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Disclaimer:  These materials are for educational purposes only, and are not a source of medical decision-making advice

PRE-OPERATIVE CARE                                                                                                                                                                                               

i. Chest X-ray - at least a new PA film. Most patients will have fairly recent films including a penetrated PA to show cardiac chamber size. These films need not be repeated. A lateral film is essential in anyone who has had a previous bypass operation to show the amount of space behind the sternum and the number of wires. For coronary artery cases a PA film is sufficient.
ii. ECG.                                                                                                                                                                                                                       
iii. Respiratory Function Tests - FEV1, Vital Capacity, PEFR. If these tests are poor, arterial blood gases breathing air are a useful baseline for postoperative care.
iv. Blood tests: Full Blood Count, Urea, Electrolytes, Liver Function Tests, Glucose, Creatinine, Coagulation Studies, Hepatitis B & C Screening, Cross Matching (Usually 2- 6 Units). If significant chest disease ABG’s.                                                                         
v. Doppler ultrasound of carotids (if previous history of stroke, TIAs or carotid bruits or age over 65 years)                                          vi. Bacteriology: Nose and throat swabs for St. Aureus, MSU, sputum if appropriate. (Performed by nursing staff.)
All patients are given Bactroban to use at home and once admitted pre operatively.
vii. Chest physiotherapy before operation in patients with known chest disease, eg. chronic airways disease. Sputum culture is particularly important in this group.
viii. Old notes, including cardiac catheter data are essential and should be obtained.  (If the cardiac catheter is more than 12 - 18 months old then may require repeating, particularly if the previous disease was single or two vessel)
ix. Transthoracic Echocardiography (TTE): Left Ventricular assessment  and Valves assessment.
x. Consent for operation. (Including documentation of the major risks.)
xi. height (cm) and weight (kg)  to calculate surface area and body mass index.

i) Anticoagulants - These are tailed off over a few days prior to operation. Patients should have a coagulation screen measured on the preoperative day to confirm a virtually normal clotting status on the day of operation. If the coagulation has not normalised then consider  the use of FFP.      Vit K is very rarely used                
 (If the operation is postponed then anticoagulants should be temporarily restarted - this is particularly important with a history of previous strokes).
ii) Aspirin and Clopidogrel- This has a significant effect in diminishing platelet function and can lead to increased postoperative blood loss. Ideally it should be stopped 7-10 days before surgery, if not, should be stopped on the day of admission of the patient - unless there is unstable angina.
iii) Digoxin - Continued until the day before operation.
iv) Diuretics and Potassium Supplements - Continued until the day before operation.
v) Beta Blockers, Calcium Antagonists, Long Acting Nitrates - Patients with coronary artery disease will frequently be taking a combination of these drugs. It is important not to interfere with these drugs in any way but to continue them until the day before operation.
vi) Antihypertensives - Maintain until operation.
vii) Monoamine Oxidase Inhibitors - Must be discontinued at least three weeks preoperatively.
viii) Anti-diabetic Agents and Steroids - Should be noted and the appropriate perioperative management will be decided by the Anaesthetist and appropriate physician. Discuss with the anaesthetist whether sliding scale insulin is required.

The definitive operating list must be submitted to the Theatre the day before surgery.   In the event of changes to the operating list it is important that Blood Bank should be informed as early as possible.
In the event of an emergency operation out of hours, all key groups must be informed. These are:
i. Theatre ii. Consultant Anaesthetist and Duty Anaesthetic SR  iii. Perfusion Technician. iv. Blood Bank.   v. CITU Staff. To confirm the availability of a bed on CITU for the postoperative care of the patient. vi.Involvement in all these tasks makes it easy to forget the patient and the anxious relatives. Clearly they must be kept informed of plans and prospects.

i. The SHO on theatre duty must be present at the scheduled starting time for anaesthesia (usually 8.30 am), prior to theatre the theatre SHO’s should attend the ITU/HDU ward round.
ii. Male patient should be catheterised by the SHO but the anaesthetic / theatre nurse will catheterise female patients unless an emergency or no female staff are available.
iii. Current X-rays and hard copies of the Angiogram if available should be put on the viewing box.
iv. Ensure that patient has been shaved properly. If not, shavers are available in the anaesthetic room to remove additional hair.
v. Patients having re do surgery require external defibrillation pads to be attached to the chest wall and the SHO must connect them once in theatre to the defibrillator
vi. Prophylactic antibiotics are given in the anaesthetic room by anaesthetist 40-60 minutes before knife to skin. 

Alterations to antibiotics may be required for example, in patients undergoing surgery for endocarditis. These will have been discussed preoperatively with Bacteriology and appropriate therapy chosen.

Current Antibiotic Prophylaxis Regime
All patients (unless beta-lactam allergic) should receive:
• Cefuroxime 1.5 g @ induction
• 750 mg 8 hourly for 48 hours

High Risk patients should also receive in addition to Cefuroxime:
• Teicoplanin 800 mg @ induction
• Then three further doses of 800 mg 12 hrly
High risk category includes any of the following:
• “Pool” patients or patients from another hospital unless recent negative MRSA screen (< one week)
• Patients received from any critical area
• Patients with no MRSA screen result available
• Emergencies
• Redo operations
• Obese patients (BMI > 30)
• Diabetic patients
• Intra cardiac procedures (Valve repair / replacements)
• Bilateral internal mammary artery grafts

Cefuroxime (beta-lactam) allergic patients should receive:
• Teicoplanin 800 mg and Ciprofloxacin 400 mg @ induction
• Then three further doses of Teicoplanin 800 mg and Ciprofloxacin 400 mg
12 hrly
All antibiotic dosages and times should be clearly recorded on the patient’s drug chart


POST-OPERATIVE CARE                                                                                                                                                                                          

The primary object of our postoperative care is to maintain an adequate cardiac output. The satisfactory performance of other sub-systems, e.g, renal function, normal consciousness etc is dependent on this. Though the primary role of open heart surgery is to improve the function of the heart and the haemodynamic situation, this may not be so in the early postoperative period for two reasons:

i. Transient but appreciable damage is done to the heart during any operation by ischaemia, cardiotomy, cooling etc.
ii. The period of perfusion imposes an insult to the entire organism. Documented physiological changes after bypass include:
     a. High extracellular (extravascular water)
     b. High extravascular total lung water
     c. Low circulating red cell mass
     d. Low total body K+
     e. Increased endogenous catecholamines.

To be able to maintain an adequate cardiac output there are four basic mechanisms which can be adjusted:
i. Heart Rate
ii. Filling Pressure (Preload)
iii. Peripheral Resistance (Afterload)
iv. Ventricular Contractility

Cardiac output is determined by the product of heart rate and stroke volume(CO = HR x SV).

The maintenance of stroke volume is central to the maintenance of cardiac output and is determined by Starling’s Law (Force of contraction is proportional to initial fibre length). In other works the fuller the ventricle at the end of diastole (within limits) the more forcefully it will eject its contents in systole.

i. Heart Rate - A heart rate of 60-100 beats per minute usually optimises cardiac output. If lower than this, despite an adequate stroke volume cardiac output will be suboptimal. Above this and the ventricular filling time is reduced such that stroke volume and hence cardiac output is reduced.

ii. Filling Pressure - The left atrial pressure is the best measure of left ventricular filling pressure and either direct left atrial pressure measurements or Mean Pulmonary Capillary Wedge pressure (which approximates the LAP) are used as a guide to transfusion requirements. CVP (right atrial pressure) is only a very crude guide to transfusion requirements. The normal left atrial pressure is 1-4 mmHg in healthy individuals. There is seldom any advantage in increasing the mean LAP to greater than 20 mmHg in postoperative surgical patients.

iii. Ventricular Contractility - Ventricular contractility can be improved by a variety of inotropic agents if cardiac output is inadequate. (See Inotropes).

iv. Peripheral Resistance (Afterload) - Under certain circumstances cardiac output may be increased by a reduction in afterload (peripheral resistance) by the use of vasodilator drugs. Mechanical devices such as IABP may also reduce afterload and increase cardiac output.

In our Intensive Care Unit cardiac output is monitored in certain patients by thermodilution techniques using Swan Ganz Catheter or Picco.  Cardiac output, cardiac index and pulmonary and systemic vascular resistances may be calculated by this method. The normal cardiac output for a healthy adult male is 5-6 litres per minute. The normal cardiac index (CI= CO\sq M of Body Surface Area) is about 3 litres\min\m2 but in the early postoperative period a figure of 2 litres\min\m2 would be regarded as acceptable.

CI 3.0-5.0 l/min/m2
ITBVI 850-1000 ml/m2
EVLWI 3.0-7.0 ml/kg
CFI 4.5-6.5 l/min
HR 60-90 b/min
CVP 2-10 mmHg
MAP 70-90 mmHg
SVRI 1200-2000 dyn.s.cm5.m2
SVI 40-60 ml/m2
SVV <=10 %

i. Inform the Duty CITU doctor and nurses of the operation, any problems including ease of coming off CP bypass, monitoring lines, inotropic support, pacing etc. 
ii. The anaesthetist will attach the patient to the ventilator. 
iii. Make base-line observations of heart rate, rhythm, arterial pressure etc. 
iv. Attach the labelled chest drains to low pressure wall suction and ensure this is functioning and measure initial drainage. 
v. Attach monitors and check zero and calibration. Zero is at the junction of the mid axillary line and the fourth intercostal space. (Remember - maladjustment of the monitoring equipment is often the cause of an apparent change in the condition of the patient, eg deteriorating arterial pressure and should always be double checked). 
vi. Order drugs and fluids on the CITU drug charts and specify guidelines for colloid and crystalloid transfusion. There is a standard daily ITU drug chart and a new in patient drug chart is written on arrival on ITU by the ITU SHO. Except out of hours / waiting list initiative cases when the theatre SHO does this. 
vii. Order initial tests: FBC, Urea and Electrolytes, Blood gases, Blood Sugar, Coagulation Screen, Chest X-ray
viii. Connect pacemaker wires. 

ix. Position the patient with 15o of head up - unless BP is low.
x. Ensure a brief operation note is recorded in the notes detailing any specific problems encountered in the operation or immediate post bypass period and in addition blood pressure, RA and LA pressures to act as a guide to the early intensive care management. (Typically the SpR or Consultant will do this.)
(Usually the ITU staff assist with iii), iv), v)and viii).

I. Fluid Replacement
Blood or colloid transfusion is required after cardiopulmonary bypass because:
i. There is bleeding via the chest drains.
ii. Following operation the circulating volume is low.

The object of colloid replacement is to prevent depletion of intravascular volume and to provide an LVEDP (measured as LA) sufficient to maintain an adequate stroke volume (rarely > 17-20 mmHg).

The colloids available for transfusion may be:
1. Blood
2. Single Donor Plasma (SDP) or FFP if there is a clotting problem
3. Hespan (Heta-Starch / Haes 6%) - Synthetic starch solution with 24 hour half life. (Avoid in large volumes).
4. Gelofusine and Haemacell are best avoided ( half life in circulation is too low.).

Our present policy is to transfuse blood only if the Hb is 8.0 g/dl or less in the early postoperative period otherwise colloids are given. If the patient is actively bleeding then a higher Hb 10 – 12 is aimed for.

A relatively low haemoglobin in the post bypass period has the theoretical advantage of reducing plasma viscosity and is particularly relevant since a low viscosity favours high graft flow after coronary artery bypass surgery. Haemoglobin rises anyway in the day following surgery as the relative haemodilution following bypass corrects itself.

Colloid transfusion is usually continued until the morning following surgery, unless blood loss via the chest drain continues.

Crystalloids (Maintenance Intravenous Fluids)

Post cardiopulmonary bypass the regime is of gradually relaxing fluid restriction. This is because:

1. Water and sodium are retained and potassium is lost
2. Water load from haemodilution prime of pump-oxygenator
3. Increase in extracellular water following bypass (20%)
4. Underlying state of cardiac failure.

For these reasons it is sensible to restrict postoperative water and sodium to minimum.
While intravenous fluids are administered, usually the first 24-48 hours after surgery, 1 ml/kg/hr of 5% Dextrose is given. After this free fluids by mouth are given.

II. Potassium
Potassium supplements are usually necessary because:
1. The diuresis associated with the haemodilution prime leads to potassium loss.
2. Potassium loss occurs after any surgery
3. Chronic diuretic therapy may have led to depletion of total body K+
4. Low potassium levels may result in increased myocardial irritability and postoperative arrhythmias.

The serum potassium is no guide at all to the total body potassium content since only 3% of total body K+ is within the serum, the rest is within the cells.

Potassium levels are measured frequently in the early postoperative period, 2 hourly for 6-8 hours then 4 hourly thereafter for 24 hours.

Potassium supplements are given in aliquots of 1 g (13 mmol) administered over 1 hour with the hourly fluids to maintain the serum K+ in the range of 4.5 – 5.0 mmol/l.

If the serum K+ is low, <3.5 mmol/l then greater than 1 g may be given in 1 hour. It is unnecessary and, may be dangerous to administer more than 2 g in 1 hour’s fluid allowance. On ITU/HDU the nursing staff typically perform this. Too rapid administration of K+ may result in asystole. KCl should never be given by direct injection.

III. Ventilation

This is largely the responsibility of the ITU Anaesthetists though decisions regarding extubation/tracheostomy ought to be taken jointly with the anaesthetic staff. In general the surgical staff do not alter the ventilation or extubate patients though the ultimate responsibility for the patient care lies with the surgical staff.

All patients return to the ITU and are ventilated initially. Extubation if contemplated on the day of operation is usually delayed until blood loss and cardiac and pulmonary function are stable.

IV. Sedation and Analgesia

Again this is largely the responsibility of the ITU Anaesthetists. Patients requiring ventilation over night are usually maintained on a Propofol infusion initially, with an opiateeg. Morphine or Fentanyl or more rarely a benzodiazepine infusion e.g. Midazolam ;as dictated by their clinical response using the smallest effective dose.

Muscle relaxants are rarely required in straight-forward postoperative patients.

1. Boluses of Fentanyl may cause sudden hypotension.
2. Before requesting sedation in a restless patient consider whether their
restlessness is not secondary to something else, eg hypoxia.

V. Antibiotics

The principle of antibiotic prophylaxis in Cardiothoracic Surgery is to give a short course of antibiotics at the time of surgery and in the immediate postoperative period. The first dose is given with induction of anaesthesia and eight hourly thereafter until the chest drains are removed. This interferes least with the normal flora of the patient. Subsequent infections are treated on their own merits based on known bacteriological sensitivities.

Current prophylaxis - Cefuroxime 750 mgs IV 8 hourly x 3 doses.
If the patient has previously been an in patient on another ward or hospital prior to surgery then also give:- Teicoplanin 800mgs 12  hrly x 3 doses

VI. Urine Output
In adults the volume of urine should be at least 20 - 30 mls/hour (0.5 ml/kg/hr). The treatment of a low urine output is based on assessment of the overall status of the patient to confirm the presence of adequate hydration and cardiac output. If the cardiac output is low efforts should primarily be directed towards its improvement.

Having confirmed that hydration and CO are adequate to ensure renal perfusion then diuretic may be employed.

1. Furosemide 10-20 mgs IV initially, larger doses may be used if small doses do not have a diuretic effect.

2. Mannitol (20%) a long acting osmotic diuretic usually given as a 100 ml infusion over 1 hour followed by 10 mls/hr. (Less common)

3. Dopamine (low dose) 3-5 ug/kg/min has a specific effect on the renal vasculature (In higher dose it has cardiac effects.).

Conversely, if urine output is high the serum potassium must be monitored carefully.

VII. Chest X-ray

These are taken immediately on return from theatre (supine), in the evening on day 0 and on days 1, 2 and 4. Always after removal of an intercostal drain but not essential after removal of a pericardial or mediastinal drain.

The following should be noted on an early postoperative film:
1. Position of ET Tube, Drains, CVP Lines, Swan Ganz if used, NG Tube etc.
2. Postoperative lung collapse.
3. Pleural effusions.
Remember: Pneumothoraces and pleural effusions may be difficult or impossible to diagnose on a supine radiograph.


i. Excessive Blood Loss

Patients tend to bleed after open heart procedures. This is because patients are heparinised during the period of bypass, though this is subsequently neutralised by protamine, and because bypass itself may disturb normal coagulation mechanisms. Excessive bleeding via the chest drains leads to excessive transfusion, which does not help natural haemostasis. Furthermore, tamponade is more common in a setting of excessive drainage.

Excessive bleeding might be considered as 1 litre in eight hours after return to the ITU or more than 200 mls per hour for several hours. However, exact limits are impossible to specify.

In the face of excessive bleeding the following steps should be taken:

1. Perform a coagulation screen.
2. Notify the Duty Registrar/SR
3. Ensure adequate cross matched blood is available.

Coagulation defects may be the primary cause of a generalised bleeding tendency. Common abnormalities found include prolonged TCT (indicating unneutralised Heparin) and low platelet count. Diagnosis and treatment of coagulation problems are discussed with the Duty Haematologist and one or more of the following may be administered:
1. Protamine (30-50 mg IV slowly) - rapid administration of Protamine may cause sudden hypotension.
2. Fresh Frozen Plasma (FFP)
3. Fresh Blood (rarely available) – Typically use Packed red cells to keep Hb > 10g/dl.
4. Platelets (in multiples of 5 units) especially if the patient was on aspirin
prior to surgery..
5. Cryoprecipitate if fibrinogen low

A Haemostatic Pack is available which consists of 5 units of platelets and 4 units of FFP usually only issued in the event of significant bleeding after discussion with the on-call haematology technician.

After administration of haemostatic agents coagulation should be rechecked if bleeding persists.

Despite the importance of correction of coagulation defects, in the face of heavy blood loss it is better to reopen the chest to exclude a surgical site for bleeding and to reduce transfusion needs while the patient is still well. This is a clinical decision taken by one of the more experienced members of the surgical team. If the patient’s condition is stable then reoperation is best performed in theatre. If the patient is unstable or tamponade occurs emergency reopening of the chest can easily be performed on the ITU.

If sudden heavy blood loss occurs after a period of hours of acceptable drainage volumes, a surgical site for bleeding is likely and reoperation should not be delayed.

Blood loss after repeat cardiac operations if often high and the above the criteria may be modified when dealing with such patients. The recent use of Aprotinin (Trasylol) or Tranexamic acid (Cyclokapron) in these cases has greatly reduced blood loss.

ii. Tamponade

This is a clinical syndrome of falling cardiac output due to compression by the accumulation of blood and/or clot in the pericardial cavity. The classical features are:

1. Falling arterial pressure with rising heart rate.
2. Rising CVP or LAP (or stable high atrial pressures with a blood balance changing in a negative direction).
3. Moderate or heavy blood loss which fluctuates particularly if the drains tend to block.
4. Increasing peripheral vasoconstriction with decreasing toe temperature.
5. Falling urine output.
6. Acidosis (Metabolic)
7. Arrhythmias.
8. Pulsus Paradoxus (the normal inspiratory fall in systolic BP is not seen).

All the above clinical features may not be present and a high index of clinical suspicion should be maintained.

The diagnosis may be difficult to distinguish from low cardiac output to ventricular dysfunction. Various distinguishing tests have been used but are all of limited volume. Chest X-ray is of little value in the diagnosis of acute postoperative tamponade.

If a diagnosis of tamponade is made, repeat sternotomy is usually undertaken immediately on the Intensive Care Unit. Remember, tamponade rarely occurs suddenly but often “creeps up on you”. In certain circumstances repeat sternotomy may be justified simply to exclude the diagnosis.

iii. Low Output State (LV dysfunction)

The clinical findings may be:

1. Blood pressure - low
2. Peripheral vasoconstriction
3. High LAP
4. Low urine output

This clinical syndrome corresponds to a cardiac index below 1.5 - 2.0 l/min/m2. Treatment of this syndrome is designed to optimise the determinants of stroke volume and cardiac output which are:

1. Heart Rate
2. Ventricular Filling Pressure (LAP) (Preload)
3. Myocardial Contractility
4. Peripheral resistance (Afterload)

although the diagnosis of a low output syndrome is usually clinical this is often confirmed by the measurement of cardiac outputs and resistances with the Thermodilutation method via a Swan Ganz catheter. Having confirmed a low cardiac output attempts are made to increase this by manipulation of the listed determinants.

1. Heart Rate

The following ranges are optimal in the adult; sinus rhythm 80-120/min.

a. Bradycardia

This may lead to a low cardiac output as the postoperative heart is unable to elevate the stroke volume beyond certain limits. Ventricular pacing is the commonest method of rate augmentation using the epicardial wires positioned during surgery.

Pacing procedures

• Use the demand mode
• set rate well above the spontaneous rate at 3-4 V
• Determine the threshold by reducing voltage until pacing ceases
• Pace at 1-1.5 V above threshold

In the absence of pacing wires or if the rhythm is sinus Atropine 0.3 mg - 0.6 mg IV may be used. In exceptional circumstances an Isoprenaline infusion may be utilised (see later) N.B.increases myocardial energy demands.

b. Tachycardia

Sinus tachycardia should not be treated empirically, a cause should always be looked for, eg hypovolaemia, pain, hypoxia. Other tachyarrhythmias causing a low cardiac output should be treated on their own merits.

2. Left Ventricular Filling Pressure

The LAP (=LVEDP if Mitral Valve is normal) is a determinant of stroke volume as described by Starling’s Law. Each person has a different LV function curve and therefore the LAP at which stroke volume is maximal is uncertain and may indeed change as the state of the ventricle changes. In surgical patients there is little to be gained by increasing the LAP to greater than 20 mmHg. (If a Swan Ganz Catheter is in situ the mean PCWP or PADP should approximate to the mean LAP).

3. Myocardial Contractility (Inotropic Agents)

Inotropic agents infused intravenously may be used to enhance myocardial contractility. A variety of these are used in our practice. A few general points on the usage of inotropic agents are:

i. Before initiating inotropic agents a more senior member of the surgical team should be notified.

ii. Once initiated and a stable haemodynamic situation established the infusion should be maintained for several hours before any attempt at withdrawal is made.

iii. The clinical effect is usually measured in terms of a satisfactory systolic or mean arterial pressure. The infusion rate is titrated to achieve this level.

iv. Specific guidelines regarding increases (usually only conducted in the presence of a Doctor) or decreased in inotropic agents must be given to the nurses responsible for that patient on the ITU. Reductions in catecholamine infusions should always be gradual (eg 1 ml/hr if mean BP and urine output maintained).

a. Dobutamine (Dobutrex)

A synthetic drug increasing cardiac output without a significant increase in peripheral resistance. It may cause tachycardia and its effect on blood pressure is often not marked. It increases urine flow by increasing cardiac output.

Therapeutic Range 2.5 - 10 ug/kg/min

Infusion Recipe 6 x body Weight (kg) in 100 mls of
5% Dextrose (1ml/hr = 1ug/kg/min)

b. Dopamine (Intropin)

A naturally occurring precursor of adrenaline, acts by releasing endogenous Noradrenaline. In low doses, 3-5 ug/kg/min it has a specific effect on dopaminergic receptors in the renal vasculature increasing renal blood flow and hence urine output. It is for this effect that we are currently using this agent most frequently. In higher doses, 5-15 ug/kg/min it increases cardiac output, raises blood pressure, LAP and heart rate. Above 15 ug/kg/min tachycardia and peripheral vasoconstriction are limiting factors in the use of high dosage.

Therapeutic Range 3-5 ug/kg/min (Renal Vasodilator)
5-15 ug/kg/min (Inotrope)

Infusion Recipe 6 x body Weight (kg) in 100 mls of
5% Dextrose (1ml/hr = 1ug/kg/min)

c. Phentolamine/Noradrenaline Mixture (Canadian Cocktail) or Noradrenaline alone

Noradrenaline has a powerful inotropic effect on the heart through it also produces severe vasoconstriction which may be harmful by increasing afterload. To offset the vasoconstrictor effect phentolamine (Rogitine), a peripheral vasodilator, is used in combination.

Therapeutic Range 5 - 50 drops/min

Infusion Recipe 4 mg Noradrenaline/2.5 mg Phentolamine in 250 mls 5% Dextrose

In desperate circumstances even bigger doses including double or quadruple strength mixtures may be utilised.

d. Isoprenaline

This drug is a powerful Beta-stimulator which increases myocardial oxygen demand. It has a powerful Inotropic and chronotropic effect but is liable to provoke ventricular arrhythmias. It is seldom used now.

Isoprenaline infusion:
Add 2mg (2ml ampoule) found in the fridge to 500mls Glucose 5%
Titrate according to patients heart rate and blood pressure.
Use a giving set with a burette for safety
Usual doses (Bradycardia) 1-4 mcg/min I.e: 0.25-1ml/min

Or:    0.4 mg in 100 mls 5% Dextrose             (Therapeutic Range 5 - 15 mls/hr)

e. Adrenaline

Rarely used in our practice because of its severe vasoconstrictive and arrhythmogenic effects.

Therapeutic Range Starting Dose - 5 mls/hr

Infusion Recipe 2 mg in 100 mls 5% Dextrose.

f. Calcium Chloride

Intravenous calcium chloride (2 - 10 mls of 10% solution) produces a marked positive inotropic effect though it may provoke arrhythmias particularly in the presence of hypokalaemia. Its effect is short-lived and is usually used while preparations are made for infusion of another inotropic agent.

g. Enoximone

This is a Type III phosphodiesterase inhibitor (Cardiac specific) and has direct myocardial effects. It has an effect on myocardial contractility and is an ionodilator.

4. Peripheral Resistance (Afterload)

If the cardiac output remains low after determinants 1 - 3 have been optimised and peripheral constriction is still present then a reduction in peripheral resistance may permit an increase in cardiac output. This is only possible with an adequate mean arterial pressure and an LAP which has been optimised, infusion of GTN/Sodium Nitroprusside or Phentolamine may be used to achieve this in combination with inotropic agents. In addition to this, mechanical circulatory support may be used to reduce afterload - IABP.


Though many varieties of LV assist-devices and artificial hearts are available we only have access to the intra-aortic balloon pump. This consists of a balloon inserted directly or percutaneously via the femoral artery and positioned in the descending aorta. It inflates during diastole and deflates during systole and is synchronised with the ECG.

We use this device to wean some patients from cardiopulmonary bypass, occasionally in postoperative low output state and preoperatively occasionally, eg post-infarction, VSD, unstable angina and those with very poor LV function. This predominantly supports the left heart.

The intra-aortic balloon pump has the following beneficial effects:

1. Reduces afterload - decreased systolic aortic pressure, increase diastolic aortic pressure.
2. Increases coronary perfusion by inflating during diastole.
3. Reduces myocardial oxygen consumption as a consequence of (1) and (2).
4. Decreases LAP (Preload).
5. Increase in stroke volume and cardiac output.

The technical aspects of counter-pulsation are supervised by the perfusion technicians and their advice should always be sort if there is a problem with the IABP. If a satisfactory haemodynamic situation is achieved then the balloon is usually removed after 24-48 hours. Heparin is administered while the IABP is in situ to prevent thrombosis occurring in the legs and on the balloon.

IV. Postoperative Hypertension

Postoperative hypertension is common particularly after coronary artery bypass grafting Excessively high blood pressure levels obviously predispose to bleeding from grafts and other incisions in the heart in the early postoperative period and should be avoided. We normally treat a blood pressure of greater than 130 - 140 systolic in the early postoperative period. The first step in management is to ensure adequate sedation, after this specific drug treatment may be instituted.

1. GTN (Nitrocine)

This drug is particularly useful in the management of CABG cases both intraoperatively and postoperatively. It has a vasodilator effect on veins and arteries and specifically improves subendocardial perfusion. It relives myocardial ischaemia by reducing Preload and Afterload. GTN is short acting and can be used safely to reduce hypertension in any postoperative patient. A 5 mg ampoule is diluted in 500 mls, 5% Dextrose and the infusion rate is titrated to give a satisfactory hypotensive effect.

2. Trimethaphan (Arfonad)

A ganglion blocker which reduces blood pressure by vasodilation. An advantage is its short duration of action but it is not always effective and tachyphylaxis occurs so other agents may need to be employed. 250 mgs Arfonad are diluted in 250 mls 5% Dextrose and the infusion rate is titrated against its clinical effects. ( Less commonly used)

3. Other hypotensive agents

The agents listed below are those used in certain circumstances, usually by those familiar with their usage.

• SNP infusion (50 mgs in 500 mls of 5% Dextrose) Titrate against effect Note that excessive doses lead to cyanide accumulation.
• Phentolamine (IV 2.5 mgs aliquots)
• Hydralazine (IV 2.5 mg aliquots)
• Chlorpromazine (IV 5 mgs aliquots + 2.5 mg aliquots thereafter)
• Labetolol (IV 50 mgs or an infusion). (Dangerous in asthmatics).

All the above agents should be administered cautiously since their effect is unpredictable and severe hypotension may result. Since they are all vasodilators their effect if profound may be reversed by rapid administration of volume.

V. Cardiac Arrest

It is the responsibility of all Doctors who may be called upon to resuscitate a patient to know where emergency equipment is stored and to be familiar with each item. Familiarise yourself with their storage position on the wards and ITU.

Most arrests occur in ITU, where the patient will be ventilated with intravenous, intra-arterial and ECG monitoring. In such cases:

1. Delegate someone to inform the ITU anaesthetist, cardiac registrar/SR on call
2. Commence external cardiac massage.
3. Hand ventilate with 100% F1O2
4. If VF/VT - Externally defibrillate - 50 J initially

• if unsuccessful increase to 100 J and repeat up to 300 J
• Give Lignocaine 100 mgs IV bolus
• Check serum K+
• If repeated VF start Lignocaine infusion.

5. If asystole or severe bradycardia:

• start pacing 80 – 90 demand
• if cardiac output is inadequate or no pacing wires give:

IV Atopine 0.3mg as a bolus dose.
IV Adrenaline 10 mls 1:10,00 via central line IV.
Calcium Chloride 10 mls 10% solution. Direct intracardiac injection
may be required.

These dosages may be repeated. In the case of severe bradycardia Isoprenaline
may be administered ( Note: Isoprenaline significantly increases myocardial energy demands.)

6. Bicarbonate Administration
This is almost exclusively in ITU in very unwell / unstable patients
• Arterial blood monitoring is usually available
• Administration of bicarbonate is best based on early blood gas analysis showing severe metabolic acidosis (i.e. increasing base deficit)
• If acidosis exists administration of 50 mls aliquots of 8.4% sodium bicarbonate is indicated
• blood gas analysis is then repeated

7. Emergency Sternotomy

Whatever the cause or other treatment instituted in a cardiac arrest, cardiac output must be maintained either by external or internal cardiac massage.

In this Unit, in early postoperative patients we favour early repeat sternotomy and internal massage, since this exclude tamponade, and particularly in the presence of prosthetic valves, it is likely to be less damaging to the heart.

If experienced help is not immediately available do not hesitate to reopen the chest. You will be criticised more for failing to do this than you will for doing it unnecessarily.

To do this, having donned a mask, gown and gloves:
• Clean the area while ECM is maintained as far as possible.
• Position towels or a “Steridrape”
• Reopen the incision with a scalpel
• Remove all wires with a wire cutter
• Spread the sternum with a large retractor
• If tamponade is the cause of the arrest it will be immediately obvious and the haemodynamic status will improve
• Try not to dislodge epicardial wires, coronary vein grafts and in particular internal mammary grafts.
• Commence internal massage by positioning the right hand behind the heart and the left hand anterior to the heart, compressing the heart between the two.
• Drugs may be administered directly into the ventricle as required.

Decisions regarding discontinuation of resuscitation will be taken by senior staff, but patients have survived and left hospital after >1 hour of cardiac massage.

VI. Arrhythmias

There are a variety of reasons for arrhythmia in the postoperative period, such as:

• Cardiac irritability from incisions, cooling, ischaemia etc
• Acidosis
• Hypoxia
• Digoxin
• Catecholamine infusion
• Hypokalaemia

Where possible if such a cause is present it should be corrected, if not empirical treatment should be used. In general, there is a tendency to over treat arrhythmias, provided that heart rate and blood pressure are within normal limits most rhythm disturbances will sort themselves out with the passage of time. Nevertheless, prompt treatment of serious arrhythmias is necessary to prevent reduction in cardiac output. This is very much a growing area of cardiovascular pharmacology and in one where we frequently as help from the on-call cardiologist.

1. Bradycardia

• Institute Pacing
• Atropine 0.6 mg IV if sinus bradycardia
• Isoprenaline infusion (rarely)
• Ask Cardiologist to insert transvenous wire if no epicardial wire or these are malfunctioning

2. Atrial Fibrillation/Supraventricular Arrhythmia

This is a stable rhythm for most patients so that cardioversion in the early post-operative period is rarely indicated urgently. Control of fast AF in the post-operative period is indicated if the rate is greater than 120/min. We employ the following drugs:-

a) Amiodarone

This is a powerful drug for the control of atrial and ventricular arrhythmias.

The dosage regime is as follows (via a central line):-

300 mgs in 100mls 5 % Dextrose over 1 hour
then 900 mgs in 250 mls 5% Dextrose over 23 hours

The initial oral dose is then 200 mgs tds for 1 week reduced thereafter to bd followed by maintenance od.

( Note. Some has a preference not to use this agent first line and prefers Digoxin)

b) Cardioversion

A DC shock applied to the chest is an effective way of restoring sinus rhythm, particularly supraventricular tachycardia. This is usually carried out by the Cardiologist.

3. Ventricular Arrhythmias

VF\VT - See cardiac arrest

c) Verapamil

The quickest drug in treating atrial fibrillation and other SVT. 5 mgs should be injected slowly IV and this dose may be repeated in 5 minutes provided the BP is maintained. The maximum effect occurs within 2-3 minutes and persists for 20 minutes. Verapamil should not be given to any patient who has received a Beta-blocker within the preceding four hours and with caution with patients on Digoxin or other anti-arrhythmic therapy since asystole can occur.

If catastrophic hypertension occurs following Verapamil administration its effect may be reversed by intravenous administration of Calcium Chloride

Sometimes the effect of Verapamil is maintained by giving it orally in a dose of 40 - 120 mgs tds.

If the patient converts to sinus rhythm no further therapy is usually given. If the patient remains in AF the patient is often digitalised.

d) Digoxin

To control fast AF a digitalising dose is given, the total dose required being 900 mcg\m2 in divided doses of six hourly intervals IV. It is unwise to exceed a dose of 0.125 mgs six hourly in patients who have taken Digoxin pre-operatively.

The maintenance dose is usually 1\6 - 1\4 of the digitalising dose. Care is required in the intravenous administration of Digoxin and it should be slowly as an infusion with ECG monitoring. Relative contra-indications to its administration are:

Low Serum K+ or ventricular ectopics

Ventricular Ectopics

These are treated in the early post-operative period if they are:-
i) Frequent (> 12/min)
ii) Multifocal
iii) "R on T"

Treat first by increasing serum K+ to greater than 4.5 mmol by potassium administration.
Magnesium sulphate 1 gm or 4 mmoles IV will help reduce myocardial irritability.
If they persist give an IV bolus of Lignocaine 1 mg/kg followed by an infusion (3 g Lignocaine in 500 ml of 5% Dextrose). The infusion is usually started at 3 mg/min for a few hours then reduced to 1 mg/min for 24 hours. Lignocaine is a negative inotrope and may cause hypotension. Non-cardiac tissue effects include altered consciousness, parathesia and convulsions.

Amiodarone (see above) is increasingly used for the same purpose.

vii) Neurological Complications

There has been much recent interest in neurological abnormality after cardiopulmonary bypass. The majority of these abnormalities are minor and recover spontaneously. It is important to establish early after operation that there is no gross motor deficit and that the patient is regaining consciousness in the normal way. Failure to do so in the normal way is commonly due air embolism. In this situation the overall prospect for recovery is good. If there is a real possibility of neurological injury give Dexamethasone 8 mg IV stat and 4 - 6 mg 8 hourly thereafter for 24 hours.

If fits or convulsions occur control with -

• IV Midazolam or Diazemuls 5 - 10 mg IV stat
• Phenytoin as directed by Neurologists
• Muscle relaxants and heavy sedation may be used but may also obscure evaluation of the neurological status

Serious neurological complications may necessitate -

• Prolonged ventilation including tracheostomy
• Nutritional support
• Pressure area care
• Long term catheterisation

viii) Post Operative Psychoses

These are multifocal in origin and often occur in the intensive care environment. They usually resolve spontaneously and it is uncommon to require psychiatric help. The following drugs may be of value:-

Heminevrin 0.8 % IV infusion 90 ml.hour initially until the desired effect is achieved then 10 - 40 ml/hour. (Severe cardiorespiratory depression may occur in overdosage)

Haloperidol 2 - 10 mg IM repeated as necessary

Chlorpromazine 50 mg IM repeated as necessary

ix) Renal Failure

Renal failure is much less common after cardiac operations than was the case some years ago. There is often an obvious cause for post-operative renal failure, usually severe hypotension before or during operation. Often the urine output is well maintained for 24 hours and we think that we have "got away it". But then the urine volume falls below 20 ml/hour, the blood urea rises and the urine urea falls. Renal failure may be said to be present when the urine volume is 20 ml/hour or less, accompanied by a urine urea less than 5 times the blood urea. Acute tubular necrosis can be regarded as established when the urine sodium is high, potassium low and urea low. In the face of impending ARF we employ three measures:-

1. Dopamine 3 - 5 ug/kg/min
2. Mannitol 100 ml 20% solution over 1 hour followed by 10 ml/hour
3. Frusemide infusion 1 – 5ml/hr (Conc. 10mg/ml) or bolus doses of up to 500
mgs 6 hourly

If there is no response to these measures regard renal failure as established and -

1. Restrict Fluids 500 ls/24 hours + measured losses
(Insensible losses = 400 ml/m+/24 hours)

2. Discontinue above measures 1 - 3 if unsuccessful

3. Review dose levels of all drugs, particularly nephrotoxic antibiotics

4. If anuric remove urinary catheter

5. Institute haemofiltration.

We notify the Renal Physicians that Haemofiltration is our preferred treatment of established renal failure and ask for their continued follow up..

Haemofiltration is indicated for :-

1. Hyperkalaemia
2. Fluid Overload (Often evident as pulmonary oedema/poor blood gases)
3. A blood urea over 50 mmol/l

Before resorting to HF for hyperkalaemia (K+) 6.0 mmol/l) several measures may be instituted:-

1. 10 ml 10% Calcium Gluconate protects against arrhythmias

2. Correct acidosis with 8.4% Bicarbonate as appropriate

3. Calcium Resonium 15 mg tds via the NG tube / PO

4. Glucose/Insulin infusion - (50 ml 50% Dextrose with 12 units of actrapid insulin) repeated as necessary with monitoring of the blood glucose

If a patient goes on to require formal haemodialysis, they remain under our care on our ward under go to B5 for HD as required.

x) Nutrition

All patients after any operation are in a catabolic state and are breaking down their own stores of fat and protein to repair the damage done at operation. Most cardiac surgical patients are able to drink on day 1 and eat on the second or third day if they are inclined to. Such patients require no special treatment but when a patient remains seriously ill on a ventilator, arrangements need to be made to feed them. The simplest way to do this is via a fine bore nasogastric tube with an appropriate liquid diet provided by the Dietician. If the feed is not absorbed then parenteral nutrition should be resorted to. Diarrhoea is common with enteral nutrition and is not a reason for abandoning the enteral route but should be treated symptomatically. Full strength feeds may be introduced at an infusion rate of 25 - 30 ml/hour over 3 - 4 days. Aspiration of the tube will reveal significant gastric retention if this is suspected. Commercially available feeds contain 1 Kcal/ml of feed and about 5 m Nitrogen/litre.

If enteral nutrition fails then we resort to parenteral nutrition via a "Nutricath" silicon catheter inserted via the infraclavicular route, usually by our Anaesthetic colleagues. General guidelines regarding TPN are difficult to provide since hospital policy is currently changing.

xi) Acid-Base Balance
A progressive metabolic acidosis usually indicates poor tissue oxygenation due to poor perfusion or reduced saturation of arterial blood. Treatment is directed towards improving and maximising arterial oxygenation and cardiac output, but empirical correction of a metabolic acidosis may be needed. 8.4% sodium bicarbonate (1 mmol/ml) should be used according to the following scheme which gives half of a conventionally calculated correction.

Base Deficit
Dose Na Bicarb Repeat Blood Gas Analysis
4 or less Nil 3 hours

5 - 6 either Nil 1\2 hour

or BD x kg 1\2 hour
3 x 2

>6 BD x kg 1\2 hour
3 x 2

Sodium bicarbonate infusion may be dangerous both because of the danger of sodium overload, induction of a more severe intracellular acidosis, estracellular metabolic alkalosis and consequent hypokalaemia and shift of the oxyhaemoglobin curve to the left thus impairing delivery of oxygen to the tissues. Administration of NaHCO3 is best discussed with one of the senior members of the team and is usuallt performed on ITU.

5. Routine Care in the Post-Operative Period

i) Ward Transfer\Day 1

Decisions regarding HDU / ward transfer of patients following a routine post-operative course will be made by the duty Senior SpR during the ITU ward round.

To be fit for transfer patients have to be stable haemodynamically, off the ventilator and extubated, fully conscious with minimal blood loss via the chest drains.


On the morning of the first post-operative day patients will require the following investigations -

U & E Creat - Serum
Blood Gases
INR - Valves

ii) Removal of Lines and Chest Drains

a) LA Lines are almost never used. However if present they are usually removed by the ITU SHO on the day following surgery unless directed otherwise. (Ask if in doubt). Chest drains should be left for 2 - 4 hours after removal of LA lines at least. Schwann Ganz lines are used more commonly, particularly in unwell patients to assess cardiac output and estimate LA pressures. If in situ they have to be removed by the SHO rather than the nursing staff.

b) Chest Drains are removed when they stop draining. This is usually when the hourly loss is less than 30 ml for 3 consecutive hours and is serous fluid. IN practice this is usually at some time during the first or second post-operative day. Drains are only removed on medical instructions. The mattress suture is tied as the drain is withdrawn and the site sprayed with iodine spray. A check X-ray is required after removal of a pleural drain though not after removal of a mediastinal or pericardial drain. Satisfactory analgesia must be administered prior to removal of chest drains, sometimes entonox or tramadol / morphine

c) Internal Jugular Lines\Pericardial Lines\Urinary Catheter

For ward transfer one central line, one peripheral line and the urinary catheter are usually left at least until the morning of day 2. The peripheral line is left until the morning of day 3.

d) Arterial Lines in routine cases are usually removed on the first or second post-operative day in HDU but may be maintained if repeat blood gas or potassium sampling is necessary.

e) ECG Monitoring is usually continued until day 3 on the ward.

iii) Anticoagulants

All patients with mechanical valves require long term oral anticoagulant therapy. Normally Warfarin is the drug of choice. Warfarin is normally commenced on the evening of day 1. It is extremely difficult to predict an initial dose of Warfarin even if patients have taken the drug before, since hepatic metabolism of this drug may be impaired by cardiopulmonary bypass and other drugs given in the peri-operative period. The initial Warfarin dose is usually moderate, say about 5 mg for about 3 days to reach a therapeutic dosage is guided by regular measurements of the INR. Anticoagulant clinic follow up must be arranged for patients at their local hospital or GP practice prior to discharge. A proforma letter requesting the monitoring of warfarin is sent to the GP with the TTH summary.

iv) Diuretics

Patients retain fluid after cardiopulmonary bypass. The extent of this is monitored by the difference between pre-operative and post-operative body weight, charted daily by the nurses. Patients with a significant increase in body weight are treated with diuretics for several days, usually Frumil (5/40) (Co-Amilofruse) After coronary artery bypass grafting diuretics may often by stopped before discharge. After mitral valve replacement the situation is different since the patients have been in borderline cardiac failure pre-operatively and usually require at least their pre-operative dose of diuretics. Dosages of diuretics in patients after valve surgery needs to be based on a general assessment of the patient, eg, presence of oedema, JVP, heptomegaly, body weight etc.

v) Digoxin

Most patients on Digoxin pre-operatively are restarted on Digoxin after operation. In this situation the "maintenance" dose is usually restarted at some point in the post-operative period when it is felt to be appropriate. It is usually unnecessary to "re-digitalise" the patient formally. If for any reason in the post-operative period a patient requires formal digitalisation this is based on the dosage schedule mentioned under "arrhythmias".

vi) Antiplatelet Agents

Most patients with coronary artery disease will be taking Aspirin. This should be discontinued before operation (except in cases of unstable angina) and restarted as soon as possible afterwards. Currently we use 150 mg of enteric-coated (EC) Aspirin.

vii) Beta-Blockers

After coronary artery bypass grafting the use of Beta-Blockers has been shown to reduce the incidence of supraventricular arrhythmias. Therefore in patients on Beta-Blockers pre-operatively these are usually re-started post-operatively - Atenolol 25 -50 mg daily. Contra-indications to restarting Beta-Blockers would be bronchospasm and hypotension.

viii) Ace-Inhibitors

Some patients are on these drugs to improve poor myocardial function. It is best to restart these drugs in the early postoperative period and allow the cardiologists to tail them off as the myocardial performance improves postoperatively.

ix) Physiotherapy

Regular chest physiotherapy both before and after extubation are keystones in the post-operative management of cardiothoracic patients. Adequate analgesia and encouragement must be provided by the medical staff.

x) Routine Ward Management

Patients sit out of bed and commence mobilisation on Day 2 after open heart surgery. Mobilisation is the best form of physiotherapy and thereafter they should be encouraged to be as active as possible.

Routine blood investigations and chest X-ray are performed regularly on all patients and entered into the post-operative charts. Typically Day 1,2, and Day 4.

Patients are usually discharged home 6 - 8 days after surgery.

Prior to discharge the pacing wires are removed 24 hours before (or day 3/4 ) provided the INR is not too high (>2.5)

• Out-patient drug treatment is prescribed
• Anticoagulant follow-up is organised
• Out-patient appointments with the Cardiologist (At 3months) and Surgeon (At six weeks) are arranged
• A discharge note must be sent to the GP
• A full discharge note must be sent to the GP as soon as possible after discharge ( This is usually dictated by the SpR)
• An information sheet is given to the patient containing details about resumption of their normal activities

Appendix 1:  Normal Values: 
Parameters of CV performance :
CVP 1-8mmHg
PCWP 6-12mmHg
CI 2.4-4.0 L/min/m2
SVR 770-1500dyn.s./cm5
SVRI 1600-2400dyn.sec.cm-5.m-2
PVR < 200 dyn.sec/cm5
PVRI 200-400dyn.sec.cm-5.m-2
SVI 40-70ml/beat/m2
LVSWI 40-60 g.m/m2
RVSWI 4 - 8 g.m/m2
RV EF 46-50%
RV EDV 80-150ml/m2 
Cardiac chambers pressures:
Site pressure mmHg saturation%
LA: 4-12 98
RA: 1-8 70
LV: 85-150/4-12 98
RV: 15-28/0-8 70
Aorta: 120/80 98
PA: 15-30/3-12 70
PAWP: 4-12

O2 consumption: 110-150ml/min/m2
AVA 2.6-3.5 cm2
MVA 4-6 cm2
EF 55-70%

pH 7.35-7.45 ([H+] 35-45nmol/l)
PaO2 10-13kPa (75-100mmHg)
PaCO2 4.7-6kPa (35-45mmHg)
HCO3 22-27
BE ±2

Lactate 0.5 - 1.6 mmol/l

Conversion: kPa to mmHg Xby 7.5                  mmHg to kPa Xby 0.133
Resp.failure PaO2<8 or PaCO2>7
Predicted normal PaO2=  104 - (age in years X 0.27)

Appendix 2:  Organ system failure scoring system:

Cardiovascular faliure:
• Heart rate =< 54/min.
• Mean ABP=< 49mm Hg.
• VT or VF.
• CI =< 2.01 l/m2.
• Serum pH =< 7.24 with pCO2 =< 49mm Hg.

Respiratory failure:
• Respiratory rate =< 5/min or=>49/min.
• PCO2 => 50mmHg (6.7 kPa).
• AaDO2 => 350 mmHg (46.7 kPa).
• Dependent on ventilator after 4 days.

Renal failure:
• Urine output =< 479 ml/24 h
• Serum crestinine =>300 micmol/l
• Serum urea => 35 mmol/l

Hematological failure:
• WBC =< 1000/mm3
• Platelets =< 20 000/mm3
• Haematocrit =< 20%

Neurological failure:
• GCS =< 6 in absence of sedation

Liver failure:
Clinical acute renal failure,
and P< 0.66,
where log(P/1 - P) = 10 - (4.3 X prothrombin ratio) - (0.03 X creatinine) - (0.85 X ENC)
ENC = +1 in presence f encephalopathy.
ENC = -1 in absence of encephalopathy.
System failure occurs when one or more of the above criteria are met.
AaDO2: alveolar - arterial oxygen difference.

A complication that arises when other diseases produce a severe and progressive form of systemic inflammatory response.
Diffuse infiltrates (all 4 quadrants) on CXR, and hypoxemia that was resistant to supplemental oxygen. (CXR is not reliable for distinguishing ARDS from cardiogenic pulmonary edema). Diffuse inflammatory injury in the lungs, Exudative material accumulates and eventually obliterates the alveolar airspaces.
ARDS is an infammatory process, not an accumulation of watery edema.
PaO2 < 8.0 kPa (60mmHg).
PCWP < 18mmHg.
PaO2/FiO2 < 26.6 kPa (200mmHg).
In ALI <40kPa(300mmHg).

• Intracranial hypertension.
• Blood products, catheter sepsis, drugs.
• Pneumonia, pulmonary contusion.
• Cardiopulmonary bypass.
• Pancreatitis.
• Translocation, Endotoxemia.
• Urosepsis, amniotic fluid embolism.
• Long bone fracture.

Tachypnea, progressive hypoxemia resistant to supplemental oxygen PaO2/FIO2 < 200), within 24 hours CXR shows bilateral pulmonary infiltrates. No evidence of left heart failure (PCWP < 18mm gH).

Pneumonia , Acute pulmonary embolism, cardiogenic (hydrostatic) pulmonary edema.

Fever, tachypnea, rales

Ventilator management:
• Peak inspiratory pressure (PIP) are kept below 35cm H2O by using tidal volumes of 7-10 ml/kg.
• External positive endexpiratory pressure (PEEP) 5-10 cm H2O is added to prevent compression atelectasis and to limit phasic collapse of the distal airways.
Inflation volumes of 5-8 ml/kg can result in CO2 retention, but in the absence of adverse effect, the hypercapnia is allowed to continue (permissive hypercapnia)

• CVP & PCWP overestimate cardiac filling volumes during positive-pressure mechanical ventilation, particularly when PEEP is applied.
• Dobutamine is used to augment COP in ARDS.
• Dopamine should be avoided because of its propensity to constrict pulmonary veins which will raise PCWP and reduce LVEDV.
• Vasodilators should also be avoided because of their propensity to increase intrapulmonary shunt, which will add to the primary gas exchange abnormality in ARDS (vasodilator prostaglandin are the exception).
• Steroids: the results do not favor the use of steroids in ARDS.
• Surfactant: not successful in adults.
• Antioxidants: nitric oxide can improve oxygenation and reduce pulmonary artery pressure in ARDS, mortality is unchanged. N-acetylcysteine may improve survival (one report).

PCWP < 18mmHg.
PaO2/FiO2 < 26.6 kPa (200mmHg).
In ALI <40kPa(300mmHg).

Respiratory failure:
PaO2 < 8.0 kPa (60mmHg).
Type I :
PaCO2 < 6.6 (50mmHg).
Type II:
PaCO2 > 6.6 (50mmHg)


SIRS: Systemic inflammatory Response syndrome 2 or more of the following: • Temperature > 38 or < 36. • HR > 90. • RR > 20. Or PaO2 < 4.3 kPa (32mmHg). • WBC > 12000 or <4000/mm3 or >10% immature forms.

Causes of SIRS:(initial stimuli) • Trauma. • Burns. • Pancreatitis. • Infection. initial stimuli--> cytokines, TNF, IL-1, IL-6, complement, coag. Systems (from endothelium, Macrophages, Lymphocytes). ______________________________ 
Signs of systemic inflammatory response (Fever & Leukocytosis) are called the "Systemic Inflammatory Response Syndrome" SIRS.

• Fever + Leukocytosis = SIRS
• SIRS + Infection = Sepsis
• Sepsis + Multiorgan dysfunction
= Severe sepsis
• Severe sepsis + Refractory hypotension = Septic shock

The signs of inflammation are not evidence of infection.

Multiple Organ Dysfunction Syndrome (MODS): is an inflammatory-mediated injury involve two or more organs.

- Empiric antibiotic therapy: if sepsis is suspected but not yet documented antibiotics directed at the common organisms: Vancomycin (staphylococci, enterococci, streptococci). Aztreonam or an aminoglycoside (gram -ve enteric organisms). Clindamycin or Metronidazole or Imipenem (Bacteroids fragilis).

- Steroids: have not proven beneficial and may be harmful in patents with severe sepsis and septic shock.

- Anti-inflammatory antibodies: tested without success.

- Antioxidant therapy: N-acetylcysteine showed promising results in ARDS.

TSS: Toxic shock syndrome:


Nosocomial infection in ICU:
• Gram +ve: 40% (staph aureus,
coag. -ve staph., enterococci ).
• Gram -ve: 40 % (pseudomonas, coliforms).
• Fungal infection 20%.

Appendix 3:        
Insulin Sliding Scale Regime

50ml normal saline containing 50 units Actrapid insulin- via syrige driver pump and iv line.

BM READING infusion Rate (1 or 2 hourly)
< 4 mmol/l     0 unit/hour
4-7                1
8-11              2
12-17            3
18-28            4
>28               medical review

• Assumes parallel continuous iv dextrose 6gms/hr and KCl 3mmol/l/hr (equivalent 5% dextrose/KCl 1L/8hrs).
• Tightness of control is a function of frequency of BM sampling and dosage alteration.

Appendix 4:      Dosage of Inotropees:

Epinephrine: positive inotrope & chronotrope (beta1, beta2, alpha)
(1-4 mcg/min)
Adverse effects: increase myocardial O2 consumption, Tachycardia, Arrhythmia, metabolic acidosis (alpha)
• 0.005-0.02mcg/kg/min alpha = beta
• < 0.05 mcg/kg/min (beta) potent inotrope
• > 0.1mcg/kg/min (alpha) increase SVR can produce severe vasoconstriction.
Starting dose:0.015mcg/kg/min
(1 mcg/min).
UHW: 2mg in 50ml dextrose 5%

Dosing: 0.008-0.06 cg/kg/min
Norepinephrine: raises BP & SVR, less positive inotropy.
(2-100 mcg/min)
Adverse effects: increase myocardial O2 consumption, visceral & renal ischaemia, metabolic acidosis (by increasing anaerobic glycolysis & lactate production ), exacerbates hyperglycemia.

2-4mcg/min can increase to 8-12
UHW: 4mg in 50ml dextrose 5%

Dosing: 0.03-0.3 mcg/kg/min (edmunds)
UHW: upto 1mcg/kg/min
40mg / 250ml
10-500 mcg/min
Dopamine: raises BP & SVR
beta1, DA, increase NA
0.5-2 mcg/kg/min DA
2-10mcg/kg/min beta1
>10mcg/kg/min alpha1,beta

Invalidates PCWP as a measure of left ventricular filling pressures.
I.: cardiogenic shock, circulatory shock synd associated with systemic vasodilation (Septic shock).

Infusion: 6X body wt(kg) in 100ml of 5%dextrose 1ml/hr=1mcg/kg/min
Dobutamine: Strong Beta1 agonist with mild beta2 effect.
2.5 - 20 mcg/kg/min (1ml/hr=1mcg/kg/min)

Not indicated as monotherapy in patients with cardiogenic shock as it may decrease BP because of decrease in systemic vascular resistance effect (baroreceptor mediated).
CI: hypertrophic cardiomyopathy.
increase COP, decrease SVR
Increase coronary blood flow
Loading dose 90mcg/kg
Maintenance : 5-20mcg/kg/min 
0.75mg/kg bolus, then
50mcg/kg bolus, then

10mg in 50ml 5% dextrose.start with 5 mls/hr.
• Potent beta adrenergic non selective agonist devoid of alfa activity.
• Dilates skeletal, renal & mesentric vascular beds;
• Decrease diastolic BP., causes tachycardia (secondary to direct and baroreceptor reflex effects on SA & AV nodes).
• Decrease PVR.
• May ---> RV ischaemia.
(1mg in 250ml 5% dextrose or 0.4 mg in 100ml)
Calcium chloride
Iv 2-10mls of 10% solution
Vasopressin (Petrissin)ADH:
0.1-0.4 units / min ( not more )
Indications for inotropes:
• Low BP. (syst. 90mmHg)
• Low CI (< 2.2L/m/m2) with elevated PCWP (>15mmHg).
• Elevation of arteriovenous O2 difference (> 5.5 ml/dl).
• Clinically: evidence of low tissue perfusion ( oliguria, cyanosis, cool extremities, altered mentation).

Start inotropes after correction of noncardiac factors: hypovolemia, arrhythmias, hypoxia & acidosis.

Appendix 5:  

Acid base Disorder                     Primary change                                  Compensatory change

Respiratory acidosis                    increase PaCO2                                 increase HCO3
Respiratory alkalosis                   decrease
 PaCO2                                decrease HCO3
Metabolic acidosis                       decrease HCO3                                  decrease PaCO2
Metabolic alkalosis                      increase HCO3                                    increase PaCO2
Respiratory compensation:
Chemoreceptors in the carotid body at the carotid bifurcation in the neck and in the lower brain stem.
• Met acidosis ---> inc ventilation --> dec arterial PaCO2
• Met alkalosis ---> dec ventilation --> inc arterial PaCO2

Metabolic compensation:
The kidneys compensate for respiratory acid base disorders by adjusting HCO3 reabsorption in the proximal tubules. This response appear in 6-12 hours. Because of this delay in renal compensation, respiratory acid-base disorders are classified as acute(before renal compensation begin) and chronic (after renal compensation is fully developed).

Correction of acidosis with sod. Bicarbonate: 8.4% in mls
(Body wt X base defficit) / 3
GIVE 1/2 of that amount

Appendix 6: Antifibrinolytic Drugs

Aprotinin (Trasylol):
A polypeptide, Serine protease inhibitor isolated from bovine lung that inhibits multiple proteases, preserve adhesive platelet receptors (GPIb) antifibrinolytic by inhibiting plasmin. In high dose it inhibit kallikreins. Aprotinin has been showen to reduce blood loss and transfusion requirements in ptatients who have undergone heart surgery.
High dose:
(Loading ) 2,000,000 KIU (280mg) 200ml, over 30min after induction of anaesthesia.
(Maintenance) 500,000 KIU/hour.
• Aprotinin reduces Inflammatory response.
• Excreted by kidneys, removed by haemofiltration.
• It elevate ACT (absorbed by kaolin but not by celite) so a celite ACT should be>750.
The wory is that it can block the graft in case of redo CABG.
Tranexamicacid (Cyclokapron):
10g infusion over 2 hours at anaseth. Induction. Or:
2g bolus, 8g during bypass.
10mg/kg loading dose. Followed by 1mg/kg/h for 12 hours.


Appendix 7: FORMULAS:
(normal 2.5-4.2l/min/m2)
Normal BMI < 25 kg/m2
BMI = Wt(kg)/ Ht(m)2
Normal BSA 1.6 - 1.9 m2
BSA = [Ht (cm) + Wt(kg) - 60 ]/100
Dubois formula:
BSA = Wt(KG)XHTX71.84 / 10000
BSA = sq root of ht(cm)Xwt(kg)/36000
Infusion rate = R / C (ml / min)
R: desired dose rate mcg/min
C: drug concention in infusate mcg/ml
Coronary Perfusion Pressure
(CPP) = Aortic P - Right atrial P
CPP should be at least 15mmHg for satisfactory CPR
Gorlin formula:
Valve area = valve flow/
(C)X (44.3)X Sq root of pressure
C= 1 in AV, C= 0.85 in MV

Kilopascal(kPa)= 0.133 X mmHg

mmHg = 7.5 X kPa

Ideal Body Weight (IBW)
Male IBW (kg) = 50+2.3(ht inch-60)
Female IBW(kg)=45.5+2.3(ht inch-60)
Plasma Osmolality = 2[Na+K]+[G]+[Urea]
Plasma osmolality = 290mosm/L
Urine osmolality =300-1400mosm/L
Anion Gap = [Na+K]-[Cl+HCO3]
Normally 10 to 16mmol/l
Bed bound medical pt. Needs:
8-12g of Nitrogen/day
(1g N=6.25g protein)
Predicted normal PaO2=
104 - (age in years X 0.27)
Wt(kg)= 2 X ( Age + 4 ).
BP(Syst.)mmHg = 80 + ( 2 X Age ).
Blood volume: 80 X Wt (kg).
Insensible fluid loss= 20ml/kg/day.
UOP = 1 ml/kg/hr.
Correction of acidosis with sod. Bicarbonate:
8.4% in mls
(Body wt X base defficit) / 3
GIVE1/2 of that amount
C to F degrees:
• X 9/5 + 32
F to C degrees:
• -32 then multiply X 5/9

Lung cancer:
5-year mortality from the time of presentation remains at approximately 85-90%. 80% will be inoperable at presentation, 20% will proceed to attempted resection, of whom 5-10% will be alive 5 years later.
(From BTS Guidelines):
Adenocarcinoma 30-35%
Squamous cell carcinoma ~ 30%
Large cell carcinoma ~ 10-20%
Small cell lung carcinoma ~ 15-25%

Operative Mortality:
Lobectomy 4%
Pneumonectomy 8%

Inoperable at operation: 5-10%
In sq cell lung cancer < 5% show brain metastases (MRI or CT) or bone metastases (bone scan) this percentage is higher in adenocarcinoma and highest in SCLC.
After surgery:
5 year survival rates (NSCLC):
T1-2 N0 50-70%
T1-2 N2 20-30%
T3 N0 45%
T3 N1 37%
T3 N2 0%

< 5% of SCLC are operable.

5 year survival rates superior sulcus (Pancoast tumours): ~ 30%

50% of all lung cancers have extrapulmonary spread at the time of diagnosis.
The average pt with a diagnosis of lung cancer has a 5-year survival of only 10-15%.

Solitary pulmonary nodule (SPN): 35% are malignant. 23% solitary metastases.
Differential diagnosis of SPN: neoplastic, infectious, inflammatory, vascular, traumatic, congenital, rheumatoid nodule, intrapulmonary lymph node, plasma cell granuloma and sarcoidosis.
Survival After AVR:
a) Early (hospital) death - 3-6% (<5%)
b) Time-related survival:
• 5 years - 75%cts (80-90%)glenn's
• 10 years - 60%
• 15 years - 40%
c) Mode of death
• Early due to CHF, hemorrhage, infection, CVA
• Sudden - 20%
• Device related - 20%

Incidence of rereplacement: 8-17%
Risk of rereplacement: 10%

Etiology of AV disease:
Rheumatic 30-40%
Congenital ~30%
Degeneative ~20-30

Bicuspid AV 0.9-2.0% of normal population.
MVR: Operative mortality: 2.5% for males and 3.9% for females for first time elective cases.
MVR+CABG: Coincident CAD increases operative risk (mortality 6.1% men, 12.2% women).
5-year survival after MVR: 80%.
10 year survival 50 - 87%.
5-year survival(CABG+MVR) 66%
10-year survival(CABG+MVR) 31%
-Freedom from failure at 10 years: 60-78%
-14 years freedom from operation: 27- 43%
Thromboembolism and Bleeding:
- Freedom from thromboembolism at 10 years is similar whether mechanical or bioprosthetic valves are implanted with a rate of 1.6 - 2.9% per patient year.

- between 20-60% of patients have bioprosthetic valve implantation are anticoagulated long term.
- The incidence of anticoagulant-related hemorrhage is between 0.18-2.2 per patient year.
Bleeding is most common in the CNS, GI and GU tracts.
Mechanical Valve Thrombosis and Structural Failure:
Bjork-Shiley valve has a thrombosis rate of 0.28% per patient year.
St. Jude valve has a thrombosis rate between 0.09 and 0.3%
Prosthetic Valve Endocarditis: several series have reported rates of endocarditis of 0.06 to 0.4%, early mortality as high as 75%
Mitral Stenosis
20-40 years from Rheumatic fever to onset of sypmtoms
Onset of symptoms to disability- 10 years
Atrial fibrillation 30-40% more common in older patients.
10 year survival-- Overall 50-60%
Asymptomatic => 80% (60% no progression of symptoms)
Symptomatic 0-15%
Severe pulmonary hypertension <3%
Older patients with atrial fibrillation 25%
Normal sinus rhythm 46%
Causes of death:
CHF 60-70%
Systemic embolism 20-30%
Pulmonary embolism 10%
Infection 1-5%
Mitral valve prolapse is most common form of valvular heart disease
Affecting 2-6% of population

Post-infarct VSD
Location: 60% anterior, 40% posterior
Occurrence: 1-2% of MI
Timing: 2-3 days post MI up to 2 weeks
Results or Repair
Survival: 35% early mortality
Functional status: good
Modes of death:
50% CHF, acute 10% sudden death
5% CHF, chronic, intractable.

Coronary Artery Bypass surgery:
Emergent CAB for hemodynamic instability during acute MI can salvage over 50% of such pts.
•40% of patients studied for symptoms will have significant stenoses in all 3 vessels.
•95% of patients with 1 completely occluded artery will have a significant stenosis in at least one other artery.
•10-20% of patients with significant disease will have L main involvement.
•Diffuse distal disease unsuitable for CAB is uncommon.
•Current hospital mortality is about 3%, most from acute cardiac failure.
•5-year survival is 88%
•10-year survival 75%.
•IMA graft favorably affects the mid- and long-term survival (after 6 years).
•About 25% of all deaths after CAB are unrelated to ischemic heart disease or CAB.
Freedom from angina:
•About 60% of patients are free from symptoms at 10 years.
Freedom from MI:
•Perioperative incidence is 2-5%
•5-year freedom is greater than 95% after CAB
Freedom from sudden death:
•Uncommon after CAB; 97% freedom at 10 years
•Poor preoperative LV function is the most significant risk factor for sudden death postop
Neurologic events:
•Up to 75% of patients may have subtle neurologic deficits in the perioperative period.
•Gross neurologic defects occur in less than 1% of younger patients but up to 5% of patients over age 70.

Graft History
A. Vein grafts:
• 10% close within the first few weeks if antiplatelet therapy is not used.
• 10-year patency is about 50-60%
•B. IMA grafts:
• Intimal hyperplasia also develops; the IMA is highly resistant to atherosclerosis
• 10-year patency is about 90%
• 5-10% develop late stenoses, but most of these do not progress to occlusion.

Reintervention after CAB
• Most interventions are reoperative CAB, although PTCA used in about 25% of cases.
• 90% of patients are free from reoperative at 10 years.
•IMA grafting reduces reoperations and extends time to reoperation.
• Overall risk for reoperative CAB is about twice that of first CAB (~6%).
• 10-year survival after reoperative CAB is about 65% .
Infective Endocarditis (IE):
0.3-3 per 1000 hospital admissions
Native valve endocarditis (NVE):
predisposing factor in 55-75%
Mortality 20-30%
Prosttic valve endocarditis (PVE): 7-25% of cases of IE
Mortality 23-70%
Early PVE within 60 days of surgery. The limit will change to 12 months.

Outcome of patents undergoing surgery using circulatory arrest:
•CVA ~ 7%
•Tranient neurological disturbance 20%
Results After Operation for aortic dissection:
1) Early (hospital) death
• Ascending aorta - 5-10% (up to 30%)
• Arch - 10-25% (up to 50%)
• Descending - 10% (up to 25-60%)
2) 10 year survival - 46%
• 1/3 late death related to residual old false channel or redissection
3) Aneurysm of false channel
• Uncontrolled hypertension - 50%
• Controlled blood pressure - 10-20%
4) Redissection - 10% (Marfan higher)
Renal dysfunction: Acute renal insufficiency or renal failure cmplicates 15 % of CPB procedures, 2% require dialysis.

Neurological injury: 0.8 - 5% reported with CVA post CPB, reported mortality reach 20% in this group.
The incidence of cognitive impairment or delirium is 50% in the first week.

Bleeding complications:
The incidence of re-exploration is 4.2% was identified as a strong independent risk factor for mortality, renal failure, prolonged mechanical ventilation, ARDS, sepsis, atrial arrhythmias.

Appendix 9: ABC
Potential Reversible causes of cardiac arrest:
• Hypoxia
• Hypovolemia
• Hypo/hyperkalemia & metabolic disorders
• Hypothermia
• Tension pneumothorax
• Tamponade
• Toxic / Therapeutic disorders
• Thrombo-embolic and mechanical obstruction




To download Thoracic clerking book: http://www.ctss.org.uk/4.html

Pre-operative Care of Thoracic Surgical Patients

Pre Operativ1.Admission and Pre operative work up
Most of thoracic surgical patients are referred due to bronchial or pleural malignancy for primary operative treatment, others are referred with bullous lung disease, empyema or for diagnostic biopsy of lung, mediastinal tissue or pleura.
Thoracic patients need thorough assessment prior to surgical intervention as they are often elderly, have multiple co morbidities and are very frequently smokers. The patients are often admitted two or three days prior to surgery.
The patients should be clerked once admited. The following investigations should be arranged:

1 Chest X ray – An up to date CXR is required, both to reassess the pulmonary pathology and assess heart size. A note should be made of any significant changes in the size of any lesions and the presence of any new pathology e.g. pleural effusion, pleural thickening etc.
3 Pulmonary function tests – Obtained on the ward by the ECG technicians
4 Blood Tests - FBC, Coagulation screen, ESR
• U & E’s, Creat, LFT’s, Calcium, CRP
• Group and Save
• ABG’s on air – If significant SOB / Low O2 Saturation

5 Bacteriology – Nose/Throat swabs for MRSA screening. Urine and sputum as necessary
6 Chest Physiotherapy – This is particularly important as many thoracic surgical patients have significant lung disease
7 Old Notes / Referring Hospital Notes/X rays – These are extremely important as they will have details of investigations so far including details of histology and cytology. They provide the necessary information to allow pre operative planning of surgery.
8 Assessment of Cardiovascular function – Any patients with significant history or risk factors for ischaemic heart disease should undergo Echocardiography and Exercise Tolerance testing (ETT with the Standard Bruce Protocol). If a thoracic surgery patient undergoes ETT then one of the Cardiothoracic SHO’s on the ward will be asked to supervise the test in the Cardiology Out patients department.
9 Consent – This should be completed once the procedure has been finalized with the appropriate Consultant Cardiothoracic Surgeon.
Consent – The major risks of thoracic surgery including, mortality, DVT, PE, Infection, Pneumonia, MI, Angina and the possibility of inoperability should be discussed. The patients should also be informed of the fact that they will have venous lines, arterial lines, central lines, urinary catheter and epidural after most thoracotomies whether they have Lobectomy, Pneumonectomy, pleuropneumonectomy or decortication.



2. Pre operative modification of treatment

This is very similar to the advice give in the Cardiac Surgical patient; the majority of medication should be left unchanged.

Anticoagulants - should be stopped so that the INR is less than 1.4 ideally pre operatively. If necessary iv unfractionated heparin should be started in their place. If the coagulation has not normalized pre operatively, then discuss with the appropriate SpR about the use of FFP. (Vitamin K is almost never used, as it makes re anticoagulation extremely difficult) If the operation is delayed then anticoagulation must be temporarily restarted.
Aspirin – This should be withheld at for ideally 2 weeks preop, however if this is not possible then it should be stopped on admission and restarted immediately post op.
Monoamine oxidase inhibitors – Stop 3 weeks prior to surgery. 
Anti diabetic agents / Steroids - Discuss with the anaesthetist re. The timing of stopping of anti diabetic agents, the use on insulin sliding scale pre operatively and the use of iv steroids to cover the necessary stress response of major surgery in those on long term oral steroids. 
All other medications should continue unhindered
Of special note as pre-operative prophylaxix  is the use of digoxin in thoracic surgical patients: -

Digoxin 500mcg PO at 22.00hrs the night before surgery
Digoxin 500mcg PO at 07.00hrs the morning of surgery

l All patients will have been seen by an anaesthetist and a pre med will also have been

3. Arrangements for Surgery

These follow similar principles to the preparation of an operation list for Cardiac surgery, i.e. all results should be in the notes, the pre operative bronchoscopy report and histology/cytology if performed should be in the notes, as should the reports of any Echo / ETT tests. The most recent CXR and any CT scans must be available to go to theatre with the patient.

a) Prior to any major pleural / lung resection every patient undergoes rigid bronchoscopy and this should be noted on the operating list and the patient should be consented for “Rigid Brochoscopy +/- Biopsy”.

b) Those patients undergoing diagnostic bronchoscopy or mediastinoscopy should always be consented for biopsy also.

The typical routine request for blood products pre operatively are as follows: -

Pleuropneunonectomy 4 – 6 units
Pneumonectomy 2-4 units
Lobectomy 2-4 units
Decortication 4 units
Pleural/ Lung Biopsy 2 units
(Open / VATS)
Mediastinoscopy 2units
Bronchoscopy +/- Biopsy G & S

4. Operating theatre

Thoracic operating days are typically the responsibilities of the resident doctor (SHO) are similar to the cardiac patients. Once in the anaesthetic room, the patients X rays should be put up on the x ray box in theatre, in male patients the urinary catheter should be placed once the anaesthetist is happy for you to do this and the operation site should be inspected to ensure it has been adequately shaved on the ward. If not there are safety razors in the anaesthetic room to complete the shave. When the patient is asleep and all the lines are in situ you should assist in positioning the patient on the operating table prior to surgery. When entering Cardiothoracic theatres the wearing of masks is mandatory.

Peri and Post Operative Management

1.) General Principles
Thoracic surgical patients have very intense monitoring in the immediate postoperative period, intensive physiotherapy (which is essential), high intensity nursing in Thoracic HDU and the ward of significant medical input.

2.) Intraoperative Care
The patients will be catheterised by the SHO in the anaesthetic room once the patient is asleep, the x rays placed on the x ray box in theatre and the patient placed on the appropriate side. The patient will be moved into theatre. The anaesthetist wills mange fluids / blood intraoperatively and will the initial dose of antibiotics.

3.) Management in Recovery
Thoracic surgical patients are routinely woken in theatre and go to general recovery, in recovery a chest x ray is performed to ensure the lung is fully expanded, a FBC, U&E's, and ABG should be performed, if the patient has had significant blood transfusion the coagulation should also be checked .The SHO involved in the patients operation should arrange this, including phoning the labs/ X ray. The intercostal drains are placed on low suction as appropriate: -

Lobectomy / Decortication / Lung Biopsy
Drains on suction at 5 - 10 cm H2O  (3-5 kPa)

Drains NEVER on suction
(This would cause Mediastinal shift, impairment of venous drainage and Cardiac Arrest)

The CXR and blood results should be reviewed prior to return to the ward.

4.) Early Post Operative Care

a) Antibiotic Prophylaxis
The normal regime is cefuroxime 1.5g iv at induction followed by 3 doses of cefuroxime 750mg iv
If the patient was an inpatient in another hospital prior to surgery then additional prophylaxis: -
Teicoplanin 400mg iv at induction, Teicoplanin 400mg iv 3 doses post op should be given
If the patient is on a treatment regime of antibiotics for a confirmed infection these should be continued and altered according to any sensitivities obtained.

b) Thromboprophylaxis

The current regime is the use of TED stockings and Enoxaparin 40mg SC BD until mobile, early mobilisation is also part of the regime and the patients will often be moved to the chair on the first day.

c) Analgesia and Antiemetics

After the majority of thoracic procedures the patients will have an epidural in situ, in addition to this regular paracetamol and diclofenac, if there are no contraindications, should be prescribed. Once the epidural has stopped at between 2 and 3 days post op, Sevredol 10 - 20mg PO 1 - 2 hourly should be considered.

Postoperative nausea is relatively common thus regular antiemetics are helpful, typically we use:-

Metoclopramide 10mg tds iv
Ondansetron 4mg tds iv
Cyclizine 50mg tds iv (Slowly)

d) Investigations post op

CXR are performed immediate postoperatively and then as clinically indicated and after the removal of any intercostal drains. The first morning: FBC, U & E's

e) Urine Output

This is monitored hourly and we aim for a minimum of 0.5ml/kg/hr, post op thoracic surgical patients are very sensitive to fluid, especially those undergoing Pneumonectomy. Pulmonary oedema in these patients is extremely serious, relatively easily precipitated and frequently fatal.

Thus fluids should be given with care, assessing CVP and response to a small fluid bolus (i.e. Haes 6% 250ml over 1 hr). If urine output is falling in the face of a high CVP, then small boluses of Frusemide 10 – 20mg iv should be considered. If this is unsuccessful consider starting Dopamine at a so called “ Renal Dose” i.e. 2.5 – 5.0 mcgs/kg/min
Maintaining an adequate CVP.

5.Management of Chest Drains

A significant proportion of patients have intercostal drains insitu, they are initially on suction in most patients, except those who have undergone Pneumonectomy or pleuropneumonectomy where the drains are NEVER on suction.

The use of suction and the removal of drains is assessed on both the activity of drain i.e. how much they bubble and also on the CXR i.e. the degree of inflation of the remaining lung tissue. Drains are almost always taken out one at a time and a chest film should always be performed post drain removal. The site of insertion of the drain should be inspected periodically as infection is possible and any air leak at the site should be noted.

The decision to remove suction and to remove a chest drain is typically made by one of the SpR’s on the morning ward rounds.

6.Continuing Care /Referral

Many of the patients undergoing thoracic surgery require oncological referral for Radiotherapy / Chemotherapy, a referral form for the referral of patients to  Consultant Clinical Oncologist.

1. Lung cancer patient should be followed-up for a period of five years post lung cancer surgery. This should consist of an initial six-weeks appointment post hospital discharge followed by six-monthly follow-up for the first two years and then yearly to complete the five years. At each follow-up, patient symptoms (to detect lung cancer recurrence or metastasis) should be reviewed, patient should be examined appropriately and a CXR should be performed. If in doubt,  flag the CXR to the consultant or check for the formal report from the radiologist.

If patient wants to be followed-up locally, then please document in the clinic letter the patient’s preference and ask the referring chest physician to follow-up patient according to above protocol.

2. Patient with benign conditions (pneumothorax surgery, lung/pleural biopsies) should be discharged to the care of the referring chest physician, after the six-week appointment.

3. Patient who underwent metastasectomy should be referred back to the referring physician after the six-weeks follow-up.

4. Patient who had undergone endobronchial resection of carcinoid should be followed-up for life. This should consist, initially of OPD alternating with check bronchoscopy at regular intervals until consecutive check bronchoscopies are NAD. Then they should be followed-up yearly in OPD.

5. Patient with mesothelioma should have a six-weeks and then a three months appointment. Thereafter they should be discharged to their local chest physician.

6. Patient post decortication for empyema should be discharged to the care of their referring physician after the six-weeks appointment. If patient had a long-term intercostals chest drain or has undergone a Claggett’s procedure, then OPD management needs to be discussed with the responsible consultant.