Crit Care Bible PDF

The Critical Care Bible 1  Student, you do not study to pass the test. You study to prepare for the day when you are the only thing between a patient and the...

The Critical Care Bible 1  Student, you do not study to pass the test. You study to prepare for the day when you are the only thing between a patient and the grave This bible is an amalgamation of resources from: - UptoDate - eTG (The Australian Therapeutic Guidelines) - Davidson’s Surgical Textbook - Oh’s Intensive Care Textbook - Emergency and Trauma Care Textbook - On Call Textbook - Life in the Fast Lane Website - Some Orthopaedic Textbook - A bunch of other textbooks - And past Crit Care and Surg exam questions 2 Contents Page - Resuscitation - Trauma o Basic Life Support o The Primary Survey o Advanced Life Support o Airway Adjuncts o Choking Management Pathway o C-Spine Precautions - Cardiac Emergencies o Tetanus o Chest Pain Pathway o Coagulopathy of Trauma o Pericarditis o The Glasgow Coma Score o Aortic Dissection o Focused Sonography Assessment for Trauma (FAST) Scan o Hypertensive Crisis o The Exploratory Laparotomy (Abdominal Trauma) o Heart Failure and Acute Pulmonary Oedema o Pelvic Fractures o STEMI o Traumatic Brain Injury o Supraventricular Tachycardia o Emergency Burr Holes o Atrial Fibrillation o Spinal Cord Trauma o Bradyarrhythmias o Tension Pneumothorax o Syncope o Haemothorax - Vascular Emergencies o Flail Chest o Acute Ischaemic Limb o Chest Drain Insertion - Respiratory Emergencies o Pericardial Tamponade o Pulmonary Embolus o Pericardiocentesis o Acute Exacerbation of COPD o Crush Syndrome o Acute Exacerbation of Asthma o Compartment Syndrome o Pneumonia o Traumatic Amputation - ENT Emergencies o Burns o Epiglottitis o Escharotomy o Quinsy o The Emergency Thoracotomy o Foreign Body Aspiration o Health Safety in Trauma o Massive Epistaxis o The Surgical Cricothyroidectomy - Anaphylaxis o Wound Management - Neurological Emergencies - Orthopaedic Emergencies o Stroke o Falls (Osteoporosis) o Seizures o Upper Limb Injuries o Delirium o Lower Limb Injuries o Meningitis o Open Fracture Management o Low Back Pain o Closed Fracture Management o Cerebral Abscess o Soft-Tissue Injuries - Ocular Emergencies - Anaesthetic Medicine o Endophthalmitis o Preoperative Assessment o Angle-Closure Glaucoma o Airway Assessment o Retinal Detachment o Rapid Sequence Induction o Eye Trauma o Volatile Agents – Inhalational o The Red Eye o Neuromuscular Blockers o Amaurosis Fugax o Depth of Anaesthesia Monitoring - Endocrinological Emergencies o Endotracheal Intubation o Myxoedema Coma o The Difficult Intubation o Thyroid Storm o Obstetric Anaesthetics o Hypoglycemia o Anaesthetics in Trauma o Diabetic Ketoacidosis o Transplantation Surgery o Adrenal Crisis o Neurological Determination of Death - Environmental Emergencies o Anaesthesia for the Obese Patient o Cold Injuries o Pain o Resuscitation of the Drowning Victim o Analgesic Drugs o Hyperthermia o Patient Controlled Analgesia o Australian Snake Bites o Neuropathic Pain o Australian Spider Bites o Regional and Local Anaesthesia - Toxicological Emergencies - Intensive Care Medicine o Management of the Poisoned Victim o Overview of Shock o Acute Paracetamol Toxicity o Hypovolemic Shock o Alcohol Poisoning o Cardiogenic Shock o Toxidromes o Obstructive Shock o Distributive Shock o Management of Shock o Fluid Resuscitation o Arterial Line/ Central Venous Cannula o Sepsis o Multiple Organ Dysfunction Syndrome o Oxygenation o Ventilation o Acute Respiratory Failure 3  Approximately 75% of deaths from cardiac arrest occur in the pre-hospital setting Basic Life Support Site of Compressions: - Lower half of the sternum - Compression applied too high is ineffective and if applied too low may cause regurgitation and/or damage to internal organs Method of Compressions: - In infants use the two finger technique - In children, can use one or two hand technique - In adults, use two handed technique - A person requiring chest compressions should be placed on their back on a firm surface - Rescuers should allow complete recoil of the chest after each compression Rate of Compressions: - Rate of 100 to 120 per minutes (almost 2 compressions/ second) - Compressions less than 100 or greater than 140 compressions per minute are associated with lower rates of survival Depth of Compressions: - The lower half of the sternum should be depressed approximately one third of the depth of the chest with each compression - This equates to more than 5 cm in adults, approximately 5 cm in children and 4 cm in infants CPR fatigue: compression rate and depth quality decreases even within one minute Minimise Interruptions to Compressions: - Interruptions lead to decrease in coronary perfusion pressure and a decreased likelihood of defibrillation success - These adverse effects commence within 10 seconds of stopping CPR Rib fractures and other injuries are common but A defibrillation shock is indicated for In patients with an ICD or a acceptable consequences of CPR given the treating ventricular fibrillation (VF) and permanent pacemaker the alternative of death pulseless ventricular tachycardia (pVT) defibrillator pad/ paddle is placed on the chest wall ideally at least 8 cm Pregnant Women: from the generator position - Standard CPR should be commenced Pads are placed on the exposed chest in immediately an anterior-lateral position or an - A towel, cushion or similar object can be placed anterior-posterior position Energy Levels: under the right hip to tilt the woman’s hips Monophasic: the energy level for (approx. 15-30 degrees) to the left but leave her Defibrillation Precautions: adults should be set at maximum shoulders flat to enable good quality chest - Defibrillation should not be attempted (usually 360 J) for all shocks compressions in an oxygen-enriched atmosphere (e.g. - The reason for this position in pregnant women when high-flow oxygen is directed Biphasic: the default energy level for is to move the weight of the pregnant uterus off across the chest) adults should be set at 200 J for all her major blood vessels in the abdomen - Avoid placing the defibrillator pads shocks over ECG electrodes (risk of burns or sparks) Compression: Ventilation Ratio - Avoid having a person in direct or 30:2 indirect contact with the victim during defibrillation (a shock may be received) The tidal breath should be delivered within 1 - Avoid having the victim in contact with second, and the desired tidal volume to be metal fixtures e.g. bed rails delivered is one that results in a visible chest rise - Avoid delivering the shock with a gap between the pad and chest wall (spark hazard) 4  The intraosseous route Advanced Life Support A precordial thump is no longer recommended for ventricular fibrillation should be considered for administration of medications if venous access is not immediately available Mechanical devices (such as LUCAS) may be useful alternatives to manual CPR in situations where traditional CPR is difficult or hazardous (e.g. during transport) Chest compressions should be continued up until defibrillation, including during charging of the defibrillator CPR should also be commenced again immediately following defibrillation (without checking the rhythm), and continued for at least 2 minutes unless signs of life return (the victim becomes responsive or starts breathing) Cardiac Arrest Medications A compression: ventilation ratio of 30:2 is After each 2 minutes of recommended before the airway is secured, and CPR (or if signs of life Atropine – cholinergic/ cardiac glycoside after the airway is secured with endotracheal return), the underlying toxicity intubation the recommended ventilation rate is 8- rhythm should be Anti-venom – snake, funnel-web spider, box 10/minute checked, and if a rhythm jellyfish venom compatible with a return Benzodiazepines – sympathomimetic toxicity of spontaneous Calcium – hypocalcemia, hypermagnesaemia, Hyperventilation during cardiac arrest is associated circulation is observed at hyperkalemia, beta blocker/ calcium channel with increased intrathoracic pressure, decreased that time then a central blocker toxicity coronary and cerebral perfusion and a decreased pulse should also be Digoxin-specific antibodies – cardiac glycoside rate of return of spontaneous circulation checked toxicity Flumazenil – benzodiazepine toxicity Epinephrine: Survival after cardiac Epinephrine – beta-blocker/ calcium channel Beneficial effect is to increase the perfusion arrest is largely blocker toxicity pressure to the heart and brain dependent on the Glucagon – beta-blocker/ calcium channel The initial dose is 1mg and should be repeated patient’s co-morbidities blocker toxicity approximately every 5 minutes and initial hypoxic insults High-dose insulin/ dextrose – beta-blocker/ to the heart and brain calcium channel blocker toxicity Shockable Rhythms: Lipid emulsion – local anaesthetic agents - Ventricular fibrillation is asynchronous chaotic Waveform Capnography Magnesium – hypomagnesaemia, ventricular activity that produces no cardiac output hypokalaemia, hypercalcemia, tricyclic - Pulseless ventricular tachycardia is a wide complex During CPR: antidepressant/ cardiac glycoside toxicity, regular tachycardia associated with no clinically - Confirming tracheal torsade de pointes detectable cardiac output tube placement Naloxone – opioid toxicity - Monitoring the Potassium – hypokalaemia Non-Shockable Rhythms: ventilation rate to avoid Pyridoxine – isoniazid toxicity - Asystole is characterised by the absence of any hyperventilation Sodium bicarbonate – hyperkalemia, tricyclic cardiac electrical activity - Assessing quality of antidepressant/ sodium-channel blocker - Pulseless electrical activity (PEA) is the presence of compressions toxicity coordinated electrical rhythm without a detectable - Identifying ROSC during cardiac output CPR (by an increased CO2 value) 5  Assess Severity: Choking Management Pathway - Easiest way to assess severity is to assess for effective cough Effective Cough (Mild Airway Obstruction) - The person with an effective cough should be given reassurance and encouragement to keep coughing to expel the foreign material Ineffective Cough (Severe Airway Obstruction) Conscious Person: - Send for an ambulance and perform up to 5 sharp, back blows with the heel of one hand in the middle of the back between the shoulder blades - An infant may be placed in a head downwards position prior to deliver back blows, i.e. across the rescuer’s lap - If back blows are unsuccessful the rescuer should perform up to five chest thrusts - To perform chest thrusts, identify the same compression point as for CPR and give up to five chest thrusts - The infants should be placed in a head downwards and on their back across the rescuer’s thigh, while children and adults may be treated in the sitting or standing position - If the obstruction is still not relieved and the person remains responsive, continue Past Exam Question: alternating five back blows with five chest A 42 year old man undergoing chemotherapy for lymphoma has a cardiac arrest on thrusts the ward. After initial resuscitation attempts he has an ECG trace showing regular ventricular depolarization but has no palpable pulses. Unconscious Person: Which of the following pathologies is not a likely cause for his presentation? - Call and ambulance and start CPR a) Pulmonary embolism b) Tension pneumothorax Past Exam Question: c) Cardiac tamponade An elderly man collapses on the street in front d) Anaemia of you. e) Hyperkalemia What is your first action? Answer: d) Anaemia is not part of the 4Hs/4Ts a) Ensure there is no visible danger to yourself before approaching him Past Exam Question: b) Look for airway obstruction by opening his A 74 year old man is recovering in hospital after a myocardial infarction. Whilst mouth attending to his regular medications, a nurse witnesses a sudden loss of c) Assess his responsiveness by gently shaking consciousness. When the biphasic defibrillator is brought into the room, what him and asking “Are you alright?” energy should be used for the initial shock? d) Protect his cervical spine by in-line immobilisation a) 2 joules/kg e) Call for emergency services to attend b) 4 joules/kg Answer: a) BLS: Danger c) 100 joules d) 200 joules e) 360 joules Answer: d) Biphasic defib Past Exam Question: Regarding adult basic life support in cardiac arrest, which of the following is correct? a) The ratio of compressions to ventilations may be altered depending on the number of rescuers b) The recommended compression: ventilation ratio is 30:2 c) Five initial rescue breaths should be given d) A radial pulse should be checked before commencing chest compressions e) Cardiopulmonary resuscitation should not be commenced if there is abnormal or irregular breathing Answer: b) 6 Top 5 to rule out: “Chest pain is an MI until proven - Acute coronary syndrome The Chest Pain Pathway otherwise, put an ECG on” - Aortic dissection - Pulmonary embolism Oxygen is only indicated if hypoxaemic - Tension pneumothorax Aspirin 300mg chewed or (O2 saturation < 94%) or in shock - Pericardial tamponade dissolved before swallowing For persisting chest pain, add an opioid: IV fentanyl or IV morphine M O N A Glyceryl trinitrate spray sublingual, Contraindications to Aspirin: repeat every 5 minutes if pain persists - Patient unable to chew or swallow, including GCS > 15 - Allergy to aspirin Other indications for GTN: Contraindications to GTN: - History of active bleeding disorder - Acute cardiogenic pulmonary oedema - Allergy - Recent or current ulcer or - Autonomic dysreflexia (with a systolic - Heart rate 150 bpm gastrointestinal bleeding BP > 160mmHg) - Systolic BP < 100mg - Irukandji syndrome (with a systolic BP - Acute CVA > 160mmHg) - Head trauma Precaution of using GTN in a suspected Side Effects of GTN: inferior MI – there is a higher risk of - Dizziness developing hypotension - Hypotension - Syncope - Reflex tachycardia - Vascular headaches Chest Pain Investigations Chest Pain Notes: - Oesophageal spasm also A standard 12-lead electrocardiogram (ECG) is obtained for all ED patients presenting responds to GTN with chest pain, an ECG should be obtained and interpreted within 10 minutes of - Pericarditis pain is positional – patient presentation – American College of Cardiology and American Heart Association worse when lying supine, relieved when leaning forward The sensitivity of ECG for acute MI is low – a single ECG detects fewer than 50% of MIs - Cocaine increases the metabolic demands of the heart via its stimulant effects and also Cardiac Biomarkers (Troponin I and T): causes coronary artery - Cardiac biomarkers must be repeated, never send just one sample of troponin testing vasoconstriction and promotes following chest pain thrombus formation (can cause - An early negative troponin does not rule out myocardial ischaemia chest pain, and risk of ACS) - In the setting of MI, troponin I and T detect elevations within 3 hours, peak at 12 - Oesophagitis or hours, and remain elevated for 7-10 days musculoskeletal causes such as - Creatine kinase MB (CK-MB) isoform levels rise to twice normal at six hours and peak costochondritis are diagnoses of within approx. 24 hours – CK-MB is not recommended anymore exclusion only - If patients have symptoms for more than 2 hours and the initial value of troponin T is below the level of detection (38) - Subacute course (without acute onset of chest pain) - Evidence suggesting cardiac tamponade - A large pericardial effusion - Immunosuppression and immunodepressed patients - A history of therapy with vitamin K antagonists - Acute trauma - Failure to show clinical improvement following seven days of appropriately Past Exam Question: dosed NSAID and colchicine therapy A 25 year old woman who presents to the - Elevated cardiac troponin, which ED with sharp central pain. You make the suggests myopericarditis/ provisional diagnosis of pericarditis. perimyocarditis Which of the following is true of this condition? Pericardial Effusions: (Measured on end-diastole by Echocardiogram) Small effusions (50 to 100 mL) – only seen posteriorly, less than 10mm in a) It has a high fatality rate in young people thickness on Echo b) It is occasionally associated with pulsus Moderate effusions (100 to 500 mL) – tend to be seen on the length of the paradoxus posterior wall, 10-20mm on Echo c) It commonly presents with pleuritic pain, Large effusions (>500 mL) – tend to be seen circumferentially, >20mm on worse on sitting up Echo d) It commonly presents with ECG changes such as PR elevation The size and rate of fluid accumulation determines the haemodynamic e) It is usually managed as an outpatient in consequence of pericardial effusion people aged less than 30 years old Pericardial effusion may need pericardial drainage Cardiac tamponade occurs when the intrapericardial pressure due to the b) Pulsus paradoxus is a sign of cardiac tamponade, which can accumulating pericardial effusion is elevated enough to impair filling of the develop from pericardial effusion from pericarditis cardiac chambers 8  Especially abrupt, transient, severe increases in Risk Factors blood pressure, e.g. cocaine, large catecholamine Aortic Dissection Hypertension releases, high-intensity weight lifting Males over 60 years old Anatomical Classification Bicuspid aortic valve The Stanford System Hypertension is present in 70% of type B Coarctation dissections but only 25-35% of type A dissections Iatrogenic (i.e. cardiac Type A - Dissections that involve catheterisation) the ascending aorta (and may Marfan or Ehler-Danlos Marfan syndrome is an autosomal dominant progress to involve the arch or syndrome condition that causes mutations in the FBN1 gene descending aorta) Turner Syndrome that makes fibrillin, this results in abnormal Type B – All other dissections Vasculitis Syndromes connective tissue Family History Ascending aortic dissections are Death from aortic dissection can almost twice as common as be from: descending dissections Immediate management: - Oxygen and maintain saturation >95% - Rupture of the pericardium The right lateral wall of the precipitating cardiac tamponade ascending aorta is the most - Insert two large IV cannulae and arrange - Acute dissection into the aortic common site immediate cross-match of 6 units of pRBCs - Relieve pain with titrated IV morphine valvular annulus leading to severe aortic regurgitation Syncope, hypotension and/or Give IV beta-blocker (esmolol or metoprolol) - Obstruction of the coronary artery shock: more common with slowly until the pulse is 120mmHg Hypertension in an asymptomatic patient - Obstructive sleep apnoea does not need to be assessed immediately, - Alcoholism May have symptoms of acute, irrespective of how high the BP is, and the - Renal artery stenosis ongoing target-organ damage BP may be safely brought under control - Parenchymal renal disease over the following hours or days - Renal tumours Signs of End-Organ Damage - Gestational Cardiovascular: Overly aggressive treatment may cause - Pre-eclampsia - Myocardial ischaemia/ infarction syncope, cortical blindness with occipital - Congenital adrenal hyperplasia - Aortic regurgitation (aortic stroke, myocardial ischaemia and death - Hypothyroidism dissection) - Hyperthyroidism - Absent pulse (aortic dissection) Do not treat the BP reading – only treat - Acromegaly Respiratory: the complications associated with it - Conn’s syndrome (primary - Pulmonary oedema (LVF) hyperaldosteronism) Central nervous system: Adverse Effects of Antihypertensive Agents - Cushing’s syndrome - Mental status change Thiazide diuretics – hypercholesterolaemia, - Phaeochromocytoma - Hyperreflexia hyperglycemia, thrombocytopenia and gout - Polycythaemia vera Beta-blockers – bradycardia, postural - Acute intermittent porphyria - Seizures hypotension, depression and cold peripheries - Raised intracranial pressure - Coma ACE inhibitors – angio-oedema, cough, postural - Hypertensive retinopathy -Medication induced – oral hypotension, hyperkalaemia, progression of renal failure and first-dose hypotension contraceptives, corticosteroids, Features of Hypertensive Angiotensin II receptor blockers – similar to cyclosporin Retinopathy ACE inhibitors but cough is less common Calcium channel blockers – headaches, MAOI antidepressant in combination None – no detectable abnormality sweating, palpitations and ankle oedema with a sympathomimetic or other Mild – focal and generalised psychoactive drug, or a food Alpha blockers – first dose hypotension arteriolar narrowing, copper and Vasodilators – minoxidil can cause sodium and containing tyramine (found in silver wiring of arterioles, water retention, leading to ankle oedema, and cheese or wine) can precipitate a arteriovenous (AV) nipping rarely pericardial effusion, also hypertrichosis hypertensive crisis Moderate – blot, dot or flame- shaped haemorrhages, cottonwool Hypertensive Encephalopathy spots, microaneurysm, yellow and white exudates - The DBP is usually >140mmHg associated with headache, lethargy, confusion, Severe – papilloedema (in addition vomiting and blurred vision – focal neurological signs, fits and coma develop later to haemorrhages and exudates) - Urine microscopy RBC casts, granular casts or dysmorphic RBCs (>70%) are suggestive of renal disease Retinopathy is indicative of - Retinal haemorrhages, exudates or papilloedema on fundoscopy increased risk of stroke, myocardial - Aim to initially reduce MAP by 25% or a DBP of 100-110mmHg within first 2-4 hrs infarctions and death - Use atenolol, long-acting nifedipine or captopril - If unsuccessful, give hydralazine slow IV boluses every 15-30 minutes Catecholamine Crisis - If still unsuccessful, arrange for ICU admission, give sodium nitroprusside IV with intra-arterial BP monitoring Phaeochromocytoma (rare neuroendocrine adrenal tumour Preeclampsia and Eclampsia associated with paroxysmal pallor, palpitations and perspiration, Hypertension at any level between 20 weeks gestation and 2 weeks postpartum, associated with intermittent and associated with oedema and proteinuria (>0.3 g/24h), indicates preeclampsia alarmingly high BP) Complications include: oliguria, placental insufficiency, haemolysis, thrombocytopenia (HELLP syndrome with haemolysis, elevated liver enzymes and Diagnosis is by measurement of encephalopathy) plasma or urinary catecholamines Treatment: - Near term is immediate birth of the baby and magnesium sulfate - A direct alpha-blocker such as - Magnesium sulfate does not significantly lower the BP, use other drugs such as phentolamine is given in boluses for nifedipine, hydralazine, labetalol or nitroprusside marked elevation of BP - Diuretics are avoided as the patient is already volume depleted from an activated - Once stable, continuous IV infusion renin-angiotensin system of phentolamine is commenced - Beta blockers must not be used Active seizures are treated with loading bolus of magnesium sulfate IV followed by alone, as unopposed alpha additional bolus if recurrent, supplemented if necessary with an IV benzodiazepine stimulation may increase the BP such as diazepam 10  Heart failure is a complex syndrome in which structural or functional Heart Failure and Acute impairment of the heart reduces ventricular filling or ejection of blood. Pulmonary Oedema Heart failure is usually a consequence of myocardial damage. Heart failure with reduced left ventricular ejection fraction (HFrEF) is Heart failure can be predominantly left-sided, heart failure with a LVEF of 40% or less typically presenting with pulmonary congestion and dyspnoea, or predominantly right sided, Causes of Heart Failure: Precipitating Factors of Heart Failure: typically presenting with elevated venous - High blood pressure pressure, peripheral oedema and liver - Coronary artery disease - Lack of adherence to drug therapy for congestion heart failure - Diabetes mellitus Both coexist in biventricular heart failure - Excessive fluid, salt or alcohol intake - Arrhythmias - Tachyarrhythmias - Excess alcohol intake - Bradyarrhythmias General Principles of HFeEF Management - Use of recreational - Myocardial ischaemia or infarction (most Treat all patients with: stimulant drugs common cause) - ACEi or ARB - Certain cardiomyopathies - Drug therapy - Beta blocker - Valvular heart disease - Infection - Aldosterone antagonist - Hyperthyroidism - Pulmonary embolism Consider: - Chronic lung disease - Iron deficiency - Anaemia - Loop diuretics - Pulmonary embolism - Hyperthyroidism - Hydralazine - Pericardial effusion - Acute valvular dysfunction - Digoxin - Ivabradine Acute Cardiogenic Pulmonary Oedema Prehospital Treatment - Acute cardiogenic pulmonary oedema is a medical emergency The patient should sit as upright as possible - It presents as rapid onset of severe dyspnoea, often first occurring at during treatment for acute cardiogenic night, as well as tachypnoea and tachycardia, with or without poor pulmonary oedema peripheral perfusion (ashen colour, sweaty, cool peripheries are reduced capillary return), agitation and restlessness, and widespread Use: lung crackles (although occasionally only wheezing may be detected) Frusemide 20-80 mg, IV or IM, repeated 20 - Exhaustion and altered conscious state will ensue if treated minutes later if necessary - The clinical features stem from the two major pathophysiological Plus (if O2 saturation is less than 94%) high- processes: intra-alveolar fluid accumulation and extreme sympathetic flow oxygen (titrated to response) via an nervous system activation oxygen mask fitted with a reservoir to maximise inspired oxygen delivery Patients who are taking oral frusemide may need a higher dose of parenteral frusemide If clinical response to oxygen and frusemide therapy is inadequate, consider adding glyceryl trinitrate Hospital Treatment Treatment includes: Frusemide 20-80 mg IV, repeated 20 minutes later if necessary - Consider inserting an indwelling catheter to monitor urine output - Consider using a glyceryl trinitrate infusion If the patient does not respond to these measures, intubation is - If pulmonary oedema remains severe and necessary. Signs of non-response include: does not respond promptly to the above measures, start non-invasive ventilation with - Patient exhaustion 100% oxygen – CPAP - Declining level of consciousness - Acute pulmonary oedema can be associated - Increasing confusion and agitation with acute anxiety and distress – use morphine - Rising partial pressure of carbon dioxide (PaCO2) - If pulmonary oedema is not responding to - Failure to maintain an adequate partial pressure of oxygen (PaO2) above measures, consider adding dobutamine 11  Do not use prasugrel for STEMI patients who weigh less than 65 kg, aged 75 or older or who have had a previous ischaemic attack Dual Antiplatelet Therapy: Do not use 2-4L/min via facemask or nasal prongs Aspirin + a P2Y12 inhibitor Clopidogrel for breathless or hypoxic patients OR ticagrelor for Ticagrelor patients who OR have second or Prasugrel third degree AV Defibrillation block Acute Management Ventricular fibrillation Percutaneous Coronary Cardiac Monitoring Intervention (PCI) Oxygen ECG Aspirin Identification of STEMI Sublingual nitroglycerine Unfractionated Venous access heparin Fibrinolytic Therapy Pain relief OR Enoxaparin Pain produces catecholamines, OR A side effect is a hypotensive Clopidogrel Bivalirudin which increases ischaemia bradycardic response (the Bezold- Jarisch reflex) Should be taken within 5 minutes of arrival Fibrinolytic agents take 30-45 minutes on Enoxaparin Alteplase average to reperfuse the occluded artery OR OR Reperfusion Therapy Unfractionated Reteplase Heparin OR PCI is more beneficial than Tenecteplase Inferior MI: fibrinolytic therapy in reducing - Need to consider the presence of a right mortality, recurrent myocardial ventricle infarction infarction and stroke - Associated with significant increased If PCI is available within 90 minutes Killip Classification of Severity of mortality, the severest form and associated of first medical contact, PCI is Infarction with cardiogenic shock preferred over fibrinolytic therapy - Patients with RV infarction are very preload If PCI cannot be delivered promptly, Class I – No failure sensitive and can develop severe hypotension in fibrinolytic therapy should be given Class II – Mild to moderate heart failure response to nitrates within 30 minutes of the patient (S3, rales 50% lung fields) - Secondary to oxygen supply-and-demand Class IV – Cardiogenic shock Complications of MI problems rather than thrombosis - Common in postoperative and ICU patients - Arrhythmias Past Exam Question: - Postinfarction Angina and Regarding unstable angina pectoris, Takotsubo’s Cardiomyopathy: which of the following statements is Reinfarction - Triggered by emotional or physical stress true? - Cardiac failure and Cardiogenic Shock - The chest pain mimics acute coronary - Mitral regurgitation syndrome a) A normal ECG and normal serial - Cardiac rupture - Systemic emboli troponins makes the diagnosis very - Post-MI pericarditis unlikely b) The absence of cardiac risk factors excludes the disease A pericardial rub may develop 24-72 c) Pain commonly radiates to the back hours after large, usually anterior MI d) It is treated with thrombolysis or percutaneous coronary intervention e) Beta blockers have been shown to Dressler’s syndrome is characterised by fever, reduce mortality pleuropericardial pain and rub, arthralgia and elevated inflammatory markers Answer: e) 12 Supraventricular Tachycardia SVT is any tachycardia that requires atrial or AV nodal tissue for initiation and maintenance - SVTs are usually conducted rapidly through the bundle Distinguishing between AV node-dependent and independent SVTs branches so that QRS complexes are narrow can be difficult - All narrow-complex tachycardia are SVT and wide-complex tachycardia are usually ventricular Vagal manoeuvres or drugs that prolong AV nodal refractoriness - However, SVT may be wide complex in the setting of bundle may assist in diagnosis branch block (BBB) and pre-excitation Supraventricular tachycardia can be converted to sinus rhythm by manoeuvres that enhance vagal tone Avoid in older patients and These include the Valsalva manoeuvre and carotid sinus massage those with vascular disease If these manoeuvres are ineffective in restoring sinus rhythm, use one of the following drugs with close blood pressure monitoring: Adenosine is best given rapidly, followed by rapid saline flush, this is most effective via a proximal venous cannula 1. Adenosine 6 mg IV by rapid bolus Adenosine is relatively contraindicated in patients or acute bronchospasm If this is ineffective, give a second bolus of 12 mg after Adverse effects of adenosine: flushing, dyspnoea 2 minutes and chest pain Classically associated with a If this is ineffective but well sense of “impending doom” tolerated, give a further Adenosine causes transient dose of 18 mg heart block in the AV node It is considered a class V Metallic taste is a hallmark antiarrhythmic agent side-effect of adenosine 2. Verapamil 5 to 10 mg IV over 2 administration minutes Verapamil is generally safe, however it can If this is ineffective but well cause occasionally cause profound depression of tolerated, give a further heart rate and/or contractility, particularly in dose of 5 to 10 after 30 patient who have pre-existing myocardial minutes disease or those taking beta blockers 3. Pre-treatment with calcium gluconate can Metoprolol tartrate 2.5 to 5 mg IV reduce the hypotensive effect of verapamil over 2 minutes without affecting the antiarrhythmic effect If this is ineffective but well Do not give verapamil to a patient with a wide- tolerated, give a further complex tachycardia unless it is known to be of dose of 2.5 to 5 mg after 10 supraventricular origin minutes If the QRS complex is wider than 0.14 seconds, ventricular If SVT persists, direct current (DC) Verapamil blocks tachycardia is more likely than cardioversion, intravenous voltage-dependent paroxysmal supraventricular 4. amiodarone or overdrive pacing calcium channels tachycardia may be required Considered a class IV antiarrhythmic agent Past Exam Question: What electrocardiogram (ECG) feature would you expect to find in typical supraventricular tachycardia? a) Delta waves b) Irregular rhythm c) Ventricular ectopic complexes d) Absent P waves e) Wide QRS complexes Answer: d) 13  Atrial fibrillation is the most frequently Atrial fibrillation is associated with Atrial Fibrillation encountered cardiac arrhythmia and becomes more common as people age heightened risk of thromboembolism such as stroke and other cardiovascular events 1. Determine the type of AF (paroxysmal, persistent, or permanent) Atrial fibrillation usually presents with Paroxysmal – terminates spontaneously within 7 days an irregular ventricular Persistent – lasts longer than 7 days or is terminated pharmacologically rate of around 160 to or electrically 180 beats per minute Permanent – does not terminate, even with cardioversion attempts Patients may have 2. Identify and correct (if possible) underlying causes of AF symptoms of palpitations, shortness of breath and fatigue, but many patients are Cardiovascular Causes: Noncardiovascular Causes: asymptomatic - Hypertension - Hyperthyroidism - Valvular heart disease - Autonomically mediated (vagal) causes - Coronary artery disease - Alcoholism (“holiday heart”) or alcohol - Heart failure or cardiomyopathy withdrawal - Genetic or familial causes - Obstructive sleep apnoea or obesity - Post cardia surgery - Pharmacologic agents (e.g. stimulants) - Congenital heart disease - Excessive physical exertion - Sick sinus syndrome - Sepsis - Pacemaker - Pulmonary disease (e.g. COPD) 3. Determine patient-specific factors that influence choice If presenting with atrial fibrillation and haemodynamic between rate-control and rhythm-control strategies compromise – consider immediate cardioversion Patients with AF persisting for longer than 48 hours have an Favouring Rate Control Favouring Rhythm Control increased risk of developing a left atrial thrombus Persistent AF More symptomatic Less symptomatic Age < 65 y If AF persisted longer than 48 hours, or if duration of AF is Age > 65 y No hypertension unknown, do not perform acute cardioversion unless left atrial Hypertension HF clearly exacerbated by thrombus has been excluded, or the patient has had No history of HF atrial fibrillation therapeutic anticoagulation for the previous 3 weeks Previous failure of No previous failure of antiarrhythmic drug antiarrhythmic drug If atrial thrombus has not been excluded, or the patient is not anticoagulated, rate control is the preferred initial treatment Step 4. Choose an appropriate pharmacologic agent considering patient-specific factors and comorbidities Synchronised DC electrical cardioversion Rate Control Algorithm Target resting HR 35% EF < 35% Beta-blocker Beta-blocker Beta-blocker with or Flecainide Diltiazem Diltiazem without digoxin Propafenone Verapamil Verapamil Sotalol Amiodarone Amiodarone Digoxin Dronedarone Diltiazem and verapamil Amiodarone can Sotalol Amiodarone have negative inotropic also be used for Beta blockers: effects and should be rate control in Atenolol avoided in patients with LV patients with LV Catheter ablation Metoprolol dysfunction dysfunction 14  - Bradycardia is defined as a heart rate less than 60 beats per minute Bradyarrhythmias - Slow heart rate may be physiologically normal for some people (especially if very fit) - Junctional escape rhythm and Wenkebach block are also seen in the general population and are usually asymptomatic Bradycardia can be due to sinus node - People with asymptomatic bradycardia usually need no treatment dysfunction (formerly called sick sinus - Intermittent severe bradycardia can cause syncope syndrome), which is characterised by sinus - Chronic bradycardia can cause fatigue, shortness of breath on exertion and dizziness bradycardia, sinus pauses and junctional - Bradycardia can cause haemodynamic compromise with signs of poor perfusion, leading or ventricular escape rhythms. It is often to hypotension and syncope, altered conscious rate, ischaemic chest pain and heart associated with paroxysmal atrial failure fibrillation (‘tachy-brady’ syndrome). Chronic sinus node dysfunction associated Drugs that can cause bradycardia: with symptoms is an indication for Digoxin, beta blockers, verapamil, diltiazem, amiodarone permanent pacing but rarely requires Combinations of drugs that block the atrioventricular (AV) node should be used with acute intervention caution, avoid the combination of verapamil and a beta blocker Bradycardia may be associated with AV block, which is classified as: Due to complete interruption Complete dissociation between of AV conduction, and may or atria and ventricles Third degree block (complete heart block) may not be symptomatic Intermittent AV conduction (intermittent dropped beats) Second degree block: At the level of the AV node and Progressive lengthening of PR interval with is usually transient, eventual dropped ventricular conduction Mobitz 1 or Wenkebach block asymptomatic and benign At the level of the His-bundle and distal conduction system Intermittent dropping of ventricular conduction Mobitz 2 block and is usually symptomatic and progresses on to complete heart block First-degree block Prolonged PR interval (more Management of Acute Bradyarrhythmias than 0.2 seconds), which is usually benign and does not require treatment During evaluation of a patient with an acute bradyarrhythmia: - Maintain a patent airway If the bradycardia is due to AV block complicating acute - Assist breathing as needed myocardial infarction, the best approach is reperfusion - Give oxygen, monitor with pulse oximetry therapy to urgently reopen the affected coronary artery - Monitor heart using a 12-lead ECG - Monitor blood pressure - Establish IV access For bradycardia occurring with AV block in inferior myocardial infarcts, - Prepare for transcutaneous pacing the AV block is usually at the end of the AV node and is transient and not haemodynamically significant Atropine may be required When bradycardia is due to sinus node dysfunction or block at the level of the AV node, atropine is the most effective treatment: For bradycardia occurring with AV block in anterior myocardial infarcts, the AV block is at the level of the distal conducting tissues in Atropine 0.5 mg IV, repeat after 3-5 minutes if the ventricle and is likely to be permanent and associated with necessary, up to a maximum of 3 mg haemodynamic compromise Emergency temporary pacing is usually required Atropine is an anticholinergic (antimuscarinic) drug If atropine is ineffective, consider transcutaneous or It inhibits the action of the parasympathetic nervous system to allow for an temporary transvenous pacing unchallenged sympathetic response (blocks the vagus nerve on the heart and increases the rate of the SA node) If pacing is delayed or not immediately available, consider using: Adrenaline is preferred if systolic blood pressure is Isoprenaline 2-10 mcg/min by IV infusion very low (less than 80 mmHg) because OR isoprenaline may further reduce blood pressure Adrenaline 2-10 mcg/min by IV infusion 15  Syncope is transient loss of consciousness and postural tone from reduced cerebral Syncope perfusion, followed by spontaneous and full recovery Causes of Syncope Presyncope refers to a reduction in cerebral perfusion resulting in a sensation of impending loss of consciousness, although the Arrhythmias: patient does not actually pass out Tachyarrhythmias: - VT (may be in setting of ACS) - An abnormally prolonged QT is associated with an Prolonged QTc: - Rapid AF or flutter (usually with associated WPW) increased risk of ventricular arrhythmias, especially - Hypokalemia - Rapid SVT (usually with associated WPW) Torsades de Pointes - Hypomagnesemia - Torsades de pointes (usually with prolonged QT) - QTc is prolonged if > 440ms in men or > 460 ms in - Hypocalcemia Bradyarrhythmias: women - Hypothermia - Sinus arrest - A normal QT is less than half the preceding RR - MI - Second and third degree (complete) AV block interval - Post-cardiac arrest - Sick sinus syndrome - Raised ICP - Pacemaker malfunction A disease characterised by abnormal sinus node - Congenital functioning with resultant bradycardia and cardiac Obstructive lesions or ‘low-flow’ conditions, insufficiency Asymmetrical sometimes precipitated by exertion: septal hypertrophy - Aortic stenosis Left ventricular hypertrophy (asymmetrical septal produces deep, - Pulmonary stenosis hypertrophy) in the absence of hypertension or aortic narrow (“dagger- - Hypertrophic cardiomyopathy stenosis like”) Q waves in - Pulmonary embolism the lateral and - Aortic dissection - Also called neurocardiogenic syncope or reflex- inferior leads mediated syncope Vasovagal syncope - Excessive vagal tone associated with standing, An exaggerated emotion, fear, stress, hunger response to carotid Carotid sinus hypersensitivity - Or raised intrathoracic pressure from coughing, sinus baroreceptor micturition, swallowing, defecation, sneezing stimulation Peripheral vascular: Results in syncope - Orthostatic (postural) hypotension Syncope on turning head from transient - Drug induced diminished - Volume depletion cerebral perfusion Nitrates, hydralazine, prazosin, ACE inhibitors, - Autonomic failure antipsychotics, levodopa Cerebrovascular: - Subarachnoid haemorrhage - Vertebrobasilar insufficiency Occlusion or severe stenosis of the proximal - Subclavian steal subclavian artery results in retrograde flow in the ipsilateral vertebral artery Psychogenic: - Hyperventilation - Psychogenic collapse Neurological: - Dementia - Confusion and cognitive impairment - Pre-existing weakness Past Exam Question: - Parkinson disease, or other movement disorders including normal pressure hydrocephalus A 50 year old woman is brought to the ED after collapsing at - Cerebellar lesions with ataxia home while standing at the sink. She says that she remembers feeling hot and nauseated before developing tunnel vision and Metabolic disorder: then passing out. She is usually well and takes a single anti- - Electrolyte abnormality hypertensive agent. In physical examination, she is now well. - Dehydration, renal failure, hepatic failure There are no significant cardiovascular findings and no focal Sensory impairment: neurological deficits. - Cataracts, age-related macular degeneration, What is the most likely cause for her syncopal episode? glaucoma - Impaired balance and proprioception a) Vasovagal syncope Musculoskeletal: b) Transient ischaemic attack - Arthritis, obesity and physical inactivity c) Orthostatic hypotension d) Ventricular tachycardia e) Ventricular fibrillation Answer: a) 16 Acute limb ischaemia is the most common vascular emergency Can also be from trauma Acute Ischaemic Limb The most common causes are embolus from the left atrium in association with atrial fibrillation and acute thrombosis at Paralysis, paraesthesia and muscle tenderness are the a site of long-standing atherosclerotic narrowing cardinal signs of complete acute ischaemia, when they are present the limb must be revascularised within 4-6 - At first, acute complete ischaemia is associated with intense distal hours if it is to be saved and full function restored arterial spasm and the limb is ‘marble’ white - As the spasm relaxes over the next few hours and the skin fills with Fasciotomy should always be considered upon deoxygenated blood, mottling appears successful reperfusion to avoid compartment syndrome - This is light blue or purple, has a fine reticular pattern and blanches on pressure: so-called ‘non-fixed mottling’ - This this stage, the limb is still salvageable -As ischaemia progresses, blood coagulates in the skin, leading to mottling A few hours can make the difference that is darker in colour, coarser in pattern and does not blanch between amputation or death, and - Finally, large patches of fixed staining progress to blistering and complete recovery of limb function liquefaction - Attempts at revascularisation at this late stage are futile and will lead to life-threatening reperfusion injury Acute Embolus Thrombosis In Situ The treatment of embolism is urgent embolectomy, Patients with thrombosis in situ should undergo usually without prior angiography angiography if possible, treatment comprises a combination of medical therapy, thrombolysis, angioplasty and bypass Femoral embolus is usually associated with profound ischaemia to the level of the upper thigh because the deep A limb affected by stable chronic ischaemia suddenly femoral artery is also affected deteriorates to the thrombosis in situ on top of atherosclerosis Acute embolic occlusion of the aortic bifurcation (saddle embolus) leads to Triggers: absent femoral pulses and a patient who - ‘Silent’ or overt MI (drop in blood is mottled to the waist pressure) - Malignancy (increase in thrombogenicity of the blood) Such patients may also present with - Septicemia (especially pneumococcal paraplegia due to ischaemia of the and meningococcal) cauda equina, which may be irreversible - Dehydration from any cause Embolectomy can be performed under Many patients can be managed medically local/regional or general anaesthetic If the limb remains threatened then it may be possible to clear the thrombus by open surgical or endoluminal means, to dissolve the clot by means of thrombolysis or bypass the affected segment 17  Risk Factors (Virchow’s Triad): Pulmonary Embolus Acute pulmonary embolism is a form of venous thromboembolism - Malignancy It is the obstruction of the Hemodynamically unstable or stable - Pregnancy pulmonary artery or one of its - Hospitalisation branches by material Source: lower extremity proximal veins - Recent surgeries (thrombus, tumor, air, fat) (iliac, femoral, popliteal) - Inherited thrombotic disorders - Immobilization Chest X-Ray - Hormone therapy - Normal X-ray - Obesity - Smoking Hampton’s Hump - Recent travel Westermark’s Sign Arterial Blood Gas (ABG) ECG - Hypoxemia - Sinus tachycardia - Widened Aa Gradient - T-wave inversion (V/Q mismatch) - S1Q3T3 Pattern - Respiratory alkalosis + - Right ventricular hypocapnia strain - Severe: metabolic acidosis from lactate Presenting Symptoms Physical Examination Treatment (in order of likelihood): (in order of likelihood): 1. Resus for Haemodynamically Unstable - Dyspnea at rest or exertion - Tachypnea 2. Fibrinolytic therapy (short-term) - Pleuritic pain - Calf or thigh swelling, - Alteplase - Cough erythema, oedema, tenderness - Tenecteplase - Orthopnea - Tachycardia 3. Anticoagulation (long-term) (LMWH) - Calf or thigh pain/ swelling - Rales - Dalteparin - Wheezing - Decreased breath sounds - Enoxaparin - Hemoptysis - Elevated JVP - UFH (renal disease) - Syncope - Fever Clinical symptoms of DVT 3 Other diagnosis less likely than PE 3 Wells Criteria for Pulmonary Embolism HR > 100 1.5 High risk: >6 Immobilization (>3 days) or surgery within 4 weeks 1.5 Moderate: 2-6 Previous DVT/ PE 1.5 Low: 10 minutes presenting with cerebral oedema - Recent internal bleed (2-4 weeks) - Ventricular drainage (to relieve acute hydrocephalus) - Uncontrolled hypertension (180/110 mmHg) and posterior fossa decompression are treatments of - Remote ischaemic stroke choice for large space-occupying cerebellar infarcts - Major surgery within 3 weeks 28  A seizure is an ‘episode of abnormal neurological function caused by an A seizure can be an acute event or Seizures abnormal discharge of brain neurons’ can be the result of a past neurological insult (e.g. stroke, head injury or hypoxic brain injury) - The focus for seizure activity is a group of neuronal cells which have highly permeable plasma membranes and are therefore in a hypersensitive state During a seizure, energy demands - Hyperexcited neurons fire impulses that increase in frequency and amplitude until impulses are increased by 250%, there is spread to adjacent normal neurons 60% increase in cerebral oxygen - Excitation of the subcortical area of the basal ganglia, thalamus and brainstem areas results in consumption and cerebral blood the tonic phase of seizure (muscle contraction with excessive tone), autonomic signs and flow also increases by 250% in an symptoms, apnoea and loss of consciousness attempt to keep up with cerebral - Hyperexcitation is interrupted by inhibitory neurons in the cortex, anterior thalamus and basal oxygen and glucose demands ganglia, resulting in the clonic phase of seizure (alternating muscular contraction and relaxation) Status epilepticus is traditionally defined as 30 minutes or more of: One of the major pathophysiol