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EMERGENCY MANUAL

Current evidence based guidelines for management of medical emergencies

FORWARD
This Manual is intended for use by primary carers who are called upon to manage medical emergencies in both community and hospital settings. It should be emphasised that the management protocols contained in the Manual are intended as a guide and should not be seen as appropriate for every patient and in all circumstances. In particular, great care should be taken to individualise treatments to account for individual patients comorbidities, and to ensure familiarity with the doses, indications, contraindications, reactions and interactions of all medications used. For many conditions, a distinction has been made between hospital and prehospital treatments. However, as treatment protocols may vary somewhat from setting to setting particularly in more remote areas - it is important to become familiar with the way in which emergency services and treatment protocols vary in the specific location concerned. Communication by telephone, fax and internet is now so advanced that ongoing management decisions can often be made in consultation with specialist colleagues. This should be encouraged as it always improves patient outcomes, and is essential when transfer of care is contemplated. Chris Cooper Convenor, Course in Emergency Medicine Department of General Practice University of Sydney September 2006

CONTENTS
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. APPENDIX 1. APPENDIX 2. APPENDIX 3.
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CARDIAC ARREST ACUTE CORONARY SYNDROMES ATRIAL FLUTTER AND FIBRILLATION SUPRAVENTRICULAR TACHYCARDIA (PSVT) VENTRICULAR TACHYCARDIA CARDIOVERSION SINUS BRADYCARDIA ATRIOVENTRICULAR RHYTHM AND BLOCK ACUTE PULMONARY OEDEMA ARRYTHMIAS IN HEART FAILURE ACUTE LIMB ISCHEMIA TEMPORAL ARTERITIS DEEP VEIN THROMBOSIS PULMONARY EMBOLISM SHOCK ACUTE ASTHMA CROUP COMPLETE UPPER AIRWAY OBSTRUCTION ACUTE EXACERBATION OF COPD PNEUMOTHORAX COMMUNITY ACQUIRED PNEUMONIA HYPOGLYCEMIA DIABETIC KETOACIDOSIS HYPEROSMOLAR HYPERGLYCAEMIA LACTIC ACIDOSIS IN DIABETES MENINGOCOCCAL DISEASE MENINGITIS STATUS EPILEPTICUS ACUTE STROKE ACUTE ANAPHYLAXIS DRUG OVERDOSE ACUTE UPPER GASTROINTESTINAL BLEED HYPERKALEMIA URGENT ELECTROLYTE ABNORMALITIES PAEDIATRIC FLUID REPLACEMENT INTEROSSEOUS INFUSION NEEDLE PLACEMENT IV DRUG INFUSIONS EMERGENCY TELEPHONE NUMBERS PAEDIATRIC DRUG DOSES

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CARDIAC ARREST
INITIAL RESPONSE
1. Check for responsiveness Shake and shout 2. Call for help Ring 000. Advise cardiac arrest, CPR in progress 3. Look, listen, feel for respirations

COMMENCE BASIC CPR


Indication for CPR: not conscious+ not moving + not breathing normally1 Do not attempt to find carotid pulse; difficult, unnecessary, time consuming.2 Any attempt at CPR is better than no attempt at all.1 Early basic CPR increases survival by 50%. Basic CPR does not restore sinus rhythm it supports circulation pending the arrival of a defibrillator. 1. External cardiac compression. Cardiac compression centre of chest ie over lower half of sternum1 Compressions should be delivered hard and fast.1 Ignore number of compressions per minute.1 Compressions to ventilations 30:2 (for 1 & 2 person, children & adults)1 Interruptions to compressions should be minimised no pause for ventilations1 NOTE: Compressions are more important than ventilations. There is growing evidence that chest compressions alone are as effective as compressions plus ventilation in the first 10 minutes of resuscitation. This is of particular relevance when lay operators are reluctant to administer mouth-to-mouth resuscitation. 2. Assisted ventilation Clear airway: head tilt, jaw thrust, clear oropharynx with sweep with index finger. Insert Guidels airway or endotracheal tube. Ventilations by bag and mask, mouth to mouth. Compressions to ventilations 30:2 for both 1 or 2 person CPR)1 Ignore number of ventilations per minute.1 Overventilation should be avoided.1

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3. Defibrillation. If a defibrillator is available, defibrillation shock should be delivered as an initial manouver before 1 & 2 above. Give three shocks in quick succession. Shock strengths: a. Monophasic defibrillator: all shocks 360 joules1 b. Biphasic defibrillator: all shocks 200 joules1 After each defibrillation attempt, give two minutes of CPR before checking rhythm. NOTE: There is some evidence a short period of 5 chest compressions prior to defibrillation improves chances of reverting to sinus rhythm. 4. Adrenaline. When adrenaline is available it should be given IV every three minutes irrespective of the rhythm, in order to maintain vascular tone. 5. Subsequent treatment If an electrocardiogram is available, treat according to the rhythm underlying disorder (see below). If rhythm is unknown all subsequent treatment should be based on the assumption that the underlying rhythm is ventricular fibrillation.
REFERENCES

1. International liaison committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations. Resuscitation. 2005: 67(2-3): 157-341. 2. Introduction to the International Guidelines 2000 for CPR and ECC Circulation. 2000;102:I-1. 3. Therapeutic guidelines: Cardiovascular. Version 4, 2003.

VENTRICULAR FIBRILLATION
(or pulseless ventricular tachycardia) Treatment should be given on a background of ongoing basic CPR as outlined above. 1. Defibrillation. Perform as initial manoeuvre. Single shock (ie not stacked shocks) for VF or pulseless VT.1 2. Adrenaline 1mg (1ml of 1:1000 or 10mls of 1:10000 solution) IV Give every 3-5 minutes. Defibrillate within 30secs of each bolus unless found to be in asystole. If there is no venous access, adrenaline can be given via ETT at twice the IV dose. 3. Antiarrhythmic therapy. If still in VF after x3 cycles of adrenaline consider: a. amiodarone 5 mg/kg IV, via a central line over 20 minutes then 10 to 15 mg/kg over 24 hours
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b. sotalol 1 to 2 mg/kg IV, over 10 to 30 minutes, repeat if necessary at 10 minute intervals c. lignocaine 75 to 100 mg IV, over 1 to 2 minutes, followed by 4 mg/minute for a maximum of 1 hour, then 1 to 3 mg/minute by IV infusion. 4. Sodium bicarbonate. If resuscitation is prolonged beyond 10 to 15 minutes, or if pH<7.2 on blood-gas analysis, use sodium bicarbonate 8.4% (1 mmol/mL) 1 mmol/kg IV, over 5 to 15 minutes. If unable to establish IV access and patient is intubated all drugs (except bicarbonate) may be given down ETT at twice normal dose.
REFERENCES

1. International liaison committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations. Resuscitation. 2005: 67(2-3): 157-341. 2. Introduction to the International Guidelines 2000 for CPR and ECC Circulation. 2000;102:I-1. 3. Therapeutic guidelines: Cardiovascular. Version 4, 2003.

ASYSTOLE
Treatment should be given on a background of ongoing basic CPR as outlined above. NOTE: Asystole occurs in about 20% of cardiac arrest, and its prognosis is uniformly poor. When asystole occurs as the initial rhythm it is often secondary to underlying problems which may require specific treatment. These include hypoxia, hyper/hypokalemia, acidosis, drug overdose and hypothermia. 1. Adrenaline 1mg (1ml of 1:1000 or 10mls of 1:10000 solution) IV Give every 5 minutes. If there is no venous access, adrenaline can be given by intratracheal administration at twice the IV dose. Evidence regarding efficacy is conflicting. 2. Atropine 1.0mg IV. Repeat every 3-5 minutes to total dose of 0.04mg/kg.(ie about 3mg for 70kg man). 3. Sodium bicarbonate If resuscitation is prolonged beyond 10 to 15 minutes, or particularly if pH<7.2 on blood-gas analysis, give sodium bicarbonate 8.4% (1 mmol/mL) 1 mmol/kg IV, over 5 to 15 minutes. NB: Defibrillation shocks should not be administered in asystole it is ineffective and shocks may damage the myocardium. However care must be taken to exclude apparent/artifactual asystole due to: incorrect lead placement very fine VF

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If unable to establish IV access and patient is intubated all drugs (except bicarbonate) may be given down ETT at twice normal dose.
REFERENCES

1. International liaison committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations. Resuscitation. 2005: 67(2-3): 157-341. 2. Introduction to the International Guidelines 2000 for CPR and ECC Circulation. 2000;102:I-1. 3. Therapeutic guidelines: Cardiovascular. Version 4, 2003.

PULSELESS ELECTRICAL ACTIVITY (P.E.A.)


Definition: Electrical activity but no output. Includes electromechanical dissociation, idioventricular rhythms, and bradysystolic rhythms. Treatment is as for asystole. PEA may be secondary to underlying problems which may require specific treatment. These include: cardiac tamponade (including left ventricular rupture), severe hypovolaemia, tension pneumothorax, pulmonary embolus, and overdosage of calcium channel blockers. 1. Adrenaline 1mg (1ml of 1:1000 or 10mls of 1:10000 solution) IV Give every 3 minutes. If poor response after multiple boluses consider high dose 5mg (5mls of 1:1000). Defibrillate within 30secs of each bolus (i.e. at least every 3 minutes) unless found to be in asystole. 2. Atropine 1.0mg IV. Repeat every 3-5 minutes to total dose of 0.04mg/kg.(i.e. about 3mg for 70kg man) 3. Consider specific drugs (see below) NB: If unable to establish IV access and patient is intubated all drugs (except bicarbonate) may be given down ETT at twice normal dose.

ADDITIONAL DRUGS IN SPECIFIC CIRCUMSTANCES


1. Calcium chloride 10mls 10% solution IV Indications: pre-existing suspected or proven: hypocalcaemia, hyperkalemia, hypermagnesemia, or calcium channel blocker toxicity. 2. Sodium bicarbonate 100mls of 8.4%solution IV Indications: prolonged arrest (>15 mins), tricyclic OD, hyperkalemia. 3. Magnesium 10mmol (2.5g) IV Indications: pre-existing suspected or proven hypomagnesaemia.
REFERENCES

1. International liaison committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations. Resuscitation. 2005: 67(2-3): 157-341. 2. Introduction to the International Guidelines 2000 for CPR and ECC Circulation. 2000;102:I-1. 3. Therapeutic guidelines: Cardiovascular. Version 4, 2003.
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PAEDIATRIC CARDIAC ARREST


Current guidelines recommend: Interosseous access rather than IV access unless prior IV access Mouth-to-nose ventilation is an alternative to mouth to mouth Two-thumb, chest-encircling compressions for children <2 yrs Compression to ventilation ratio: 15:21 Adrenaline (1:1000) Adrenaline (1:10000) Cardioversion initial shock Amiodarone Lignocaine
REFERENCES

0.01 mls/kg 0.1 mls/kg 2 joules/kg1 5mg/kg 5 mg/kg

Cardioversion subsequent shocks 5 joules/kg1

1. International liaison committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations. Resuscitation. 2005: 67(2-3): 157-341. 2. Introduction to the International Guidelines 2000 for CPR and ECC Circulation. 2000;102:I-1. 3. Therapeutic guidelines: Cardiovascular. Version 4, 2003.

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ACUTE CORONARY SYNDROMES


Acute coronary syndromes (ACS) are clinical syndromes consistent with myocardial infarction or accelerated angina, characterised by chest pain or discomfort at rest or for >10 minutes which is unrelieved by anginine, or which is associated with syncope or cardiac failure. Associated symptoms of dyspnoea, diaphoresis, nausea or vomiting may be prominent or occasionally occur in isolation. Atypical presentations are more common in women, diabetes, and in the elderly.

IMMEDIATE PREHOSPITAL TREATMENT


1. Arrange urgent ambulance transport. 50% of fatalities following ACS occur within 2 hours of onset of chest pain, and are due to reversible arrthymias. The immediate and urgent requirement is to ensure access to a defibrillator in order to avoid early avoidable cardiac death from treatable arrthymias. All Australian ambulances now carry defibrillators. 2. Oxygen at least 8L/min. 3. Antiplatelet therapy. Aspirin 150mg P.O. crushed or dissolved to hasten absorption. This has a major influence on outcome. PLUS Clopidogrel Initial loading dose 300 mg. NB: If early cardiac surgery is considered likely clopidogrel should be withheld until the coronary anatomy is known. 4. Nitrates Providing BP>100 mm HG a. glyceryl trinitrate spray 400 micrograms sublingually, repeat after 5 minutes if pain persists (up to a maximum of 2 metered doses) OR b. glyceryl trinitrate tablet 600 micrograms sublingually, repeat every 3 to 5 minutes up to a maximum dose of 1800 micrograms (3 tablets) If possible, ensure cannula inserted before giving anginine as may cause precipitous hypotension. Give 1/2-1 SL (1/4-1/2 if first nitrates or in the elderly). Repeat 5-15mins PRN. providing BP>100 mm Hg. If >3 doses required consider glyceryl trinitrate paste, patch or infusion c. Glyceryl trinitrate paste 2.5-5cm
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d. Glyceryl trinitrate patch 25 or 50mg. Remove and wipe skin if BP falls <100mmHg. Remove after 18 hours, reapply after 6 hours. NB: Avoid nitrates if the patient has used sildenafil (Viagra) in the previous 24 hours or tadalafil (Cialis) in the previous five days. 5. Morphine 2.5-5mg IV Providing BP>100 mm Hg. (+/- Maxalon 10mg IV q8h) Repeat PRN until pain relieved, and providing BP>100 mm Hg, to max 10mg IV. 6. B-blockers: Consider if tachycardic and no contraindications. a. Metoprolol 5mg q5min IV x3, then 50mg q6h PO, OR b. Atenolol 5mg q5min IV x2, then 100mg/day PO 7. Take a 12-lead ECG providing it does not delay transfer. The ECG is the sole test which further defines acute coronary syndromes and determines the need for emergency reperfusion. 8. Telephone receiving facility of incoming patient with ACS.

1. NON-ST SEGMENT ELEVATION ACUTE CORONARY SYNDROME (NSTEACS)


NSTEACS is defined as an acute coronary syndrome which occurs in the absence of ECG changes of ST segment elevation or left bundle branch block.

TREATMENT IN HOSPITAL
Risk stratification. All patients NSTEACS should undergo risk stratification. Risk stratification determines subsequent management. (See Table next page)

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Risk Criteria
High risk ANY of the following: Repetitive or prolonged chest pain. At least one elevated cardiac biomarker. Persistent ST segment depression or new T wave inversion. Transient ST elevation in two leads. Hemodynamic compromise. Sustained VT Syncope Left ventricular ejection fraction <0.40 Prior PCI within last 6/12 Prior CABG Known diabetes Chronic kidney disease Intermediate ANY of the following: Chest pain at rest now resolved. Age >65 years Known CAD No high risk ECG changes (above) Two or more of the following: HT, family history, current smoking, hyperlipidemia. Presence of known diabetes. Chronic kidney disease Prior aspirin use Low ACS without high or intermediate risk features.

Management
Aggressive management with: platelet inhibitors, antithrombin therapy, B blockers, glycoprotein IIb/IIIa inhibitors Arrange coronary angiography and revascularisation.

Accelerated diagnostic evaluation to allow reclassification as high or low risk.

May be discharged with upgraded medical assessment for followup.

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Management of 'high risk' NSTEACS


1. IV glyceryl trinitrate Indications: Persistent or recurrent rest pain + ischaemic changes on ECG + poor response to glyceryl trinitrate sublingual, paste or patch. Give: 10 micrograms/minute by IV infusion, increase by 10 micrograms/minute every 3 minutes until pain is controlled, providing the systolic blood pressure (SBP) >95 mm Hg. Then: titrate to relieve pain and to keep BP>100 mm Hg. NB: Avoid nitrates if the patient has used sildenafil (Viagra) in the previous 24 hours or tadalafil (Cialis) in the previous five days. 2. Antithrombin therapy Give low molecular weight heparin (LMWH) or unfractionated heparin (UFH): LMWH is generally preferred. UFH requires constant monitoring, but has the advantage that may be easily reversed in high-risk patients who may require urgent intervention. NB: Care should be taken in the elderly and in those with impaired renal function, in whom the dose should be reduced to once daily. Enoxaparin 1 mg/kg SC, twice daily OR Dalteparin 120 international units/kg SC, twice daily to a maximum of 10 000 units OR dalteparin 120 international units/kg SC, twice daily to a maximum of 10 000 units OR unfractionated heparin 5000 units bolus IV, followed by 1000 units/hour by IV infusion, then adjust according to APTT. Monitoring: activated partial thromboplastin time (APTT) should be checked initially every 6 hours, aiming for a range of 60 to 80 seconds, and should be checked daily once therapy has been stabilised. 3. Beta blocker (Unless contraindicated) Give: atenolol 25 to 100 mg orally, once daily or metoprolol 25 to 100 mg orally, twice daily. Patients in whom Bblockers are contraindicated give:

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Nondihydropyridine calcium channel blocker Give: diltiazem 30 to 120 mg orally, 3 times daily OR diltiazem controlled-release 180 to 360 mg orally, daily OR verapamil 40 to 120 mg orally, 2 to 3 times daily OR verapamil sustained-release 160 to 480 mg orally, daily. 4. Glycoprotein IIb/IIIa inhibitors Indications: high risk patients with abnormal ECGs or positive troponin. a. In the coronary care unit, tirofiban (0.4 micrograms/kg/minute loading dose administered over 30 minutes, followed by a maintenance infusion of 0.1 micrograms/kg/minute for up to 72 hours), may be given, then followed by percutaneous procedures if indicated. b. In the cardiac catheterisation laboratory abciximab (250 micrograms/kg bolus loading dose, followed by a maintenance infusion dose of 0.125 micrograms/kg/minute to a maximum of 10 micrograms/minute) given over the 12 hours following the PCI. 5. Revascularisation Revascularisation should be considered in all patients who are at high risk. Clinical trials have demonstrated the benefit of an early invasive strategy
REFERENCES

1. National heart foundation of Australia/ The Cardiac Society of Australia and New Zealand. 'Guidelines for the management of acute coronary syndromes' 2006. Med J Aust 2006; 184; S1-S32 2. Therapeutic guidelines: Cardiovascular. Version 4, 2003.

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2. ST SEGMENT ELEVATION MYOCARDIAL INFARCTION (STEMI)


STEMI is defined as an acute coronary syndrome with ECG features including any of: persistent ST-segment elevation of greater than 1mm in two contiguous limb leads ST-segment elevation of greater than 2mm in two contiguous chest leads; new left bundle branch block (LBBB) pattern. NB: LBBB is presumed new unless there is evidence otherwise.

MANAGEMENT
1. Specific prehospital treatment. Where formal protocols are in place, prehospital treatment should be given, including fibrinolysis in appropriate cases. 2. Emergency reperfusion ie fibrinolytic therapy OR direct percutaneous coronary intervention (PCI), is indicated in all patients with STEMI who present within 12 hours of the onset of ischaemic symptoms. a. In general, direct percutaneous coronary intervention (PCI) is the treatment of choice, providing it can be performed promptly by a qualified interventional cardiologist in an appropriate facility. The maximum acceptable delay from presentation to balloon inflation is 60 minutes if a patient presents within 1 hour of symptom onset; or 90 minutes if a patient presents later. b. Fibrinolytic therapy. Second-generation fibrin-specific fibrinolytic agents that are available as a bolus (ie, reteplase, tenecteplase) are the fibrinolytics of choice. 3. Antiplatelet treatment. All patients undergoing reperfusion therapy for STEMI (PCI or fibrinolysis) should be given aspirin and clopidogrel unless these are contraindicated. Clopidogrel should not be given if the need for acute CABG is likely. a. Aspirin 150mg P.O. crushed or dissolved to hasten absorption. This has a major influence on outcome. PLUS b. Clopidogrel Initial loading dose 300 mg. NB: If early cardiac surgery is considered likely clopidogrel should be withheld until the coronary anatomy is known.
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4. Antithrombin agents. Give low molecular weight heparin (LMWH) or unfractionated heparin (UFH): LMWH is generally preferred. UFH requires constant monitoring, but has the advantage that may be easily reversed in high-risk patients who may require urgent intervention. NB: Care should be taken in the elderly and in those with impaired renal function, in whom the dose should be reduced to once daily. Enoxaparin 1 mg/kg SC, twice daily OR Dalteparin 120 international units/kg SC, twice daily to a maximum of 10 000 units OR dalteparin 120 international units/kg SC, twice daily to a maximum of 10 000 units OR unfractionated heparin 5000 units bolus IV, followed by 1000 units/hour by IV infusion, then adjust according to APTT. Monitoring: activated partial thromboplastin time (APTT) should be checked initially every 6 hours, aiming for a range of 60 to 80 seconds, and should be checked daily once therapy has been stabilised. Care should be taken in patients aged over 75 years, or those who have significant renal dysfunction dose adjustment is required.
REFERENCES

1. National heart foundation of Australia/ The Cardiac Society of Australia and New Zealand. 'Guidelines for the management of acute coronary syndromes' 2006. Med J Aust 2006; 184; S1-S32. 2. Therapeutic guidelines: Cardiovascular. Version 4, 2003.

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ATRIAL FLUTTER AND FIBRILLATION


INTRODUCTION
1. Atrial fibrillation rarely causes death or serious morbidity except via thromboembolism. 2. Anticoagulation should be considered in ALL patients in whom AF is discovered. 3. Rhythm control is no better than rate control. AF is frequently an asymptomatic finding, especially in the elderly. Many elderly patients and most younger patients, however, find the arrhythmia itself produces disturbing symptoms, and it is particularly in this group where one or more attempts at conversion to sinus rhythm, either electrically or pharmacologically, are commonly employed. However rate control is a perfectly acceptable first-line strategy and not just a 'fall-back' if rhythm control fails or proves difficult. In either case, due attention should be given to the question of thromboembolic prophylaxis. 4. Management requires prior assessment of ventricular function and/ or coronary artery disease. As many of the rhythm control drugs and some of those used for rate control have myocardial depressant or proarrhythmic potential, it is essential to have some idea of whether or not the patient has normal left ventricular function and/or coronary disease. This information is not always available on first presentation however. 5. Recent onset AF generally requires admission to hospital for anticoagulation. This is to avoid thromboembolism arising from 'atrial stunning' which commonly follows spontaneous or induced cardioversion.

ANTICOAGULATION
Initial anticoagulation Enoxaparin 1 mg/kg SC, twice daily OR Dalteparin 120 international units/kg SC, twice daily to a maximum of 10 000 units OR Dalteparin 120 international units/kg SC, twice daily to a maximum of 10 000 units.
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Subsequent anticoagulation is dependent on risk stratification. Anticoagulation with warfarin reduces the risk of stroke by about 70% in patients with nonvalvular AF. Aspirin at 325 mg/day seems to provide about one-third to one-half the protection provided by warfarin. Indications for warfarin are determined by three risk categories for thromboembolism*. Risk Category Risk Factors High History of Thromboembolic event or longstanding mitral valve disease 10-15% Intermediate History Thromboembolic event or longstanding mitral valve disease Low Nil

Annual risk of Thromoboembolism

3-5%

0.5-1%

Management

Long-term warfarin (unless strong contraindications.)

Long-term warfarin based on clinical judgement.

Probably no Warfarin. Consider aspirin.

Warfarin 5 mg orally, daily. (reduced in the very elderly.) Target INR: 2 to 3, or 2.5 to 3.5 (in patients who have already suffered thromboembolic event).

RATE CONTROL
1. Obtain and maintain long-term control of ventricular rate, use a c atenolol 25 to 100 mg orally, daily OR diltiazem controlled-release 180 to 360 mg orally, daily twice daily OR b metoprolol 25 to 100 mg orally OR d verapamil sustained-release 160 to 480 mg orally, daily

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2. Consider digoxin. In elderly, sedentary patients, additionally, or as standalone therapy, consider digoxin 62.5 to 250 micrograms orally, daily, according to age, plasma creatinine and plasma digoxin levels (steady state is achieved in approximately 5 days). (Digoxin alone frequently fails to control exercise-induced tachycardia. An alternative or additional therapy to control ventricular rate is often indicated.) 3. If the IV route is indicated give: a metoprolol 5 to 10 mg IV OR esmolol 500 micrograms/kg IV, over 1 minute, then titrate to achieve desired ventricular rate, typically 50 to 200 micrograms/kg/minute OR

b verapamil 1 mg/minute IV, up to 15 mg with careful blood pressure monitoring OR c digoxin 0.5mg in 20mls 5%D IV over 10-30mins. Repeat after 6hr. Then continue normal oral dose. CI: Digoxin in preceding 2 weeks. Although digoxin is often given IV in this situation and is unlikely to do any harm (whereas the other agents do have cardiodepressant potential), but is also very unlikely to have much effect on ventricular rate in the short term.

RHYTHM CONTROL: CARDIOVERSION


Pharmacological cardioversion: 1. Oral cardioversion give a flecainide 50 to 100 mg orally, 2 to 3 times daily (if normal left ventricular function and no coronary disease) OR

b amiodarone 200 to 400 mg orally, 3 times daily, aiming eventually to reduce to 100 to 200 mg per day 2. If IV cardioversion is indicated give: a amiodarone 5 mg/kg IV, via a central line over 20 minutes to 2 hours, then 10 to 15 mg/kg over 24 hours. OR

b flecainide 2 mg/kg IV, over 30 minutes. NB 1. Anticoagulation with warfarin should be started 2-6/52 before cardioversion. Transoesophageal echocardiography has 95 percent sensitivity for detecting atrial thrombus. In situations where this test is available, the demonstrated absence of thrombus at recent transoesophageal echocardiography'recent' meaning within 12 to 24 hours at most, and preferably within the previous 12 hours obviates the need for prolonged warfarin therapy prior to attempted conversion.

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2. Anticoagulation during and after cardioversion. Atrial stunning. There is significant risk of thromboembolism in the days following direct current cardioversion. This may be due to 'atrial stunning' causing weak atrial contractions for hours or days, despite sinus rhythm. Partly for this reason, but also because of the high initial incidence of relapse to AF following elective cardioversion, anticoagulation with heparin or warfarin should be initiated prior to or at the time of cardioversion, even if the transoesophageal echocardiography confirms no intra-atrial thrombus. There is no consensus on the ideal duration of postcardioversion warfarin therapy if SR is successfully restored and maintained, but current practice ranges anywhere from 1 to 12 months depending on the risk of embolismwhich in turn is a function of the presence of known risk factors for atrial thrombosis, and the perceived likelihood of relapse into AF. 3. If using flecainide, thought should be given to the possibility of accelerating the ventricular rate (a higher proportion of atrial impulses being conducted through the AV nodeespecially in atrial flutter). Consider pre-treatment with an AV nodal blocking agent such as digoxin or a beta blocker or nondihydropyridine calcium antagonist. 4. Sotalol is frequently used for attempted pharmacological reversion, but the evidence suggests it is no more effective than placebo, in contrast to its well-documented efficacy in maintenance of SR long-term. NB: If drug therapy fails to convert to SR within a reasonable time, synchronised electrical cardioversion should be considered. Long-term antiarrhythmic therapy after cardioversion, Oral antiarryhmics a sotalol 40 to 160 mg orally, twice daily (monitor for excessive QT prolongation; cease if QT or QTc exceeds 500 or increases by >20% from baseline; use low doses or not at all in patients with impaired renal function), OR

b flecainide 50 to 100 mg orally, twice daily (in patients with normal left ventricular function and no coronary disease), OR c amiodarone 200 to 400 mg orally, 3 times daily, aiming eventually to reduce to 100 to 200 mg per day.

NB 1. Amiodarone has been shown to be the most effective of these but is listed third because of its long-term adverse effect profile. 2. Long-term antiarrhythmic therapy is not required if atrial flutter or AF is associated with a transient condition, eg acute myocardial infarction (MI), cardiothoracic surgery, excessive alcohol. Consider whether the risks associated with recurrence outweigh those of long-term antiarrhythmic treatment.
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3. In patients without a precipitating cause, long-term antiarrhythmic therapy will maintain SR in about 50 percent of patients at 12 months after DC cardioversion. 4. There is no consensus about duration of anticoagulation following successful cardioversion, but as many strokes occur soon after relapse into AF, a good rule of thumb is to err on the side of continuing warfarin whenever there is thought to be a reasonable risk of relapse (i.e. generally much longer than the one month which has been common practice in the past). More invasive procedures, such as His bundle ablation with pacemaker implantation, radiofrequency ablation of atrial flutter pathway, or surgical approaches, may be considered in patients whose ventricular rate is poorly controlled with antiarrhythmic therapy.
REFERENCES

1. Non-valvular atrial fibrillation and stroke prevention. Graeme J Hankey, on behalf of the National. Blood Pressure Advisory Committee of the National Heart Foundation. MJA 2001; 174: 234-348. 2. Therapeutic guidelines: Cardiovascular. Version 4, 2003. 3. Consensus guidelines for warfarin therapy. Recommendations from the Australasian Society of Thrombosis and Haemostasis. Alex S Gallus, Ross I Baker, Beng H Chong, Paul A Ockelford and Alison M Street on behalf of the Australasian Society of Thrombosis and Haemostasis.MJA 2000; 172: 600-605

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PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA


(Narrow complex tachycardia )
NOTE: In the presence of a pre-existing (or rate related) bundle branch block, SVT may produce a wide QRS complex (>0.12 seconds) tachycardia which may be difficult to differentiate from ventricular tachycardia. If the QRS complex is wider than 0.14 seconds, ventricular tachycardia is more likely than PSVT. Verapamil must never be given to a patient with an undiagnosed widecomplex tachycardia. In such circumstances, either use adenosine, as above, or treat as sustained ventricular tachycardia.

CONVERSION TO SINUS RHYTHM


1. Manoeuvres that enhance vagal tone. a. Carotid sinus massage (firm pressure; slow circular motions; alternate sides; one side at a time; exercise care in the elderly and avoid if carotid bruit; more effective if lying flat; may reveal atrial flutter by temporarily slowing rate, even if doesnt revert), b. Valsalva manoeuvre or stimulation of nasopharyngeal afferents with icecold water. 2. Arrange transport to a hospital with cardiac monitoring facility. 3. Pharmacologic conversion. If the above is ineffective. Use, only under continuous ECG monitoring: a. Adenosine 6 mg bolus IV, over 5 to 10 seconds, if unsuccessful then followed 2 minutes later by a second bolus of 12 mg. If ineffective but well tolerated a further dose of 18 mg may be given OR b. Verapamil 1 mg/minute IV, up to 15 mg with careful blood pressure monitoring NB: Verapamil is generally safe in patients with supraventricular arrhythmias, the main concern being its ability to produce profound depression of contractility and/or heart rate in occasional patients, particularly those who have pre-existent myocardial disease. The danger of such an adverse response is also considerably greater in patients taking beta blockers prior to the administration of verapamil.
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Adenosine may be associated with transient hypotension and/or chest pain. 4. Repeat 1+2 if PSVT persists, vagal manoeuvres may be repeated, followed, if necessary, by further adenosine or verapamil. 5. Direct current cardioversion or overdrive pacing may be required. If PSVT persists.

PROPHYLAXIS
1. Occasional episodes of PSVT generally do not require prophylaxis. 2. Frequent episodes should prompt consideration of electrophysiological study and radiofrequency ablation therapy. 3. Prophylaxis. Give: a c e f. atenolol 25 to 100 mg orally, daily OR sotalol 80 to 160 mg orally, twice daily OR verapamil sustained-release 160 to 480 mg orally, daily. If the above agents fail, and in patients debilitated by recurrent symptoms, use amiodarone 200 to 400 mg orally, 3 times daily for 2 weeks as a loading dose, followed by 100 to 400 mg orally, daily b metoprolol 25 to 100 mg orally, twice daily OR d flecainide 100 to 200 mg orally, twice daily OR

REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

www.gpkit.com.au

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VENTRICULAR TACHYCARDIA
Treat only if: a c prolonged episodes if significant symptoms are present. b with haemodynamic compromise, or NB: Sustained ventricular tachycardia may initiate cardiac arrest = immediate intervention is essential.= need urgent ambulance transportation to an emergency department. 1. Arrange urgent transport immediately to a facility with cardiac monitoring facility. 2. In patients who are haemodynamically stable, use a. lignocaine 1 to 1.5 mg/kg (usually 75 to 100 mg) IV, over 1 to 2 minutes followed, if successful, by 4 mg/minute for a maximum of 1 hour, then 1 to 3 mg/minute by IV infusion OR b. amiodarone 5 mg/kg IV, via a central line over 20 minutes to 2 hours, then 10 to 15 mg/kg over 24 hours OR c. sotalol 1 to 2 mg/kg IV, over 10 to 30 minutes, repeat if necessary at 10 minute intervals, and if indicated 80 to 160 mg by IV infusion over 12 hours. 3. Direct current cardioversion. Cardioversion should be considered at an early stage if: a. acute drug therapy is unsuccessful or b. there is haemodynamic impairment 4. Correct any underlying causes such as ischaemia or electrolyte disturbances, eg hypokalaemia 5. ICD. Several large trials comparing antiarrhythmic drug regimens with ICD have now suggested that in many patients with recurrent ventricular tachycardia, an ICD may well be the most effective therapeutic option. Unless this possibility is ruled out, eg by extreme old age or coexistent malignant disease, early referral for cardiac electrophysiological opinion should be considered. 6. Maintenance. If a decision is taken to continue with long-term oral drug treatment to maintain SR then the choice of drug may be either empirical or may be decided after electrophysiological study.
24 MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

In patients with significant left ventricular dysfunction, use amiodarone 200 to 400 mg orally, 3 tds for 2 weeks, followed by 200 mg orally, on alternate days OR sotalol 80 to 160 mg orally, twice daily OR atenolol 25 to 100 mg orally, daily OR metoprolol 25 to 100 mg orally, twice daily OR

b Patients with otherwise normal hearts may also be treated with flecainide 100 to 200 mg orally, twice daily While there is increasing evidence for greater efficacy for sotalol than lignocaine in this situation, an initial trial of IV lignocaine has the advantage that, if successful, there is little toxicity likely, and if unsuccessful, any unwanted effects of the drug will wear off rapidly and allow the treating physician to move on to alternative therapies with minimal risk of additive adverse effects from multiple antiarrhythmic agents. Sinus rhythm may be maintained by continuing the successful drug. Breakthrough episodes require increased dosage or an empirical change to an alternative drug, or consideration of insertion of an implantable cardioverter-defibrillator (ICD) Criteria for determining the maintenance dosage of amiodarone are controversial. The lowest dose providing symptomatic relief may not prevent a potentially fatal episode. Plasma levels of amiodarone and its active metabolite may be of limited value in guiding dosage or for determining compliance.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

www.gpkit.com.au

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TORSADES DE POINTES
Definition. A form of polymorphic ventricular tachycardia in which the QRS axis is constantly shifting, often in patients with a prolonged QTc (>450 msec). It may occur spontaneously or during therapy with various drugs or combinations thereof, eg amiodarone, tricyclic antidepressants, phenothiazines, disopyramide, erythromycin, pentamidine, quinidine, sotalol, ketoconazole, and cisapride. For an up-to-date listing see www.torsades.org/. Torsades is frequently self-limiting and uncommonly fatal but can cause haemodynamic collapse or lead to cardiac arrest and death. 1. Any drug suspected of causing the arrhythmia should be ceased immediately. 2. Serum potassium should be checked urgently and IV potassium chloride administered to attain and maintain a level of 5 to 5.5 mmol/L. 3. If there is an underlying bradycardia (PR<60) administer atropine 0.5 to 1.5 mg IV, repeat after 15 minutes if necessary 4. The following have been reported to be successful in terminating the condition: a temporary transvenous pacing, where easily available, is probably the treatment of first choice; pace at a rate of 90 to 100 per minute OR

b magnesium sulfate 50% 4 mL (2 g) IV, over 10 to 15 minutes followed, if indicated, by 1 to 1.5 mL (0.5 to 0.75 g) per hour by IV infusion, for 12 to 24 hours OR c isoprenaline 20 micrograms IV, repeat according to clinical response, followed by an infusion at 1 to 4 micrograms/minute (occasionally higher doses may be required) OR

d lignocaine 75 to 100 mg IV, over 1 to 2 minutes followed, if successful, by 4 mg/minute for a maximum of 1 hour and then 1 to 3 mg/minute by IV infusion
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

CARDIOVERSION
1. Explain procedure and obtain informed consent (if clinical situation permits). 2. Monitor. Obtain IV access, ECG monitor, pulse oximetry. Ensure facilities for resuscitation. 3. Exclude contraindications: Digoxin toxicity, heart block. 4. Ensure patient is fasting for >6hours. If not fasting and clinical situation necessitates urgent cardioversion, intubate to protect airway. 5. Sedate with midazolam 2.5-5mg IV slowly (1-2mg increments). Monitor with pulse oximetry. 6. Synchronise defibrillator. Synchronised setting must be selected on defibrillator panel. 7. Ensure patient is not in contact with any other person or metal object. 8. Initial energies: a. Atrial flutter c. Ventricular tachycardia d. Atrial fibrillation 50 joules 50-100 joules 100 joules b. Supraventricular tachycardia 50 joules

NB: If no response wait 2-3 minutes. Attempts at cardioversion during this period may be unsuccessful. Then increase energies incrementally to maximum of 360joules.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

www.gpkit.com.au

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SINUS BRADYCARDIA
1. Treat only if symptomatic. Symptoms are uncommon at rates above 40 to 45 beats per minute. 2. Exclude reversible causes viz hypothyroidism and panhypopituitarism. 3. If acute treatment is required, use atropine 0.5 to 1.5 mg IV, repeat after 15 minutes if necessary. 4. Stop drugs which may cause or exacerbate (eg beta blockers, digoxin, sotalol, amiodarone, verapamil, diltiazem). 5. Chronic sinus bradycardia may be a feature of the sick sinus syndrome. Treat with sinoatrial or atrioventricular block or atrial tachyarrhythmia. 6. Pacing may be required if the bradycardia is symptomatic, or if intermittent tachyarrhythmia requires drug treatment which might exacerbate the underlying bradycardia.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

ATRIOVENTRICULAR JUNCTIONAL RHYTHM


Definition: Atrioventricular junctional rhythm (<60 beats per minute) is usually an escape rhythm when the sinus node is suppressed by drugs, by increased vagal tone or when there is atrioventricular nodal block. This rhythm rarely requires treatment. 1. If hypotension occurs, give atropine 0.5 to 1.5 mg IV, repeat after 15 minutes if necessary. 2. If atropine fails, use isoprenaline 20 micrograms IV, repeat according to clinical response, followed by an infusion at 1 to 4 micrograms/minute. Occasionally higher doses required especially in patients who have been taking beta blockers 3. If an isoprenaline infusion is required for more than 30 to 60 minutes, and as first choice in acute MI, use temporary transvenous pacing.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

INCOMPLETE ATRIOVENTRICULAR BLOCK


Indications Relative indications for treatment include: 1. symptoms such as syncope 2. occurring in the context of an acute MI. Management 1. Discontinue drugs which may cause AV block (such as digoxin, diltiazem, verapamil or beta blockers) 2. Further treatment depends upon the level in the conducting system at which the block is occurring: a. First-degree atrioventricular block (prolonged PR interval) requires no treatment. b. Second-degree heart block may be due to either: i. Wenckebach block (usually in the atrioventricular node) rarely requires treatment ii. Mobitz type 2 block (usually in the more distal conducting tissue) rarely requires treatment In chronic cases permanent pacing is recommended for distal block (Mobitz type 2) because of frequent early progression to third-degree atrioventricular block.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

www.gpkit.com.au

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COMPLETE HEART BLOCK


1. If acute and located in the atrioventricular node (i.e. normal qrs complex) treat conservatively. In this case the junctional escape rhythm has a rate of 50 to 60 beats per minute. Temporary pacing may be required for slow escape rates originating from a focus at any level if haemodynamic deterioration occurs. 2. If complicating AMI. Treat with urgent angioplasty i.e. concentrate on urgently reopening the culprit coronary artery (if available, or thrombolysis). 3. If occurring as wide QRS escape rhythm. Treat with urgent external transcutaneous pacing. Such a rhythm is often unstable and ventricular standstill may supervene. Many emergency departments now have facilities for and this can be very useful as a temporising measure while transvenous pacing is being organised. 4. If extreme bradycardia or hypotension a. Urgent external transcutaneous pacing If temporary pacing facilities are not immediately available, treat with: b. IV isoprenaline 20 micrograms IV, repeat according to clinical response, followed by an infusion at 1 to 4 micrograms/minute, 5. Chronic complete heart block nearly always involves the distal conducting system and permanent pacing is usually indicated.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

ACUTE PULMONARY OEDEMA


IMMEDIATE PREHOSPITAL TREATMENT
1. Sit patient up. 2. Oxygen 100% via non-rebreather 3. Frusemide 40mg IV or twice normal oral dose. Avoid if BP<100 mm Hg 4. Morphine 2mg increments IV titrate to response or maximum of 10mg IV (+ Maxalon 10mg IV q8h) Avoid if BP < 100. 5. Nitrates: a. Glyceryl trinitrate sublingual. Ensure cannula inserted before as may cause hypotension. Give 1/2-1 SL Repeat 5-15mins PRN providing BP>100 mm Hg or b. Glyceryl trinitrate paste 2.5-5cm or c. Glyceryl trinitrate patch 25 or 50mg. Providing BP>100 mm Hg. Remove and wipe skin if BP falls <100mmHg. Remove after 18 hours, reapply after 6 hours.

HOSPITAL TREATMENT
In addition to above, and if pulmonary oedema is severe, not responding, or associated with ischaemia or significant hypertension, add 1. Isosorbide dinitrate 5 to 20 mg sublingually, repeat after 30 minutes if necessary or Glyceryl trinitrate (Tridil) Infusion: 50mg (1amp) in 500mls 5%D. Start at 5ug/min (3mls/hour) and titrate to pain and to keep BP>100 mmHg. 2. CPAP at 10cm airway pressure. May need to be started early if treated before arrival. If no response after 15mins increase to 15cm 3. If confined to bed anticoagulation. When confined to bed all patients should receive: d. unfractionated heparin 5000 units SC, 8- to 12-hourly OR e. enoxaparin 40 mg (or 20 mg for low body weight) SC, OR f. dalteparin 5000 international units (or 2500 international units for low body weight) SC, daily unless other risk factors, eg AF, dictate full anticoagulation

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If pulmonary oedema remains severe and not responding, add: 4. Dopamine Must be given via central line Infusion:: 200mg (1amp) in 100mls 5%D (2mg/ml). Start at:2.5ug/kg/min (approx 5mls/hr for 70kg man) renal dose 5 ug/kg/min (approx 10ml/hr for 70kg man) ionotropic dose Increase at increments of 5 ug/kg/min (approx 10ml/hr for 70kg man) to max 20ug/kg/min (approx 40mls/hr for 70kg man). If pulmonary oedema is severe and not responding to diuretics and vasodilator, consider adding 5. Dobutamine May be given via peripheral line. Infusion:: 250mg (1amp) in 100mls 5%D (2.5mg/ml). Start at 5 ug/kg/min (approx 8ml/hr for 70kg man) Increase at increments of 5 ug/kg/min (approx 8mls/hr for 70kg man) to max 40ug/kg/min (approx 80mls/hr for 70kg man). OR 6. Milrinone 50 micrograms/kg IV, slowly over 10 minutes, followed by 0.375 to 0.75 micrograms/kg/minute IV, adjust according to clinical and haemodynamic response, up to a maximum of 1.13 mg/kg daily. PULMONARY OEDEMA IN SPECIFIC CIRCUMSTANCES: Pulmonary oedema + atrial fibrillation with rapid ventricular rate give Digoxin 0.5mg IV in 20ml 5% Dextrose over 10-30 minutes Repeat after 6hr. Avoid if received any digoxin in the last 2/52. digoxin. The following day digoxin 62.5 to 500 micrograms orally, daily, according to age, plasma creatinine and plasma digoxin level. Pulmonary oedema + hypotension (BP persistently<100 mm Hg). Dopamine Must be given via central line Infusion:: 200mg (1amp) in 100mls 5%D (2mg/ml). Start at:2.5ug/kg/min (approx 5mls/hr for 70kg man) renal dose 5 ug/kg/min (approx 10ml/hr for 70kg man) ionotropic dose Increase at increments of 5 ug/kg/min (approx 10ml/hr for 70kg man) to max 20ug/kg/min (approx 40mls/hr for 70kg man). OR Dobutamine May be given via peripheral line. Infusion:: 250mg (1amp) in 100mls 5%D (2.5mg/ml). Start at 5 ug/kg/min (approx 8ml/hr for 70kg man) Increase at increments of 5 ug/kg/min (approx 8mls/hr for 70kg man) to max 40ug/kg/min (approx 80mls/hr for 70kg man). When BP restored, give Lasix as above Pulmonary oedema + hypertension (BP persistently>160 mm Hg). Glyceryl trinitrate (as above) increase to maintain SBP >100 150 mm Hg.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.


32 MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

ARRHYTHMIAS IN HEART FAILURE


Introduction 1. Arrhythmias may rarely CAUSE heart failure if they persist for weeks to months eg supraventricular tachycardia. Control of the arrhythmia then completely reverses heart failure. 2. Arrhythmias may CONTRIBUTE to heart failure. Eg complete heart block, or tachyarrhythmias, (AF or atrial flutter with rapid ventricular response). Treatment of heart failure must then include appropriate treatment of the arrhythmia. Often it is not possible to determine how much the heart failure was due to the arrhythmia and how much to the underlying heart disease until the arrhythmia has been controlled for some time. 3. Arrhythmias frequently ARISE from heart failure. The more severe the underlying heart disease and the heart failure, the more severe and frequent the arrhythmias. a. Atrial tachyarrhythmias AF and, to a lesser extent, atrial flutter, are common in heart failure. They usually reflect atrial enlargement and are a consequence of the proarrhythmic effect of atrial stretch. In patients with substantial atrial enlargement, maintenance of SR following reversion is unlikely in the longer term. This limits the therapeutic options to ventricular rate control combined with judicious use of antithrombotic therapy, see Arrhythmias. b. Ventricular tachyarrhythmia. Consider an implantable cardioverterdefibrillator in patients with life-threatening ventricular arrhythmias, see Sustained ventricular tachycardia. Principles of antiarrhythmic therapy The principles underlying the approach to the treatment and prevention of arrhythmias in heart failure are listed below. Avoid potassium depletion from diuretic therapy. Maintain serum potassium above 4 mmol/L, preferably closer to 5 mmol/L. Use potassium-sparing diuretics freely, while remembering their potential to cause hyperkalaemia and dehydration. Avoid magnesium depletion from diuretic therapy. Advise patients to follow a prudent diet including at least two fish meals per week. Use ACEI in all patients and in maximum tolerated dose, given their proven effect in reducing arrhythmias and sudden death.

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Use beta blockers given their proven effect in reducing arrhythmias and sudden death. Where possible, use standard beta blockers instead of sotalol because of the small but definite risk of proarrhythmia with sotalol. If sotalol or amiodarone are used, use the minimum effective dose, obtain objective evidence of antiarrhythmic efficacy and monitor for possible proarrhythmia. Avoid using long-term cardiac stimulants such as beta agonists and cardiac phosphodiesterase inhibitors because of their proven proarrhythmic actions. Avoid using class I antiarrhythmic agents such as quinidine, mexilitene and flecainide because of their high proarrhythmic potential.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

ACUTE LIMB ISCHEMIA


Definition: sudden onset of severe ischaemia with associated sensory and motor loss and intense pain. Causes include thrombosis, thromboembolism from heart, aneurysm or atheroma, or thrombotic occlusion of an aneurysm. Such a source should always be sought.

IMMEDIATE PREHOSPITAL TREATMENT


1. Arrange urgent transport immediately to a facility with angiography and vascular surgery. 2. Protect limb using a cage and a heel pad, but do not elevate. 3. Analgesia: Morphine 5-10 mg IMI or IV.

INITIAL HOSPITAL TREATMENT


1. Anticoagulation with unfractionated heparin should be initiated unfractionated heparin 5000 units loading dose IV, followed by 1250 units/hour by IV infusion, then adjust according to APTT. 2. Thrombolysis is appropriate. Use a. streptokinase 2500 to 5000 international units/hour by intra-arterial infusion, with the catheter tip at the occlusion until patency is restored OR

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b. alteplase 1 to 1.5 mg/hour by intra-arterial infusion, with the catheter tip at the occlusion until patency is restored OR urokinase 50 000 to 100 000 international units/hour by intra-arterial infusion, with the catheter tip at the occlusion until patency is restored. NB: different regimens and techniques are used and expert advice should be sought 2. Warfarin maintaining an international normalised ratio (INR) of 2 to 3. Duration: 3 to 6 months (if due to embolism), long-term if embolism is from a cardiac source 3. Antiplatelet therapy. Commence aspirin if acute ischaemia is due to in situ thrombosis or atherosclerosis.
REFERENCES

Consensus guidelines for warfarin therapy. Recommendations from the Australasian Society of Thrombosis and Haemostasis. Alex S Gallus, Ross I Baker, Beng H Chong, Paul A Ockelford and Alison M Street on behalf of the Australasian Society of Thrombosis and Haemostasis.MJA 2000; 172: 600-605 Therapeutic guidelines: Cardiovascular. Version 4, 2003.

TEMPORAL ARTERITIS
Definition: Temporal arteritis is characterised by inflammation of medium size arteries, with the risk of vessel stenosis and occlusion. It occurs in people > 50 years causing pain and tenderness over the superficial temporal arteries with or without polymyalgia rheumatica. Irreversible blindness is an uncommon but devastating complication. A marked elevation of ESR is almost universal. 1. Prednisolone 1 mg/kg orally daily should be commenced immediately in patients presenting with typical clinical findings and should not be delayed pending the results of inflammatory markers. 2. Arrange early referral to a rheumatologist to oversee prednisolone therapy and for consideration of the introduction of steroid-sparing agents in selected cases.
REFERENCES

Therapeutic guidelines: Cardiovascular. Version 4, 2003.

www.gpkit.com.au

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DEEP VEIN THROMBOSIS


Introduction 1. The aim of deep vein thrombosis (DVT) treatment is to avoid complications of pulmonary embolism (PE) and post-thrombotic syndrome. Postthrombotic syndrome is characterised by recurrent pain, swelling, and increased risk of leg ulceration occurring for months or years following the primary event, and may be confused with recurrent DVT. 2. Risk of pulmonary embolism from deep vein thrombosis (DVT) is dependent on the location of the DVT, and this determines treatment protocols (see Table below). 3. DVT is confirmed by duplex ultrasound scanning and PE is confirmed by helical CT or isotope lung scan. 4. Anticoagulation is highly effective in preventing PE . 5. Graduated compression stockings reduce the incidence and severity of the post-thrombotic syndrome. Anticoagulation does little to prevent the postthrombotic syndrome. Treatment of deep vein thrombosis Iliofemoral DVT 50% risk of pulmonary embolism Anticoagulation Consider Thrombolysis PLUS Compression stockings Anticoagulation PLUS Compression stockings Anticoagulation OR Ultrasound surveillance program PLUS Compression stockings

Femoropopliteal DVT

25% risk of pulmonary embolism 5-10% risk of pulmonary embolism

Isolated calf DVT

NB: If duplex USS is not available, and clinical suspicion is high, LMWH may be started empirically on outpatient basis, pending USS,then discontinued if USS is normal

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MANAGEMENT
1. Anticoagulation Low molecular weight heparin (LMWH) LMWH has been shown to be at least as effective and as safe as an IV unfractionated heparin infusion in the initial management of deep vein thrombosis and allows treatment on an outpatient basis. Collect blood for activated partial thromboplastin time (APTT), international normalised ratio (INR) and platelet count. Give: a. Enoxaparin (clexane) 1.5 mg/kg SC, daily (maximum dose 150 mg daily) OR b. dalteparin 100 international units/kg SC, twice daily (maximum dose 10,000 international units twice daily) OR c. Enoxaparin (clexane) 1 mg/kg SC, twice daily (maximum dose 100 mg twice daily). Oral anticoagulation may be commenced on the same day as LMWH. Warfarin should not be commenced alone (i.e. without LMWH) as this is associated with a high rate of subsequent DVT recurrence. Give warfarin 5 mg orally, daily for 2 days. This initial dose of warfarin should be reduced in the elderly. Monitoring. LMWH should be given for a minimum of 5 days and until the INR has been above 2.0 on two consecutive days. The INR should be monitored daily and the dose adjusted according to INR until a therapeutic level is achieved. 2. Thrombolysis. Possible indications: ongoing hypotension, right heart failure or severe hypoxaemia, and no contraindications. Give: a. alteplase 10 mg bolus IV, followed by 90 mg by IV infusion over 2 hours (in patients below 65 kg in weight, the total dose should not exceed 1.5 mg/kg) OR b. streptokinase 250 000 international units IV, over 30 minutes, followed by 100 000 international units/hour by IV infusion for 24 to 48 hours. NB Streptokinase therapy may cause anaphylactic reactions and should not be given to patients who have previously had streptokinase therapy, because of the likely presence of neutralising antibodies.
REFERENCES

Consensus guidelines for warfarin therapy. Recommendations from the Australasian Society of Thrombosis and Haemostasis. Alex S Gallus, Ross I Baker, Beng H Chong, Paul A Ockelford and Alison M Street on behalf of the Australasian Society of Thrombosis and Haemostasis.MJA 2000; 172: 600-605 Therapeutic guidelines: Cardiovascular. Version 4, 2003.
www.gpkit.com.au 37

PULMONARY EMBOLISM
A clinical syndrome of dyspnoea, chest pain, cough, tachypnoea, tachycardia, and hypoxia (low Sa02, low Pa02) typically in association with: a normal or near normal chest examination a normal or near normal CXR specific clinical contexts (immobility, post surgery, postpartum) or risk factors (obesity, cigarette smoking, age>50) in >90% cases. PE is common, underdiagnosed and potentially fatal. Diagnosis, by V/Q or helical CT scan is dependent on consideration of the diagnosis and maintenance of a high index of suspicion. Treatment reduces mortality to < 10%.

MANAGEMENT
1. Oxygen 2. Analgesia 3. Anticoagulation If no evidence of hemodynamic compromise give low molecular weight heparin (LMWH) Give: a. Enoxaparin (clexane) 1.5 mg/kg SC, daily (maximum dose 150 mg daily) OR b. Dalteparin 100 international units/kg SC, twice daily (maximum dose 10 000 international units twice daily) OR c. Enoxaparin (clexane) 1 mg/kg SC, twice daily (maximum dose 100 mg twice daily). 4. If evidence of hemodynamic compromise: i. Anticoagulation with unfractionated heparin (UFH) 5000 units IV, as a loading dose, followed by 1250 units/hour by IV infusion. The APTT should be checked after 4 to 6 hours and the dose adjusted if not in the therapeutic range. If in the therapeutic range, the dose should be reviewed daily.

ii. Consider thrombolysis. Possible indications: ongoing hypotension, right heart failure or severe hypoxaemia, and no contraindications. Give: alteplase 10 mg bolus IV, followed by 90 mg by IV infusion over 2 hours (in patients below 65 kg in weight, the total dose should not exceed 1.5 mg/kg) OR streptokinase 250 000 international units IV, over 30 minutes, followed by 100 000 international units/hour by IV infusion for 24 to 48 hours.
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NB: Streptokinase therapy may cause anaphylactic reactions and should not be given to patients who have previously had streptokinase therapy, because of the likely presence of neutralising antibodies. iii. Consider surgical thrombectomy. Possible indications: ongoing hypotension, right heart failure or severe hypoxaemia, and no contraindications. iv. Oral anticoagulation may be commenced on the same day as LMWH. Warfarin should not be commenced alone (i.e. without LMWH) as this is associated with a high rate of subsequent DVT recurrence. Give warfarin 5 mg orally, daily for 2 days. This initial dose of warfarin should be reduced in the elderly.
REFERENCES

Consensus guidelines for warfarin therapy. Recommendations from the Australasian Society of Thrombosis and Haemostasis. Alex S Gallus, Ross I Baker, Beng H Chong, Paul A Ockelford and Alison M Street on behalf of the Australasian Society of Thrombosis and Haemostasis.MJA 2000; 172: 600-605 Therapeutic guidelines: Cardiovascular. Version 4, 2003.

SHOCK
A clinical syndrome characterised by hypotension and inadequate tissue perfusion (ie falling urine output, impaired consciousness, cold extremities), due, usually, to uncontrolled haemorrhage, sepsis or anaphlaxis.

MANAGEMENT
1. Establish IV access with x2 large bore cannulas. 2. Infuse Gelofusine at 10-20 mls/kg. 3. If cause is not immediately apparent, perform rapid, full body survey to establish underlying cause: a. Blood loss (hypotension, cold extremities, pallor) b. Sepsis (hypotension, warm extremities, fever) c. Anaphylaxis (hypotension, uricaria, wheeze, stridor) If no specific features are present, consider other causes: coronary syndromes, massive pulmonary embolism, tension pneumothorax. 4. If evidence of sepsis, take blood cultures x2 and commence: Benzylpenicillin 1200 mg IV PLUS. Ceftriaxone 50 mg/kg up to 2 g IV.. 5. If evidence of anaphyaxis treat as for Anaphlaxis.
www.gpkit.com.au 39

ACUTE ASTHMA
1. Assess severity of the attack. Clinical features Mild Physical exhaustion Talks in Pulse rate [NB1] PEF (% predicted) FEV1 (% predicted) Oximetry on room air Arterial blood gases No Sentences <100/minute >75% >75% >95% Not needed Moderate No Phrases 100120/minute 50%75% 50%75% 92%95% Perform if initial treatment response is poor (if PaCO2 >40 mm Hg treat as severe attack) Severe Yes Words >120/minute <50% <50% <92% PaCO2 >42 mm Hg; elevated or highnormal PaCO2 indicates ventilatory insufficiency requiring close monitoring and possibly ventilatory support Yes, consider ICU

Hospital admission needed?

No

Probably

Admission criteria: Patient should generally be referred to hospital if: Nebulised bronchodilators fail to relieve wheeze/SOB for >4 hours. Initial PEFR is < than 50% best/ideal reading. NB: Many other factors will reduce admission threshold: previous severe/precipitate attack, doubtful compliance, poor previous response etc.etc.

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Assessment of acute asthma in children Clinical features Altered consciousness Use accessory muscles Talks in Pulse rate PEF (% predicted) FEV1 (% predicted) SaO2 on room air Hospital admission needed? Admission criteria: Patient should generally be referred to hospital if: Nebulised bronchodilators fail to relieve wheeze/SOB for >4 hours. Initial PEFR is < than 50% best/ideal reading. NB: Many other factors will reduce admission threshold: previous severe/precipitate attack, doubtful compliance, poor previous response etc.etc. Mild No No Sentences >60 >75% >60 >94% No Moderate No Some Phrases 40-60 50%75% 40-60 90-94 Probably Severe Yes Marked Words <40 <50% <40 <90 Yes

MANAGEMENT OF ACUTE ASTHMA


Management of acute asthma is the same in adults and children. 1. Oxygen at least 8L/min to maintain PO2>94%. 2. Bronchodilators via SPACER* Salbutamol .100 micrograms MDI, 412 inhalations via a spacer** PLUS (optional) Ipratropium bromide 20 micrograms MDI, 48 inhalations (via a largevolume spacer)** Reassess immediately if no or poor response, repeat salbutamol immediately or after 20,30,60 or 120 minute intervals. In severe asthma salbutamol should be given continuously until control is achieved. Ipratropium should be repeated q2-4h. *NB Giving bronchodilators via nebulisers offers no advantage over spacers in either children or adults. If a nebuliser is used it should be driver by O2 at 8 liters/min if available. Give salbutamol 1ml (5mg) nebuliser solution+2mls NS (or one 5mg nebule) via nebuliser**

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PLUS (optional) Ipratropium bromide 2mls (500 ug) nebuliser solution (or X1 500 ug nebule) via nebuliser. 3. Hydrocortisone 100-250mg Children: 5mg/kg (max 100mg), Repeat q6h thereafter. OR Prednisone 50-75mg. Children 1 mg/kg. PO. Repeat daily. If response to 1-3 above is inadequate give the following: 4. Salbutamol IV 300ug over 5minutes, then as infusion (See IV Drug Infusions) Requires close monitoring in hospital setting. If response to 1-4 above is poor consider: 5. Magnesium sulfate 1.22 g IV Children 25100 mg/kg IV over 20 minutes. 6. Continuous Positive Airways Pressure (CPAP) if hypoxic (eg Sa02<90 mmHg, Pa02<55 mmHg) and exhausted. Start at 10cm airway pressure. If no response after 15mins increase to 15cm. Arrange CXR prior to CPAP to rule out pneumothorax. 7. If hypoxic (exhausted, shallow respiration, Pa02<50 mmHg, bradycardia) give: Adrenaline 0.3-0.5mg (0.3-0.5 ml of 1:1000 solution) IV over 1 minute. OR (if no IV access) Adrenaline 0.3-0.5mg (0.3-0.5 ml of 1:1000 solution) SC subcutaneously or via endotracheal tube for imminent cardiorespiratory arrest (exhausted, shallow respiration, Pa02<50 mmHg, bradycardia).
REFERENCES

1. Therapeutic guidelines: Respiratory. Version 3., 2003. 2. National asthma council. Asthma management handbook 2002.

CROUP
Poor prognostic indicators: Presentation early in the illness (within 24 hours of onset) ie likely to progress over 1-2 days. Younger child (smaller airway, greater obstruction). Known structural airway abnormality [eg subglottic stenosis] Past severe attack
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Admission criteria: Persistent stridor at rest. Other indications include: age less than 1 year symptoms progressed despite systemic corticosteroids doubtful parental compliance etc.etc. NB: Upper airway obstruction is made worse by changes in position and emotional distress. The child should be seated upright on its mothers lap with mother holding O2 mask away from face. Procedures causing distress should be avoided eg IMI injections. MILD CROUP (90% of cases) = barking 'croupy' cough alone 1. Paracetamol 2. Corticosteroids. Good evidence now exists for a single dose of oral prednisone 1mg/kg in most, if not all, cases of mild croup, as a means of preventing the progression to moderate or severe croup. 3. Advice to parents. Parents should be advised if cough progresses to stridor they should present directly to hospital. NB. Steam inhalation. There is anecdotal information but no clear evidence of the efficacy of steam inhalation (administered with child seated on parents lap in steamy bathroom). Boiling water should never be used for steam inhalation. Moderate croup (<5% of cases) = persistent inspiratory stridor at rest. NB This is an indication for hospital admission: While awaiting hospital transfer, give: 1. Oxygen 2. Corticosteroids: Oral: prednisone 1mg/kg or dexamethasone at 0.15 to 0.6 mg/kg. both once daily for 1 to 2 days. OR Nebulised budesonide (2mg b.d). Consider only if oral steroids not available or for children who have vomited after oral steroids. SEVERE CROUP (<1% of all cases) = biphasic stridor at rest + chest wall retractions PLUS, while waiting for hospital transfer, give the following: Nebulised adrenaline (1:1000 concentration at a dose of 0.5 ml/kg of body weight to a maximum dose of 4-5 ml delivered neat in the nebuliser bowl)
REFERENCES

Therapeutic guidelines: Respiratory. Version 3., 2003.


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COMPLETE UPPER AIRWAY OBSTRUCTION


Definition: Signs of advancing upper airway obstruction (biphasic stridor) and hypoxia (agitation -> bradycardia, obtunded, cyanotic etc) 1. The invasive procedure described below should only be considered when all other attempts to relieve airway obstruction have failed and patient is showing signs of severe advancing hypoxia. 2. In patients with impaired consciousness attempts should first be made to relieve obstruction by head tilt, jaw thrust, followed by gentle positive pressure ventilation with bag and mask. If this is not rapidly effective, move to cricothyroidotomy.

EMERGENCY NEEDLE CRICOTHYROIDOTOMY


Indication: Children < 10 years with complete upper airway obstruction which fails to respond to alternate measures. a. Position patient as above: neck extended. b. Identify landmarks: The cricothyroid membrane is identified between the lower border of the thyroid cartilage and the upper border of the cricoid cartilage.

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Mandible

Thyroid Cartilage Cricoid Cartilage Trachea

Cricothyroid Membrane

c. Prep skin and infiltrate with Xylocaine 1% (If clinical situation permits). d. Insert 12-14 gauge cannula through the cricothyroid membrane, angled at 90 to skin. When needle is placed in trachea, rotate cannula so that it is angled at approximately 45 and directed towards the lungs. e. Once placement is complete, remove needle, leaving plastic cannula in situ.
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f. A makeshift connection can be fashioned between the cannula and Ambubag (see diagram below). The cannula (1) is attached to a 3 ml syringe (3). The plunger of the 3 ml syringe is removed and attached to a bag-valve-mask device (Ambubag) via an 8 mm endotracheal connector. 3. Oxygen tubing on the Ambubag is connected to an oxygen source with a flow at 1015 L/min. Manual ventilation should be at a rate of 1-second compression with 4-second relaxation (guided with chest rise).

4. If required, a 3 way stop cock or Y connector (2) can be placed between the cannula and syringe to facilitate the escape of air in between insufflations. Lateral compressions of the chest will facilitate the escape of air. NOTE: Ventilating a patient with complete upper airway obstruction via a needle cricothyroidotomy is a life saving but time limited procedure which will lead to hypercapnea and hypoxia after 30-45 minutes after which intubation or a surgical tracheotomy will be required.
REFERENCES

Management of the Airway. The American College of Surgeons Committee on Trauma. September 2002. Chee-Fah C. Tzong-Luen W Hang C. Percutaneous transtracheal ventilation without a jet ventilator The American Journal of Emergency Medicine Vol 28, 2003 507-508.
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EMERGENCY INCISSIONAL CRICOTHYROIDOTOMY


Indication: Children > 10 years and adults. 1-3 As ABOVE 4. Transverse incision 1 cm through cricothyroid membrane. NB some means of maintaining patency of incision will be necessary, and should be obtained in advance eg 3-5 gauge endotracheal tube (depending on patient age) , or improvise with cut tube of giving set, stethoscope, outer casing of ballpoint pen etc. if nothing else available.

REFERENCES

Management of the Airway. The American College of Surgeons Committee on Trauma. September 2002.

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ACUTE EXACERBATION OF COPD


NB: Arrange CXR to rule out pneumothorax and to look for radiological evidence of pneumonia. 1. Controlled oxygen. Indicated for hypoxia, with the aim of achieving achieving SaO2 88-92%, PaO2 55 mmHg. Note however, patients with COPD are typically chronically hypoxic, and tolerant of low PaO2. No further benefit is gained in trying to obtain SaO2 >92% If patient is known to be a chronic CO2 retainer in the past, or if status unknown give LOW DOSE oxygen via NASAL PRONGS at 0.5-2 L/min, or 24% via VENTURI MASK. Monitor with ABGs and increase to 28% then 35% at hourly intervals in order to maintain Pa02>55%, providing PaCO2 does not increase >10mmHg with each increment. 2. Bronchodilators Beta2 agonists and ipratropium bromide work equally well, although some may respond better to one type of medication than the other, so treatment should be tailored to individual response. The onset of effect of salbutamol is more rapid than that of ipratropium bromide. Give via SPACER salbutamol 100 micrograms MDI, up to 8 to 10 inhalations repeated as required PLUS (optional) ipratropium bromide 20 micrograms MDI, up to 4 to 6 inhalations repeated as required *NB Generally, nebulisers offer no advantage over MDI with spacers, although the evidence for this comes from studies in patients with asthma. Nebulisers may be indicated in very unwell patients in hospital, and if used should be driven by air at 8 liters/min. Give salbutamol 1ml (5mg) nebuliser solution+2mls NS (or one 5mg nebule) via nebuliser, continuously or repeated as required. PLUS (optional) Ipratropium bromide 2mls (500 ug) nebuliser solution (or X1 500 ug nebule) via nebuliser.

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3. Hydrocortisone 100-250mg or dexamethazone 4mg IV. Repeat q6h thereafter. or Prednisone 60mg PO. Repeat daily. 4. If evidence of infection (fever, purulent sputum, leukocytosis) give: amoxicillin 500 mg orally, 8-hourly for 5 days or doxycycline 200 mg orally, as 1 dose on the first day, then 100mg orally, x1-2/day for a further 5 days. or cefriaxone 1g IV plus roxithromycin 300mg PO daily 5. If rising PCO2, increasing respiratory acidosis, or exhaustion start Continuous Positive Airways Pressure (CPAP) at 10cm airway pressure. If no response after 15mins increase to 15cm. Nebulised medications can be given via the assisted ventilation circuit. 6. If respiratory arrest immanent (exhausted, shallow respiration, Pa02<50 mmHg, bradycardia) give: Adrenaline 0.3-0.5mg (0.3-0.5 ml of 1:1000 solution) IV over 1 minute. or (if no IV access) Adrenaline 0.3-0.5mg (0.3-0.5 ml of 1:1000 solution) SC
REFERENCES

1.Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. MJA 2003 178(6 Suppl 17 Mar) 2.Therapeutic guidelines: Respiratory. Version 3., 2003.

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PNEUMOTHORAX
EMERGENCY NEEDLE DECOMPRESSION of TENSION PNEUMOTHORAX
Signs of tension pneumothorax: absent breath sounds PLUS hypotension, syncope, tracheal shift, cyanosis etc Identify landmarks: 2nd intercostal space, mid clavicular line, above 3rd rib (rather than below 2nd rib). 1. Prep skin and infiltrate with Xylocaine 1% (if patient conscious and clinical situation permits). 2. Insert12-14G cannula full length of needle to pleura. Remove metal trochar/needle, leaving plastic cannula is situ. This should be followed by rush of air and sudden clinical improvement. 3. Leave plastic cannula open and in situ until formal intercostal drain can be inserted

SIMPLE (NON-TENSION) PNEUMOTHORAX


If SMALL (<2cm rim of air around lung i.e. < 50% collapse) and no shortness of breath OBSERVATION alone is usually all that is required. If LARGE (>2cm rim of air around lung i.e. > 50% collapse) or shortness of breath SIMPLE ASPIRATION or INTERCOSTAL DRAIN.
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SIMPLE ASPIRATION 1,2,3 As above. Attach cannula to 3 way tap. Attach 3 way tap to large (50-100ml) syringe and Heimlich valve. Aspirate gently 60mls at a time; turn 3 way tap each time to expel air through Heimlich valve. Cease when resistance to aspiration is encountered, or when 2 litres have been aspirated Repeat CXR. If <20% observe. If >20% proceed to intercostal drain.

INTERCOSTAL DRAIN NB: Indications: if simple aspiration fails, pre-existing lung disease, traumatic pneumothorax, tension pneumothorax. 1,2 As above. Make 1.5cm transverse incision (along direction of rib). Incise subcutaneous tissue to muscle. Use haemostat or finger to dissect through muscle. Should feel pop and rush of air. Sweep finger inside cavity to check for adherent lung tissue. Insert chest tube posteriorly and superiorly, making sure all holes are inside cavity.
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Double clamp tube (clamps at right angles to each other) Attach free end of tube to underwater drain. Remove clamps. Secure tube with purse string suture firmly tied around tube (circle tube x3, knots x3). Cut gauze to fit around tube. Cover with adhesive tape extending in airtight series of strips from skin onto tube. Tape tube to chest.
REFERENCES

Therapeutic guidelines: Respiratory. Version 3., 2003.

COMMUNITY ACQUIRED PNEUMONIA


CAP is usually caused by a single organism, the most common being Streptococcus pneumoniae. Other important causes include Mycoplasma pneumoniae, Chlamydophila pneumoniae and Legionella species. Haemophilus influenzae is responsible for less than 5% of cases of CAP and is seen predominantly in chronic obstructive pulmonary disease. NB: Hospital admission is usually indicated but ultimately dependent on factors such as age and presence of intercurrent medical problems. 1. Benzylpenicillin 1.2 g IV, 6-hourly OR amoxy/ampicillin 1 g IV, 6-hourly until significant improvement THEN amoxicillin 1 g orally, 8-hourly OR amoxicillin 1 g orally, 8-hourly for a total of 7 days. PLUS Doxycycline 200 mg orally, for 1 dose, then 100 mg orally, daily for a further 5 days OR roxithromycin 300 mg orally, daily for 7 days. 2. If Gram-negative bacilli are identified in the sputum or blood, gentamicin should be added to the above regimen (see recommendations for risk class V). 3. If hypersensitive to penicillin ceftriaxone 1 g IV, daily OR cefotaxime 1 g IV, 8-hourly until significant improvement THEN cefuroxime 500 mg orally, 12-hourly for a total of 7 days.
REFERENCES

Therapeutic guidelines: Respiratory. Version 3., 2003.

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HYPOGLYCEMIA
RECOGNITION Symptoms of hypoglycemia are of two types: 1. adrenergic symptoms: palor, sweating, shaking, palpitations, anxiety 2. neuroglycopenic symptoms: impaired cognition, confusion, seizures, coma. B blockers mask adrenergic symptoms leading to precipitous onset of neuroglycopenic symptoms. MANAGEMENT Mild to moderate hypoglycaemia If the patient is conscious and cooperative, give sugar-containing food (fruit juice, jelly beans, honey), followed by a long-acting carbohydrate (sandwich, dried fruit). Severe hypoglycaemia 1. Adult: glucose 50% 20 to 30 mL IV given into large vein because risk of superficial thrombophlebitis. Patients should wake within 4 to 5 minutes. OR Child: glucose 10% 2 to 5 mL/kg bolus IV, then 0.1 mL/kg/minute. (Glucose 10% is recommended in children as the excessive use of glucose 50% carries the risk of deaths due to hyperosmolality.) . OR 2. Adult: glucagon 1 mg SC or IM OR Child: glucagon 0.5 mg SC or IM Followed by oral feeding as above when conscious. Patients should wake within approximately 6 minutes following glucagon administration. Sulfonylurea-induced hypoglycaemia Hypoglycaemia due to sulfonylurea overdose causes long lasting hypoglycemia: 1. Arrange urgent hospital admission. 2. Glucose 10% 2 to 5 mL/kg bolus IV, then 0.1 mL/kg/minute often prolonged treatment is required 3. Frequent monitoring of blood glucose to exclude a recurrence of hypoglycaemia. 4. Octreotide 50 micrograms SC, 8-hourly for up to 3 doses. Octreotide can reduce both the duration of intravenous therapy and the need for added boluses of 50% glucose.
REFERENCES

Therapeutic guidelines: Endocrinology, Version 3, 2004.


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DIABETIC KETOACIDOSIS
NB: Arrange urgent hospital admission. IV rehydration using normal saline should be commenced prior to transfer. 1. Oxygen 6L/min 2. Fluid resuscitation. Monitor BP, PR, UO Give normal saline 1L stat, 1L over 1 hour, 1L over 2 hours, 1L over 4 hours, 1L over 8 hours. Give hypotonic saline initially if Na>150 or serum osmolality>320mOsm/kg 3. Potassium replacement. Monitor K hourly. Start replacement when K<5. Give 20mmol (1.5g)/K/hr for first 6 hrs then 10mmol(0.75g)K/hr for next 12hrs according to clinical response. 4. Insulin infusion Monitor venous BSL hourly (ward capillary BSL readings may be inaccurate). Infusion: 20 units Actrapid in 20mls. Start at 3 units(3mls)/hr. BSL should fall at approx. 5 mmol/L/hr. If BSL not falling after 2 hours* increase infusion rate 1 unit per hour until clinical response. When BSL reaches approx 15 mmol/L: i. halve insulin infusion rate (to approx. 0.5-2.0 units/hour) and ii. start 5%Dextrose at 1L q6h Continue insulin infusion and 5%D to maintain BSL at approx 10 mmol/l until ketosis is has resolved. If sliding scale order is required, make an estimate based on clinical response or give: If BSL>22 mmol/L, give 4 units/hr If BSL18-21 mmol/L, give 3 units/hour If BSL 12-17 mmol/L, give 2 units/hour If BSL 8-11 mmol/L, give 1 unit/hour with 5%D at 50-100mls/hr.

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OR Subcutaneous insulin Monitor BSL q2h . Give sliding scale as follows: If BSL> 20 mmol/L, give 10units of Actrapid. If BSL 10-20 mmol/L, give 5units of Actrapid. If BSL> 10 mmol/L, give no Actrapid. *NB If high doses (5-50 units/hr) required to cause drop in BSL, think of inadequate resuscitation, sepsis, thyrotoxicosis, Cushings, steroids, or Bblockers. 5. Magnesium replacement Monitor Magnesium q4h and replace PRN (See Electrolyte Abnormalities) 6. Phosphate replacement Monitor Phosphate q4h and replace PRN (See Electrolyte Abnormalities) 7. Sodium bicarbonate 8.4% 70 to 100 mL IV, over 20 to 30 minutes. Treatment with bicarbonate should be reserved for those patients with severe ketoacidosis and considered only if the pH is below 7 and creating an immediate cardiovascular risk. Sodium bicarbonate should be given as an infusion of 1 to 2 mmol/kg with strict attention to potassium levels, which may fall precipitately. The aim of this treatment is to reduce the immediate risks of extremely low pH, not to normalise pH.
REFERENCES

Therapeutic guidelines: Endocrinology, Version 3, 2004.

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HYPEROSMOLAR HYPERGLYCAEMIA
Hyperglycaemic hyperosmolar state occurs primarily in type 2 diabetes especially in the elderly, and is characterised by marked hyperglycaemia and dehydration but not ketoacidosis. The major laboratory findings are extreme hyperglycaemia and plasma osmolarity over 350 mosm/L; the serum sodium is frequently 140 mmol/L or higher. Management is similar to DKA. Differences in treatment are: 1. More dilute solutions such as sodium chloride 0.45% should be used initially and given slowly. 2. Lower doses of insulin. These patients are more sensitive to insulin and require lower doses eg 0.05 to 0.1 units/kg/hour. It is not advisable to lower blood glucose rapidly. 3. Confusion may be prolonged for several days after blood glucose is restored to normal. Careful follow-up is essential. 4. Oral hypoglycaemic drugs should not be started immediately because many patients may be subsequently managed just with diet and exercise.
REFERENCES

Therapeutic guidelines: Endocrinology, Version 3, 2004.

LACTIC ACIDOSIS IN DIABETES


Lactic acidosis is most common in the setting of tissue hypoxia secondary to shock and hypotension. It also occurs in liver disease and diabetes especially if treated with metformin when renal function is impaired or in hypoxic states. Treatment is directed at removing the cause, eg restoring circulating volume in the hypotensive dehydrated patient. With severe lactic acidosis, bicarbonate therapy is mandatory and several hundred mmol may be required.
REFERENCES

Therapeutic guidelines: Endocrinology, Version 3, 2004.

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MENINGOCOCCAL DISEASE
Meningococcal disease is a hyperfulminent and uniformly fatal syndrome if untreated, which is manifest as meningitis alone (1/3 cases), septicemia alone (1/3 cases), or a combination of meningitis and septicemia (1/3 cases). Most cases appear in spring and autumn with a bimodal age distribution with peaks in early childhood and early adolescence. Effective treatment is dependent on early recognition, but this is often difficult because early presentations (mean 4-6 hours after onset) are typically non-specific and indistinguishable from other, self-limiting, febrile illnesses, such as influenza. Classic symptoms of purpuric rash, meningism, drowsiness appear late in the course of the illness (mean 13-22 hours after onset) when potentially curative treatment with penicillin is often not possible. Early diagnosis is on average dependent on recognition of symptoms of sepsis, which commence 6-8 hours after onset, are present in 70% of cases, and consist of: leg pains, cold hands and feet abnormal skin colour

TREATMENT
If menigococcal disease is suspected immediate prehospital treatment is mandatory and may be lifesaving. 1. Give benzylpenicillin 1200 mg IV immediately. (Child <1y 300mg, Child 19 years 600mg, Child >10 years). 2. In patients hypersensitive to penicillin or in remote areas where further parenteral therapy may be substantially delayed (>6 hours) give ceftriaxone 50 mg/kg up to 2 g IV.. 3. Arrange urgent transportation to hospital.
REFERENCES

1.Thompson MJ. Ninis N Perera R .Clinical recognition of meningococcal disease in children and adolescents. Lancet. 367(9508):397-403, 2006 Feb 4. 2.Therapeutic guidelines: Neurology. Version 2, 2002

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MENINGITIS
1. Prehospital treatment. If meningitis is suspected immediate prehospital treatment is mandatory and may be lifesaving. a. Give benzylpenicillin 1200 mg IV or IM immediately. (Child <1y 300mg, Child 1-9 years 600mg, Child >10 years). b. Give ceftriaxone 50 mg/kg up to 2 g IV. In patients hypersensitive to penicillin or in remote areas where further parenteral therapy may be substantially delayed (>6 hours). 2. Hospital treatment based on known or probable pathogen. c. Meningitis caused by Neisseria meningitidis (meningococcal meningitis). Give benzylpenicillin (child: 60 mg/kg up to) 1.8 to 2.4 g IV, 4-hourly for 5 to 7 days.For patients hypersensitive to penicillin (excluding immediate hypersensitivity), use cefotaxime (child: 50 mg/kg up to) 2 g IV, 6-hourly for 5 to 7 days OR ceftriaxone (child: 100 mg/kg up to) 4 g IV, daily OR (child: 50 mg/kg up to) 2 g IV, 12-hourly for 5 to 7 days. d. Meningitis caused by Streptococcus pneumoniae. For penicillinsusceptible strains (MIC <0.125mg/L), give benzylpenicillin (child: 60 mg/kg up to) 1.8 to 2.4 g IV, 4-hourly for 10 days. For strains with an MIC >0.125 mg/L use vancomycin plus either cefotaxime or ceftriaxone, Specialist advice must be sought particularly if the MIC of these cephalosporins is elevated. Rifampicin is a possible alternative to vancomycin. e. Meningitis caused by Haemophilus influenzae type b (Hib) give cefotaxime (child: 50 mg/kg up to) 2 g IV, 6-hourly for 7 to 10 days or ceftriaxone (child: 100 mg/kg up to) 4 g IV, daily OR (child: 50 mg/kg up to) 2 g IV, 12-hourly for 7 to 10 days.
REFERENCES

Thompson MJ. Ninis N Perera R .Clinical recognition of meningococcal disease in children and adolescents. Lancet. 367(9508):397-403, 2006 Feb 4. Therapeutic guidelines: Neurology. Version 2, 2002.

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STATUS EPILEPTICUS
1. Protect and maintain airway. Lie in recumbent (L) lateral position, suction, insert Guedels airway. 2. Protect patient from self injury. 3. Oxygen 6-8L/min 4. Dextrostix: if low give glucose 50mls 50% solution IV. 5. To terminate convulsion give: a. Diazepam 10 to 20mg bolus IV, not exceeding 2 to 5mg/minute titrating to response; repeat once 15 minutes later if status epilepticus continues (child: 0.1 to 0. 25mg/kg bolus IV, over 2 to 5 minutes). Monitor with pulse oximetry. OR b. Clonazepam 1 to 2mg bolus IV, not exceeding 0.5mg/minute; repeat once 15 minutes later if status epilepticus continues (child: 0.25 to 0.5mg bolus IV, over 2 to 5 minutes) OR c. Midazolam 5 to 10mg (child: 0.2mg/kg) IM, repeat once 15 minutes later if status epilepticus continues. NB if IV access not possible give Diazepam 10mg RECTALLY, either as suppository or administered PR by syringe (without needle!) OR Intranasal midazolam (0.3 to 0.5mg/kg/dose up to a maximum of 10mg). If seizures persist after repeated diazepam (eg 5mg x4 = 20mg doses) give: 6. Phenytoin 15mg/kg in 100mls NS over 1 hour (but no faster than 50mg/min). (child: 20mg/kg IV, not exceeding 25mg/minute), providing no phenytoin has been given in the preceding week. If seizures persist after valium and phenytoin, transfer to ICU or: 7. Intubation and barbiturate anaesthesia. Give thiopentone 3-5mg/kg at 25mg/min for intubation followed by infusion (See IV Drug Infusions). Plus appropriate muscle relaxant. 8. Consider and treat causes: Poor compliance ; sleep deprivation (in known epileptics); hypoxia (eg following bcardiac arrest); meningitis; drug overdose (tricyclics, theophyline, amphetamines); drug withdrawal (alcohol, benzodiazepines); metabolic (hypoglcemia, hyperthyroid); electrolyte disturbances (hyponatremia, hypocalcemia, hypomagnesemia); CVA; cerebral tumour.
REFERENCES

Therapeutic guidelines: Neurology. Version 2, 2002.


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ACUTE STROKE
Urgent transport to hospital with neuroimaging facilities. Stroke should be considered as urgent as AMI or acute trauma. Urgent CT or MRI scan. To differentiate between ischemic or hemorrhagic stroke. If CT/MRI confirms ischemic stroke give: 1. Aspirin OR clopidogrel OR aspirin + dipyridamole. Aspirin given within 48 hours reduces mortality by 20%. 2. Admission to stroke unit (>20% overall reduction in mortality) Adequate oxygenation, hydration, control of BSL, nursing care. 3. Antihypertensives. Cautious use in consultation with stroke physician if markedly elevated blood pressure (systolic greater than 220 mm Hg). 4. Unfractionated IV heparin is indicated for patients at very high risk of recurrent embolism in consultation with stroke physician. 5. Tissue plasminogen activator (alteplase, rt-PA). alteplase 0.9mg/kg (maximum of 90mg), over 1 hour with 10% of the dose given as an initial bolus. Each 50mg vial is reconstituted using the 50mL diluent provided by the manufacturer, and then the appropriate dose is administered with no further dilution. Give only in consultation with stroke physician. Improves outcomes if given to selected patients within 3 hours of onset of acute ischaemic stroke. Improved outcomes may come at the risk of symptomatic intracerebral haemorrhage (5% to 7%).
REFERENCES

Therapeutic guidelines: Neurology. Version 2, 2002.

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ACUTE ANAPHYLAXIS
Definition: bronchospasm, stridor, hypotension or severe generalised urticaria. 1. Oxygen 6L/min 2. Adrenaline 0.3 to 0.5mg (0.3-0.5 ml of 1:1000 sol) SC. Repeat at 15-30 min OR (if severe) Adrenaline 0.3 mg (3 ml of 1:10000 sol) IV over 1 minute followed by infusion Adrenaline 1mg in 250 mls 5%D (4ug/ml) as infusion at 1-10ug (0.25 2.5mls) /min, titrating to maintain BP. 3. Hydrocortisone 100mg IV or Prednisone 1mg/kg PO 4. Phenergan (H1 blocker) 12.5-25mg IV Plus 5. Cimetidine (H2 blocker) 300mg IV or Ranitidine 50mg IV If the above fails to reverse anaphylaxis, individual manifestations of anaphylaxis of hypotension, bronchospasm, stridor, should be treated as required. 6. Fluid resuscitation. If in shock fluid resuscitation with multiple IV access and transfusion. Very large volumes may be required. Should be given with adrenaline infusion as above. 7. Bronchodilators. If in bronchospasm and poor response to adrenaline, treat as for asthma (viz. continuous nebulised salbutamol, steroids, IV salbutamol) 8. Maintain upper airway. If severe upper airway obstruction (increasing stridor and hypoxia) not relieved by adrenaline consider intubation or emergency cricothyrotomy. 9. Admit for 24 hours following major anaphylaxis (stridor, bronchospasm, shock) 10. Discharge on diphenhydramine 25mg q6h and predisone 60mg/day, for 3 days.

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DRUG OVERDOSE
1. Contact Poisons Centre. Ph (02) 131126 for details of toxicology, specific and supportive treatment. 2. Activated charcoal. 1g/kg (+Sorbitol 1ml/kg of 70% solution) as slurry. May be swallowed or administered via nasogastric tube. Multiple doses (0.25g/kg at q2h) are indicated in overdose of barbiturates, theophylline, digoxin, salicylates, carbamazepine, phenytoin. NB Activated charcoal not useful for acids, alkalis, ethanol, ethylene glycol, methanol, lithium or iron. 3. IV Fluids: 1-2L NS at q2-4h depending on age, hydration, cardiovascular status. 4. Paracetamol level on all patients presenting with overdose. NOTE: a. Gastric lavage is generally not recommended unless overdose<1 hour and potentially very toxic (eg TCA or Ca channel blocker OD). If indicated, lavage via orogastric or nasogastric tube. Aspirate before lavage, then lavage with water (1ml/kg) at body temperature. Recover lavage before repeating until lavage aspirates clear. Contraindications i. corrosives. ii. petroleum derivatives. Airway must be protected with cuffed endotracheal tube where consciousness is impaired or gag reflex is absent. b. Ipecac is generally no longer used (less effective, risk of aspiration), but may be justified in serious OD when lavage not available, consciousness is not impaired and transfer to hospital is likely to be delayed (>1-2hr)

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Specific treatments
Narcotics. Naloxone (Narcan)0.4mg IV (+flush) May also be give 0.4mg IM concurrently. Repeat 0.4mg (1 amp) IV every 1-2 minutes until response. Large initial dose of 2mg (x5 amps) may also be given. If no response after maximum 10mg, suspect combined drug effect or other causes of coma. Benzodiazepines. Flumazenil (Anexate) 0.2mg IV. Repeat at 0.1mg / minute until response or total 1mg. Avoid if multiple drug OD, particularly TCAs, as flumazenil may effectively lower the seizure threshold. Paracetamol. N-acetyl-cysteine (Parvolex) 150mg/kg in 200mls 5%D over 30mins, followed by 50mg/kg in 500mls 5%D over 4 hours, followed by 100mg/kg in 1litre 5%D over 16 hours. Indication: serum paracetamol >200 mg/L (or 1300 umol/L) at 4 hours post ingestion. Warfarin: If patient normally requires anticoagulation give Vitamin K 1mg IV slowly over 10 minutes. Avoid completely if prosthetic values (give FFP only). Otherwise give Vitamin K. 5-10mg SC. PLUS Fresh frozen plasma (FFP) 2 units stat. Check INR at 3-4 hours and repeat Vitamin K and FFP prn. Heparin If APPT raised above therapeutic range in the course of normal dose schedule: Stop heparin 1/2-1hr, then adjust infusion rate according to specific protocol.. If massive inadvertent overdose: Give protamine sulphate (1mg protamine/100 units of heparin given in the preceding 15 minutes to max 50mg.) no faster than 50mg protamine over 10 minutes.

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ACUTE UPPER GASTROINTESTINAL BLEED


1. Fluid resuscitation. Monitor BP, CVP, UO. If hypotensive or postural drop (postural drop of 10mmHg=1 liter blood loss) give Hartmans solution to restore BP,CVP,UO. Start with 1 unit bolus then repeat based on clinical response. 2. Transfuse. If bleeding severe and persistent consider transfusion with O negative blood. Otherwise X-match 4-8 units. Monitor Hb and transfuse to maintain Hb>10g/dl. 3. H2 Antagonist IV. eg Zantac 50mg IV q8h, Famotidine 20mg IV q12h 4. Correct coagulopathy. i. Correct clotting abnormality.Monitor INR and APPT. If any clotting abnormality give Vitamin K 10mg IV over 10 minutes and Fresh Frozen Plasma (FFP) 2 units stat.

ii. Platetlet transfusion. If platelets<50,000 give platelets 2 units stat. 5. Maintain nil by mouth. This is usually sufficient (with bed rest) to stop bleeding. 6. Arrange endoscopy within 24hours. Arrange urgently if bleeding is persistent to locate bleeding point pending laparotomy (or to sclerose esophageal varices). 7. Obtain surgical consult if: i. Massive bleed.(eg hypotension or transfusion>5 units) ii. Recurrence of bleeding during hospitalisation iii. Bleeding for >12h iv. Age>50 v. Past history of previous bleed. 8. Octreiotide. If varices known or suspected and bleeding uncontrolled by 15 above give: Octreotide 50mcg IV over 5 mins followed by infusion 250mcg in 100mls NS at 25mcg (10mls)/hr. If no response increase to 50mcg (20mls)/hr. 9. Insertion of Sengstaken-Blackmore tube for 48hours if bleeding due to varices and no response to 1-5,8 above.

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

HYPERKALAEMIA
Urgent treatment: If K>7 or signs of cardiac toxicity (peaked T waves, prolonged PR, deep S, ventricular arrhythmias). Give: Intravenous calcium gluconate 10% 10 mL IV, over 2 to 3 minutes into a large vein (with ECG monitoring of the response, if possible). Calcium alleviates the cardiac complications by reversing the membrane depolarisation of severe hyperkalaemia. In the presence of life-threatening cardiac arrhythmia or severe ECG changes of acute hyperkalaemia. The effect is short-lived and the dose may need to be repeated in 30 to 60 minutes. Intravenous sodium bicarbonate 8.4% (1 mmol/mL) 50 mL IV over 5 to 10 minutes under ECG control. Indic: if metabolic acidosis is associated with volume depletion. This may be repeated in 60 to 120 minutes. (NOTE: to prepare an approximately isotonic bicarbonate solution, add 50 mL 8.4% sodium bicarbonate to 500 mL 0.45% sodium chloride) Glucose 50% 50 to 100 mL TOGETHER WITH a short-acting insulin 10 to 20 units, IV over 5 to 10 minutes. Insulin action promotes cellular uptake of potassium. Serum potassium will decrease by 0.5 to 1.5 mmol/L over 30 minutes. NB Hypoglycaemia, possibly due to adrenal insufficiency, must be ruled out before insulin is given. Consider: Salbutamol 0.5 mg IV (4 micrograms/kg in children) OR salbutamol 10 mg by nebuliser (2 to 5 mg in children) Beta2-adrenergic agonists promote tissue uptake of potassium, but have the potential disadvantage of precipitating cardiac arrthythmia. Either can be expected to decrease serum potassium by 0.5 to 1.5 mmol/L in 30 to 90 minutes. Other treatments: Consider if K<7 and no signs of cardiac toxicity 1. Correction of volume depletion. Any volume depletion should be corrected, to optimise renal function. Sodium polystyrene sulfonate (Resonium A) 25 to 50 g in suspension. Each gram removes about 1 mmol of potassium from the bowel, and lowers the serum potassium by 0.5 to 1 mmol/L over 1 to 6 hours. For intractable hyperkalcemia Dialysis. Where hyperkalaemia is extreme, as in extensive tissue breakdown due to rhabdomyolysis, none of the above approaches may be effective and dialysis will be required.

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URGENT ELECTROLYTE ABNORMALITIES


Hypokalemia. If in context of cardiac arrythmias give 10 mmol (0.75g) KCl over 1/2 hr in 100mls NS (less rapidly in less urgent settings). Hypocalcemia. Estimate corrected Ca = Ca + [(40-Albumin (g/L) x 0.02] If low in context of cardiac arrythmias or tetany give: Loading: Calcium chloride 10mls 10% over 10-15mins (ECG monitor) then infusion: 20mls 10% CaCl in 100mls NS over 4 hours. Hypomagnesemia. Loading: Mg 10mmol in 20mls NS over 1 hour then infusion: Mg 20mmol in 100mls NS over 4 hours. Hypophosphatemia. Infusion: Phosphate 10mmol in 20mls NS over 2 hours

PAEDIATRIC FLUID REPLACEMENT


1. Maintenance Give: N/4 if maintenance alone If <10kg: If 10-20kg: If >20kg: PLUS 2. Replacement: Give: N/2 if clinically dehydrated % Dehydration x Kg X 10 over 24 hours. 3. If circulatory collapse: Give IV fluids (normal saline) initially 10-20 ml/Kg as rapid infusion (over 15 minutes). 100mls/kg/day 1000mls + 50mls/kg/day for every kg over 10kg 1500mls + 20mls/kg/day for every kg over 20kg

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

INTEROSSEOUS NEEDLE PLACEMENT


INDICATIONS To establish parenteral means to administer fluids and IV medications in children in whom IV access is difficult or impossible.

PROCEDURE
1. Sterile technique as situation permits. 2. Local anaesthetic if patient is conscious. 3. Preferred site: the proximal anteromedial tibia, 1-3 cm below the tibial tuberosity 4. Angle 14-16 g cannula at 90 degree angle to the skin surface, approximately one to two finger breadths distal to the tibial tuberosity. With a straight steady push and/or rotary motion, push needle through subcutaneous tissue and bone until a drop or pop is felt. Once the needle has reached the bone marrow, it should be held by the bone cortex, but if necessary may be anchored with tape and/or plaster of paris. 5. Fluids usually require injection using 60 ml syringe. All fluids or drugs which are injected IV may be injected through interosseous needle, and enter the circulation at rates comparable to IV administration.

Tibial Tuberosity

Anterior Border

90 to Medial Surface

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APPENDIX 1. IV DRUG INFUSIONS


Note: Drug infusion regimes may vary at different centres.

Adrenaline
Must be given via central line Infusion: 4mg (4 amps of 1:1000) in 100mls 5%D. Start at 10mls/hr and titrate to BP and PR, to maximum of 50mls/hour.

Amiodarone
Loading: 300mg (x2 amps) in 20mls NS or 5%D IV over 60 mins. Infusion: 600mg in500mls 5%D over 12 hours.

Dobutamine
May be given via peripheral line. Infusion:: 250mg (1amp) in 100mls 5%D (2.5mg/ml). Start at 5 ug/kg/min (approx 8ml/hr for 70kg man) Increase at increments of 5 ug/kg/min (approx 8mls/hr for 70kg man) to max 40ug/kg/min (approx 80mls/hr for 70kg man).

Dopamine
Must be given via central line Infusion: 200mg (1amp) in 100mls 5%D (2mg/ml). Start at: 2.5ug/kg/min (approx 5mls/hr for 70kg man) renal dose ug/kg/min (approx 10ml/hr for 70kg man) ionotropic dose Increase at increments of 5 ug/kg/min (approx 10ml/hr for 70kg man) to max 20ug/kg/min (approx 40mls/hr for 70kg man).

Glyceryl Trinitrate (Tridil).


Infusion: 50mg (1amp) in 500mls 5%D. Start at 5ug/min (3mls/hour) and titrate to pain and to keep BP>100 mmHg.

Heparin
Loading: 5000 units IV as bolus (take blood for coags first!) Infusion: 25000 units in 500mls NS Start at 20mls (1000 units)/hour and titrate to APTT

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

Isuprenaline
Loading: 0.2mg (1 amp) in 10mls NS and give 1-3mls Infusion: 1mg in 100mls 5%D (10ug/ml). Start at 5mls/hr (50ug/hr) and increase in increments to maximum of 100mls/hr, titrating to PR and BP.

Lignocaine
Loading: 1mg/kg IV over 1 minute. Infusion: 2g in 500mls 5% D (preloaded bag). Start at 4mg/min (60mls/hr) for 2 hours, then 3mg/min (45mls/hr) for 2 hours, then 2mg/min (30mls/hr) for 24 hours.

Manitol
Loading: 1g/kg over 20 minutes. Infusion: 100g in 500mls (20% solution) at 10mls/hour

Noradrenaline
Must be given via central line Infusion: 4mg in 100mls 5%D. Start at 10mls/hr and titrate to response to maximum of 50mls/hour.

Salbutamol
Loading: 250ug (1amp) in 10mls 5%D over 5minutes Infusion: 3mg (6amps) in 100mls 5%D (30mg/ml). Start at 5ug/min (=10mls/hr). Increase in 5ug/min increments every 15-30mins until control achieved to maximum of 40mls/hour.

Sotolol
Loading: 0.5mg/kg IV in 10mls 5%D over 10-30 minutes Infusion: 80mg (8mls) into 72mls 5%D = 80mls = 1mg/ml. Give 160-240mg (160-240mls) /day

Thiopentone
Loading: 3-5mg/kg at 25mg/min Infusion: 10g in 500mls NS or 5% D (20mg/ml). Start at 2.5mg /kg/hr (ie 8.75mls/ hr for 70 kg man)

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APPENDIX 2. EMERGENCY TELEPHONE NUMBERS


Poisons information centre (National): 131126 Hospitals

Other emergency numbers

Commonwealth Carer Respite Centre 1800 059 059

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MANUAL OF MEDICAL EMERGENCIES 2nd Edition 2006

APPENDIX 3. EMERGENCY PAEDIATRIC DRUG DOSES


Neonate 3.5 15 0.05ml 0.05mg 0.5ml 0.05mg 1ml 0.1mg 0.25mls 5mg 3 2.5mls 0.2ml 0.7mg 0.3mls 1.4mg 0.3mls 15ug 0.8mls 40ug 0.6mls 3mg 0.8mls 4mg 1ml 50ug 0.3mls 1.5mg 0.4mls 2mg 7.5mls 10mls 10mls 04mls 2mg 0.8mls 4mg 1.2mls 60ug 3.5 4.0 4.5 4.5 15mls 0.6mls 3mg 1.2mls 6mg 1.5mls 75ug 0.5mls 10mg 0.75mls 10mg 0.75mls 15mg 1ml 20mg 2ml 0.2mg 2mls 0.2mg 2.5mls 0.25mg 3mls 0.3mgs 3.5mls 0.35mg 1ml 20mg 5.0 15mls 0.6mls 3mg 1.2mls 6mg 1.5mls 75ug 1ml 0.1mg 1ml 0.1mg 1.5ml 0.15mg 1.5ml 0.15mg 2ml 0.2mg 2ml 0.2mg 3.5mls 0.35mg 1.25mls 25mg 5.0 15mls 0.8mls 4mg 1.6mls 8mg 1.6mls 80ug 0.1ml 0.1mg 0.1ml 0.1mg 0.15ml 0.15mg 0.15ml 0.15mg 0.2ml 0.2mg 0.2ml 0.2mg 40 50 60 75 85 95 100 0.2ml 0.2mg 2ml 0.2mg 4mls 0.4mg 1.25mls 25mg 5.5 20mls 0.8mls 4mg 1.6mls 8mg 2mls 100ug 8 10 12 15 17 19 20 6m 1 2 3 4 5 6 7 23 115 0.25ml 0.25mg 2.5mls 0.25mg 4.5mls 0.45mg 1.5mls 30mg 5.5 20mls 0.9mls 4.5mg 1.8mls 9mg 2.3mls 115ug

Age

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Weight (kg)

DC Defibrillation 5J/Kg

Adrenaline 1:1000 Amp: 1mg in 1ml Dose: 0.01mg/Kg IV,SC,IM

Adrenaline 1:10000 Amp: 1mg in 10mls Dose: 0.01mg/Kg IV

Atropine Amp: 0.5mg in 5mls Dose: 0.02mg/kg IV

Lignocaine Amp: 100mg in 5mls Dose: 1mg/kg IV

ETT size (mm ID)

NaHCO3 Amp: 100mls 8.4% IV

Diazepam IV Amp: 10mg in 2 mls Dose: 0.2 mg/Kg IV

Diazepam RECTAL Amp: 10mg in 2mls Dose: 0.4mg/kg rectally

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Salbutamol IV Amp: 500ug in 1ml made up to 10mls with NS. Dose: 5 ug/kg IV 50 100

Fluid bolus (ml)

150

150

200

250

300

300

400

To doctors who go out into the community - along city streets, suburban thoroughfares and country roads, at all times of the year and all hours of the day and night; to manage medical emergencies in shopping centres, boarding houses and lounge rooms; who work alone, without the assistance or council of colleagues, using only what equipment they can carry, and what skills they have gained through experience; whose dedication will go unwitnessed, whose consideration will go unrecognised, who will receive no professional accolade, no great honor, and no reward - other than the gratitude of their patients. To those brave, dedicated and worthy colleagues - this manual is respectfully dedicated.

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