITH VOMITING & MUSCLE WEAKNESS

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A 49 year old woman was admitted to a medical ward because of severe vomiting and marked muscle weakness. She had been unwell for two weeks following a fall. Four days before presentation, she had developed abdominal discomfort with vomiting. The vomiting was severe and oral intake was poor. She said she had lost a significant amount of weight. She felt very weak, was anorexic and lethargic and had a dry mouth. She did not have diarrhoea or urinary symptoms. There was no significant past medical illness and she was on no medication.

She was afebrile but looked ill. BP 110/60 (sitting). Pulse 84/min and regular. Respiratory rate 18min. Chest was clear. Heart sounds were normal. Slight abdominal tenderness on deep palpation was present in the right iliac fossa. Deep tendon reflexes were 1+ and muscle power was graded as 4/5. Sensation was normal.

Initial pathology: Na+ 128, K+ 1.6, Cl- 103, HCO3- 12.5, Glucose 167, urea 34, creatinine 1.2 mg/dl and total protein was 89 g/l. Anion gap 12. Amylase was within the normal range.

CASE HISTORY 16 : A WOMAN WITH VOMITING & MUSCLE WEAKNESS

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CASE HISTORY 17 : AN INTOXICATED BABY

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An 8 month old female baby was admitted with a one day history of lethargy. She had vomited several times. Her mother said she appeared "intoxicated". Examination confirmed the obtunded mental state but she was easily rousable and muscle tone was normal. Resp rate was 60/min. Pupils were normal. There was no evidence of dehydration. Abdomen was soft and nontender. BP was 112/62. Peripheral perfusion was clinically assessed as normal. Heart and chest examination was normal. Plantar response was normal.

Investigations: Na+ 135, K+ 4.2, Cl- 116, bicarbonate 5.7, glucose 5.9 (All in mmol/l). Other results:Urine: pH 5.0, negative for glucose and ketones. Numerous calcium oxalate crystals were seen on urine microscopy

CASE HISTORY 17 : AN INTOXICATED BABY

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CASE HISTORY 18 : A SMOKER WITH FEVER & RIGORS

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A 67 year old man presented to a peripheral hospital with a 3 day history of lethargy, vomiting, fever with rigors and increasing dyspnoea. A dry cough was present. There was no pleuritic pain. He was described as a 'previously healthy heavy smoker'. There was a past history of osteoarthritis treated with simple analgesics. No other medication.

On examination, he was sweaty, pale and acutely dyspnoeic. T 38.4C BP 104/70. Pulse oximetry reading was 62% on room air. Bilateral bronchopneumonia was present on chest xray.

Initial pathology: Hb 147 g/l, Na 137, K 4.3, Cl 96, total CO2 32, glucose 130mg% urea 10.2, creatinine 0.8 mg/dl.

CASE HISTORY 18 : A SMOKER WITH FEVER & RIGORS

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CASE HISTORY 19 : A YOUNG MAN WHO INGESTED BARIUM CARBONATE

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A 22 year old man was admitted to hospital 1.5 hours after ingestion of about 10G of barium carbonate dissolved in hydrochloric acid. Symptoms included abdominal pain, generalised areflexic muscle paralysis, increased salivation and diarrhoea. BP 180/110. Pulse 92/min.

Initial biochemistry (in mmol/l) was: Na+ 140, K+ 2.1, Cl 92, glucose 50 and plasma lactate 10.2.

CASE HISTORY 19 : A YOUNG MAN WHO INGESTED BARIUM CARBONATE

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CASE 20 : A SHOCKED ALCOHOLIC WITH GIT BLEEDING

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A 60 year old man was seriously ill on arrival at hospital. The patient told of vomiting several hundred mls of dark brown fluid ‘every hour or two’ for about a day plus several episodes of melaena.Past history was of alcoholism, cirrhosis, portal hypertension and a previous episode of bleeding varices.Sclerotherapy for the varices had been performed several months previously at another hospital.

Examination: He was jaundiced and distressed: sweaty, clammy and tachypnoeic. BP 98/50, pulse 120/ min. Air entry was good. Heart sounds dual with a systolic murmur. Peripheries were cool. Abdomen was soft and nontender. Signs of chronic liver disease were present (spider naevi, gynaecomastia, testicular atrophy). Urinalysis: glucose, trace ketones.

Pathology: Na+ 131, Cl- 85 K+ 4.2, "total CO2" 5.1, glucose 52, urea 60, creatinine 1.8lactate 20.3 mmol/l. Hb 62 G/l, WCC 23.8

CASE 20 : A SHOCKED ALCOHOLIC WITH GIT BLEEDING

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