ALS Flashcards

Question

A to E - DISABILITY

Answer 1

Examine pupils (size, equality, reaction to light) Rapid initial assessment of ACVPU (formal GCS if possible) BLOOD GLUCOSE Check drug chart

Answer 2

Full clinical history Fully expose patient and examine - rashes, abdo, etc Temperature Review notes and charts

Answer 3

- crescendo angina - recurrent/unpredictable episodes of angina-like pain without specific provocation by exercise - unprovoked/prolonged episode of CP raising suspicion of MI but without ECG changes/lab evidence of MI NORMAL TROPONINS

Answer 4

Angina on exertion, occurring with increasing frequency over a few days, provoked by progressively less exertion

Answer 5

- normal ECG - acute MI changes (usually ST depression) - non-specific abnormalities (eg. TWI)

Answer 6

- ST depression - dynamic ECG changes - unstable rhythm - unstable haemodynamics - DM - high GRACE score

Answer 7

PCI if available within 120 minutes of onset of CP If PCI not possible - fibrinolytic therapy considered as alternative DO NOT wait for trops to come back in pts with STEMI

Answer 8

V1-V4 Lesion in LAD artery

Answer 9

V1-V6 and I and aVL

Answer 10

= Anterior more likely to cause impairment of LV function

Answer 11

V5-V6, I and aVL lesion in circumflex artery or diagonal branch of LAD artery

Answer 12

Leads II, III and aVF usually lesion in RCA Less commonly lesion in circumflex artery

Answer 13

when there is reciprocal ST-depression on anterior leads this could reflect ST-elevation posteriorly most commonly RCA occlusion Suspicion can be confirmed by placing V8-V10 posteriorly (posterior leads)

Answer 14

300mg Aspirin asap sublingual GTN (unless hypotensive) O2 to maintain sats in target range Analgesia - titrated IV morphine with anti-emetic

Answer 15

Previous haemorrhagic stroke Ischaemic stroke in past 6 months CNS damage/neoplasm Recent (3/52) major surgery/head injury/major trauma Active internal bleeding or GI bleed in last 1 month Known/suspected aortic dissection Known bleeding disorder

Answer 16

Refractory HTN (SBP >180mmHg) TIA in last 6 months DOACs Pregnancy or <1 week post-partum Traumatic CPR Non-compressible vascular puncture Active PUD Advances liver disease Infective endocartitis Previous allergic reaction to fibrinolytic drug

Answer 17

= hypotension, poor peripheral perfusion often accompanied by drowsiness/confusion and oliguria if develops in a patient after a STEMI consider acute complications such as myocardial rupture, papillary muscle rupture, VSD

Answer 18

Inherited (autosomal dominant) ion channel disorder Predispose to torsade de pointes VT and VF

Answer 19

caused by IHD/drug therapy/myocarditis Predispose to torsade de pointes VT and VF

Answer 20

inherited (autosomal dominant) ion channel disorder More common in SE asians

Answer 21

Rare Inherited (autosomal dominant) ion channel disorder Predispose to torsade de pointes VT and VF

Answer 22

Rare Inherited (autosomal dominant) ion channel disorder Predisposes to torsade de pointes VT and VF, especially on exercise

Answer 23

Inherited (autosomal dominant) Predisposes to VT and VF

Answer 24

Inherited (autosomal dominant) Several genotypes SCD risk is due to VT/VF Risk varies with genotype and individual factors

Answer 25

Mostly sporadic, infrequent familial incidence Risk is due to rapid transmission of AF to the ventricles, triggering VT/VF

Answer 26

Caused by conducting stem fibrosis, calcified AS, myocardial diseases, cardiac surgery, drug therapy, occasionally congenital Predisposes to ventricular standstill (asystole)

Answer 27

Caused by congenital bicuspid valve (becomes severe age 50-70) or degenerative changes Many develop HF, risk of SCD due to VT/VF

Answer 28

Multiple causes, familial in minority of cases Many develop HF, risk of SCD due to VT/VF

Answer 29

partly genetic, partly acquired SCD risk mainly due to VT/VF either due to acute ischaemia or chronic scarring

Answer 30

congenital rare cause of SCD, often on exercise, risk varies with pattern of anomaly

Answer 31

often remain at risk of cardiac arrest even when they have had corrective surgery as a child

Answer 32

Hypoxia Hypotension

Answer 33

1. check for safety 2. check for patient response 3. no response, no signs of life, no pulse --> CPR algorithm 4. response / signs of life --> urgent assessment +/- MET call

Answer 34

Agonal breathing (occasional, irregular gasps) Arm movements during CPR Seizure-like movements - can occur right at the start of arrest

Answer 35

Call for help & crash trolley Check airway +/- manoeuvres Check for breathing Check for pulse Commence 30:2 CPR

Answer 36

Depth of 5-6cm Rate of 100-120 compressions/min Allow chest to recoil completely after each compression Approx. same amount of time for compression and relaxation Minimise hands-off time If there are enough team members, swap every 2 mins

Answer 37

use what ever equipment is available immediately aim for inspiratory time of about 1 sec give enough volume to produce visible rise of chest wall add supplementary oxygen as soon as possible avoid rapid/forceful breaths If intubated (+/i iGel) - ventilate and compressions simultaneously and uninterrupted

Answer 38

= continuous real-time end-tidal CO2 Uses: - confirming correct intubation - monitoring ventilation rate - used to monitor quality of CPR - used as indicator of ROSC - prognostic indicator

Answer 39

ALS provider can immediately recognise rhythm and shock if needed This can reduce hands-off time to less than 5 seconds

Answer 40

= respiratory arrest Diagnosis can only be made if confident in assessing pulse and signs of life (e.g. perfusion/normal CRT) Ventilate patient's lungs Check for pulse every 1 minute All pts with respiratory arrest will develop cardiac arrest if it is not treated rapidly and effectively

Answer 41

If shockable rhythm, can deliver 3 rapid successive shocks Check for any rhythm change/other signs of ROSC after each shock Start 30:2 CPR if no ROSC after 3rd shock (these 3 are considered the 1st shock in the ALS algorithm)

Answer 42

rarely works Only to be used whilst awaiting defibrillator in a monitored VF/pVT arrest ulnar edge of tight fist - sharp impact of lower half of sternum from about 20cm, then retract immediately

Answer 43

First shock 120-150 J Same or higher for subsequent shocks

Answer 44

1. rhythm check - confirm shockable rhythm 2. resume compressions 3. STAND CLEAR (only person on the chest should be touching) 4. charge to appropriate energy 5. everyone to STAND CLEAR 6. when clear, deliver shock 7. immediately restart CPR for next 2 minutes

Answer 45

After the 3rd shock (whilst 2 mins CPR ongoing) - Adrenaline 1mg IV - Amiodarone 300mg IV Then further adrenaline IV after alternate shocks (roughly every 3-5 mins) If shockable rhythm persists/recurs - a further dose of 150mg amiodarone can be given after a total of 5 defibrillation attempts

Answer 46

longer interruptions in chest compressions reduce the chance of a shock achieving ROSC

Answer 47

Lidocaine 1mg/kg can be used as an alternative if amiodarone unavailable - but DO NOT give lidocaine if amiodarone already given.

Answer 48

presence of carotid pulse sudden increase in end-tidal CO2 evidence of Cardiac Output on invasive monitoring equipment

Answer 49

only when there is a rhythm that could be compatible with a pulse

Answer 50

= cardiac arrest in the presence of electrical activity that would normally be associated with a palpable pulse these Pts often have some mechanical myocardial contractions but these are too weak to produce a detectable pulse/BP

Answer 51

Survival of PEA or asystole is unlikely unless a reversible cause can be found and treated quickly and effectively

Answer 52

= the absence of electrical activity on ECG trace Important to check trace for evidence of P waves as then ventricular standstill may be treated effectively by cardiac pacing Attempts to pace true asystole are unlikely to be successful

Answer 53

Start CPR 30:2 Adrenaline 1mg IV as soon as access achieved Continue CPR 30:2 until airway secured (then continous compressions and ventilation) Recheck rhythm after 2 mins - If pulse/signs of life - commence post-resuscitation care - if no pulse/signs of life - recommence CPR Further adrenaline every 3-5 mins If at any point VF/pVT on rhythm check, switch to shockable algorithm

Answer 54

- only carried out by someone competent to intubate - no evidence that intubation is any better than bag-valve or SGA during an arrest - avoid interruptions on compressions (max 5 sec while tube going through vocal cords) - intubation may be avoided until ROSC achieved

Answer 55

4.7-6.0 kPa

Answer 56

= the partial pressure of CO2 at the end of an exhaled breath 4.3-5.5 kPa (i.e. lower than arterial)

Answer 57

During CPR, end-tidal CO2 is low (reflecting the low CO generated by compressions)

Answer 58

the more effective the compressions, the greater the end-tidal CO2

Answer 59

an increase in end-tidal CO2 during CPR may indicate ROSC

Answer 60

Low end-tidal CO2 values during CPR are associated with lower ROSC rates and increased mortality Higher values associated with better ROSC rates and survival End-tidal CO2 should be part of a multifactorial approach to prognostication (do not use alone)

Answer 61

Intubation SGA with good seal

Answer 62

10 per min

Answer 63

If pt has CVC - use this Otherwise attempt to gain peripheral access - drugs will need to be followed by a flush of 20mL fluid and elevation of extremity (for 10-20s) to allow adequate delivery to central circulation If IV access difficult, consider IO

Answer 64

Proximal humerus Proximal Tibia Distal Tibia

Answer 65

Trauma Infection Prosthesis at target site Recent IO access (last 48h) in the same limb Failure to identify anatomical landmarks

Answer 66

- extravasation into soft tissues around insertion site - dislodgement of needle - compartment syndrome (due to extravasation) - fracture or chipping of bone during insertion - pain related to drugs/fluid - fat emboli - infection/Osteomyelitis

Answer 67

Ensure adequate: - ventilation with 100% O2 during CPR - chest rise - bilateral breath sounds

Answer 68

PEA caused by hypovolaemia is usually due to severe haemorrhage Restore IV volume rapidly with fluid/blood (effective compressions require an adequate circulating volume) Urgent interventions to stop haemorrhage

Answer 69

identified on biochemical tests or suggested by Pt's PMHx IV CaCl is indicated in the presence of hyperkalaemia, hypocalcaemia and CCB overdose

Answer 70

Suspect hypothermia in any drowning incident

Answer 71

Coronary thrombosis is a common cause - if ACS is suspected as cause it may be feasible to perform PCI during ongoing CPR but this requires mechanical compressions Massive PE - consider fibrinolytic therapy immediately if suspected - if given, CPR needed for 60-90 mins after this

Answer 72

clinical Dx or focussed US of chest Decompress rapidly by thoracostomy or needle thoracocentesis and then insert a chest drain

Answer 73

difficult to diagnose in arrest (typical signs difficult to see) Focused cardiac ultrasound can diagnose pericardial effusion Have strong suspicion in an arrest after penetrating chest trauma or after cardiac surgery

Answer 74

If no specific history, may be difficult to detect but may be revealed later by lab tests Where available, appropriate antidotes should be used but a lot of treatment is supportive

Answer 75

Requires vascular access and a circuit with a pump and oxygenator Can buy time until restoration of adequate spontaneous circulation in select patients who have a reversible cause, there is little comorbidity, and arrest was witnessed/has had immediate high-quality CPR

Answer 76

If attempts at achieving ROSC are unsuccessful the team leader should discuss stopping CPR with the team Consider the circumstances and perceived prospect of a successful outcome If it was considered appropriate to start CPR, it is usually considered worthwhile continuing whilst the patient remains in a shockable rhythm or there are potentially reversible causes that can be treated Asystole >20mins in absence of reversible causes, generally constitutes reasonable grounds for stopping

Answer 77

After stopping CPR observe the patient for 5 mins before confirming death - absence of central pulse on palpation - absence of heart sounds on auscultation One or more can supplement the above: - asystole on continuous ECG display - absence of pulsatile flow on direct intra-arterial pressure monitoring - absence of contractile activity using echo After 5 mins of continued arrest, check pupil responses, corneal response, and motor response to supra-orbital pressure. Time of death is recorded as the time at which these criteria are fulfilled

Answer 78

the pharynx (soft palate / epiglottis rather than tongue)

Answer 79

Inspiratory Stridor - laryngeal level or above Expiratory Wheeze - lower airways Gurgling - liquid foreign material in upper airways Snoring - pharynx partially occluded by tongue/palate

Answer 80

= effective cough Able to answer "yes" to the question are you choking? Able to speak, cough, breathe. Mx => encourage coughing

Answer 81

= ineffective cough unable to speak, unable to breathe, attempts at coughing are silent, may lose consciousness Mx if conscious => 5 back blows, 5 abdominal thrusts Mx if unconscious => start CPR

Answer 82

Head tilt & chin lift Jaw thrust

Answer 83

one hand on pt's forehead and tilt head back fingertips of other hand under point of pt's chin gently lift to stretch anterior neck structures

Answer 84

identify angle of mandible with the index and other fingers placed behind the mandible, apply steady upwards and forwards pressure to lift the mandible With the thumbs, slightly open the mouth by downward displacement of the chin

Answer 85

checking length between pt's incisors and the angle of the jaw if in doubt, a bigger airway will be more beneficial than a smaller airway

Answer 86

only attempt in unconscious patients (vomiting or laryngospasm may occur if gossopharyngeal/laryngeal reflexes are present) - open pt's mouth - remove any foreign material if present - insert airway upside down into oral cavity until you reach junction between hard/soft palate - rotate it 180 degrees - advance airway until it lies within the pharynx remove airway if pt gags or strains

Answer 87

better tolerated than OP airway in Pts who are not deeply unconscious Size 6-7mm usually suitable for adults Can cause bleeding in up to 30% of uses If tube is too long it can stimulate laryngeal / glossopharyngeal reflexes

Answer 88

in a patient with suspected basal skull # (rare chance of inadvertently inserting into cranial vault through the fracture)

Answer 89

Wide-bore rigid sucker (yankauer) to remove liquid (blood, saliva, gastric contents) from the upper airway => use cautiously if gag reflex intact Fine-bore flexible suction catheters may be needed in pts with limited mouth opening (can also be passed through OP/NP airways)

Answer 90

- try to continue compressions throughout insertion (if necessary to stop, limit pause to 5 sec) - select appropriate size - lubricate the back, sides and front with a thin layer of lube - position so that the cuff outlet is facing the chin of the patient - ensure patient is 'sniffing the morning air' - insert in direction towards the hard palate, glide device downwards and backwards with continuous but gentle push until a definitive resistance is felt

Answer 91

- there is risk of significant leak around the cuff in presence of high airway resistance (e.g. COPD, pulmonary oedema) - may cause gastric inflation - uninterrupted chest compressions are likely to cause some gas leak, can revert to 30:2 if needed - theoretical risk of aspiration of stomach contents but rarely seen in clinical practice - may cause coughing, straining or laryngeal spasm (but not in an arrest)

Answer 92

= wide-bore tube with elliptical inflated cuff designed to seal around laryngeal opening

Answer 93

i-Gel Laryngeal Mask Airway

Answer 94

exhaled CO2 will be detectable by waveform capnography even during cardiac arrest, failure to detect any CO2 indicate that the tube is in the oesophagus

Answer 95

most often needed in patients with extensive facial trauma or severe laryngeal obstruction (eg. anaphylaxis/foreign material) => surgical airway below the level of obstruction should only be performed by those trained in the technique

Answer 96

Beneath right clavicle Left mid-axillary line

Answer 97

e.g. if permanent pacemaker, chest wall trauma Anterior/posterior - left precordium and on the back behind the heart Lateral/posterior - left mid-axillary line, on the bakc behind the heart Bi-axillary - both lateral chest walls

Answer 98

occurs in the presence of an accessory pathway in WPW syndrome produces an irregular broad complex tachycardia which might be mistaken for polymorphic VT Correct Tx is immediate defibrillation left untreated, this can leat to VT/VF causing cardiac arrest

Answer 99

management follows broad-complex tachycardia algorithm

Answer 100

when atrial beats are conducted to the ventricles during VT produces a single normal-looking QRS complex during monomorphic VT

Answer 101

can be seen in VT a wave of depolarisation travelling down from the AV node occurs simultaneously with a wave of depolarisation travelling from the ventricular focus producing the arrhythmia results in a hybrid QRS complex

Answer 102

in the presence of BBB, SVT will cause a broad-complex tachycardia however the safest approach is to regard all broad-complex tachycardias as VT unless proven otherwise

Answer 103

= polymorphic VT the axis of electrical activity changes in a rotational way, so that the overall pattern of the ECG rhythm strip is sinusoidal

Answer 104

drugs that prolong QT interval (e.g. amiodarone)

Answer 105

<60 bpm may be physiological in fit people/during sleep may be an expected result of Tx (e.g. beta blockers) Pathological bradycardia may be caused by malfunction of the SA node or partial/complete failure of AV node.

Answer 106

Atropine and/or cardiac pacing the need for treatment depends on haemodynamic effect and risk of developing asystole, rather than the precise ECG classification

Answer 107

fixed PR interval >0.20s rarely requires Tx

Answer 108

PR interval shows progressive prolongation, until a P wave occurs without a QRS complex Also called Wenckeback heart block Does not usually require immediate Tx

Answer 109

A constant prolonged PR interval, with some P waves not followed by QRS complex Occurs randomly without a consistent pattern Increased risk of progression to AV block and asystole

Answer 110

no correlation between P waves and QRS Likely to stop abruptly, resulting in asystole

Answer 111

If the SA node fails, cardiac depolarisation may be initiated from a subsidary 'pacemaker' elsewhere the resulting escape rhythm will be slower than normal

Answer 112

occurs in dying patients Commonly seen in later stages of unsuccessful resuscitation attempts Slow, irregular, wide ventricular complexes Often become progressively broader before progressing to asystole Does not generate a palpable pulse

Answer 113

= the passage of an electrical current of sufficient magnitude across the myocardium to depolarise a critical mass of cardiac muscle simultaneously the aim is to enable the natural pacemaker tissue to resume control

Answer 114

Thoracic Impedence: - ensure good skin contact (removal of drug patches, shave chest) Electrode position

Answer 115

= the absence of VF/pVT at 5s after shock delivery although, the ultimate goal is ROSC

Answer 116

used for atrial or ventricular tachyarrhythmias (not pVT or VF) the shock must be synchronised with the R wave to reduce the risk of inducing VF

Answer 117

to minimise risk, place the defibrillator electrodes >8cm away from the pacemaker or ICD if necessary use anterior/posterior or bi-axillary position you may need to deactivate the ICD with a magnet

Answer 118

= internal paddles applied directly to the ventricles requires considerably less energy (10-20 J) - do not exceed 50 J

Answer 119

SA node - 60-70bpm AV node - 40-50 bpm (narrow QRS) Distal to Bundle of His - 0-30 bpm (broad QRD)

Answer 120

when the HB occurs lower in the conducting system than bundle of His The escape rhythm is unreliable and may fail transiently (leading to syncope) or fail completely (leading to ventricular standstill / cardiac arrest) THIS WILL NEED PACING

Answer 121

= a sudden, brief loss of consciousness from a large drop in cardiac output

Answer 122

NON-INVASIVE percussion (fist) pacing transcutaneous pacing INVASIVE temporary transvenous pacing permanent pacing

Answer 123

may produce an adequate cardiac output with less trauma to the patient than CPR more likely to be successful when ventricular standstill is accompanied by P wave activity 1. with side of closed fist deliver repeated, firm thumps to precordium, just lateral to left sternal edge 2. raise hand to about 20cm above the chest before each thump 3. monitor ECG to assess if QRD is achieved by each thump 4. if initial thumps don't work, try slightly harder 6. if this still fails, move the point of contact around the precordium until a point is found that produces ventricular stimulation If does not produce a regular pulse promptly, start CPR immediately

Answer 124

- can be established quickly, widely available, easy to perform - causes discomfort in a conscious patient, not as reliable so only short-term solution

Answer 125

1. remove chest hair if needed and ensure skin is dry 2. Apply pads in conventional position (A-P if needed) 3. select appropriate pacing rate (usually 60-90) 4. set energy output to lowest setting and gradually increase until a pacing 'spike' appears on ECG followed by a QRS immediately and check a T wave follows 5. having achieved electrical capture, ensure there is a palpable pulse WARN PATIENTS THERE WILL BE DISCOMFORT

Answer 126

1 - HIGH THRESHOLD 2 - CONNECTION FAILURE 3 - LEAD DISPLACEMENT

Answer 127

>8cm from device

Answer 128

implanted device to terminate life-threatening tachyarrythmia - delivers a shock when it detects VF or fast VT - most can also function as demand pacemakers in the event of bradycardia - some devices will deliver biventricular pacing for heart failure

Answer 129

Shock Syncope Heart Failure MI Extremes of heart rate

Answer 130

when HR increases, diastole is shortened to a greater degree than systole if rate >150 this can reduce cardiac output dramatically (due to inability to fill correctly due to short diastole)

Answer 131

HR <40 often tolerated poorly especially when people have severe heart disease and cannot compensate for bradycardia by increasing SV

Answer 132

depending on the presence or absence of life-threatening features 1. no treatment needed 2. simple clinical intervention (e.g. vagal manoeuvres / percussion pacing) 3. pharmacological 4. electrical (cardioversion for tachy, pacing for brady)

Answer 133

if life-threatening features --> up to 3x synchronised DC shocks, if unsuccessful then amiodarone 300mg IV over 10-20 mins If no features, then depends if QRS narrow/broad NARROW: - irregular - Tx as AF - regular vagal manoeuvres, then adenosine BROAD: - if VT --> amiodarone 300mg IV over 10-60mins

Answer 134

for narrow complex tachycardia after vagal manoeuvres failed Give adenosine (if no pre-excitation) 6mg rapid IV bolus If unsuccessful, give 12mg If unsuccessful, give 18mg Needs continuous ECG monitoring If still ineffective, verapamil/beta-blocker

Answer 135

either under conscious sedation or GA set defib to deliver a synchronised shock (it will coincide with the R wave) Press the shock button and keep pressed until after the shock has occured (might eb a slight delay)

Answer 136

an unsynchronised shock could coincide with a T wave and cause VF

Answer 137

= cause of death in 68% of patients who have an OHCA and have survived to ITU usually manifests as coma, seizures, myoclonus, varying degrees of neurological dysfunction and brain death. Worsened by: mpaired autoregulation, hyper/hypocapnia, hypoxia/hyperoxia, hypo/hyperglycaemia, pyrexia and seizures. Thus treatment is aimed at preventing these.

Answer 138

'myocardial stunning' may result in a temporary but significantly reduced LV ejection fraction and therefore cardiac output. It typically recovers after 72h.

Answer 139

whole body ischaemia/reperfusion that occurs after resuscitation from cardiac arrest activates immunological and coagulation pathways that cause multiple organ failure and increase the risk of infection.

Answer 140

Often complicates the post-resuscitation phase. This comprises of: Post-cardiac arrest brain injury. Post-cardiac arrest myocardial dysfunction. Systemic ischaemia/reperfusion response. Persistence of precipitating pathology.

Answer 141

Any persisting pathology relating to the cause of the cardiac arrest, such as a myocardial infarction or a pulmonary embolism, will also need treatment.

Answer 142

fevers are common post-arrest continuously monitor core temperature in a ROSC pt treat any pyrexia with cooling and antipyrexials

Answer 143

First-line usually beta-blocker Can use diltiazem if BB contraindicated Digoxin may be used in patients with heart failure. Amiodarone may be used to assist with rate control but is most useful in maintaining rhythm control.

Answer 144

If AF is <48 hours PHARMACOLOGICAL - Flecanide (seek expert help) - Amiodarone (300 mg over 20-60 min followed by 900 mg over 24 h) may be used but is less often effective than drugs like flecainide and takes longer to work. ELECTRICAL

Answer 145

Do not use flecainide in the presence of heart failure, known left ventricular impairment, ischaemic heart disease, or a prolonged QT interval.

Answer 146

If the pt has been in AF for >48 hours, do not attempt cardioversion until they have been fully anticoagulated for at least 3 weeks, or unless transoesophageal echocardiography has detected no evidence of atrial thrombus.

Answer 147

For a broad-complex tachycardia, start with a 120-150 J biphasic shock and increase in increments if this fails to a maximum of three attempts. For atrial fibrillation, start at the maximum defibrillator output. Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower-energy shocks: start with 70-120 J biphasic.

Answer 148

Anterior-posterior placement

Answer 149

If cardioversion is unsuccessful at terminating the arrhythmia after delivery of three shocks of increasing energy: Give the patient amiodarone 300mg IV over 10-20 min. Attempt further synchronised cardioversion. The loading dose of amiodarone may be followed by an infusion of 900mg over 24h, given into a large vein (preferably via a central venous cannula).

Answer 150

Sinus tachycardia is not an arrhythmia. It is a common physiological response to stimuli such as exercise or anxiety. Do not attempt to treat sinus tachycardia with cardioversion or anti-arrhythmic drugs as treatment is directed at the underlying cause.

Answer 151

Used when there is evidence of life-threatening signs in bradycardia Dose = 500mcg IV Repeat to a maximum of 3mg Other drugs to use: - Isoprenaline - Adrenaline - aminophylline - glucagon (in BB/CCB overdose) PACING

Answer 152

recent asystole mobitz II AV block complete heart block with broad QRS ventricular pause > 3 s.

Answer 153

either ventricular in origin or supraventricular with BBB Safest approach is to manage as VT if in doubt

Answer 154

most likely to be AF with BBB will need careful examination of 12-lead ECG can be polymorphic VT (but this is unlikely to present without adverse features)

Answer 155

REGULAR: - sinus tachy - SVT - atrial flutter with regular AV conduction (i.e. 2:1) IRREGULAR - most likely AF - atrial flutter with variable conduction

Answer 156

If life-threatening features --> synchronised shock If no adverse features: 1. Vagal manoeuvres (record an ECG during each manoeuvre ? identify any flutter waves) 2. Adenosine 6mg -> 12mg -> 18mg (rapid IV boluses)

Answer 157

rapid narrow complex tachy with no pulse technically this is PEA and CPR should be started however, the most appropriate Tx is synchronised shock

Answer 158

patient with cardiac transplant (heart is denervated and will not respond)

Answer 159

If NO life threatening features and NO high risk of progression to asystole then do not initiate immediate treatment Monitor and re-assess Seek expert help

Answer 160

- renal failure - drugs (e.g. ACEi, ARB, NSAIDs, BBs, trimethoprim) - tissue breakdown - metabolic acidosis - endocrine disorders - diet - spurious (e.g. haemolysed sample)

Answer 161

1st degree AV block flattened/absent P waves tall, peaked T-waves ST-depression sine-wave pattern widened QRS VT bradycardia Cardiac arrest

Answer 162

T waves larger than R wave in more than one lead

Answer 163

1. cardiac protection (calcium gluconate) 2. shift potassium into cells - insulin (+ glucose) - salbutamol 3. remove potassium from body - Lokelma - dialysis 4. monitor serum K and glucose 5. prevention of recurrence

Answer 164

- confirm hyperkalaemia on VBG - protect heart with CALCIUM CHLORIDE 10% - shift potassium into cells - give sodium bicarb - consider dialysis and need for mechanical chest compressions for prolonged CPR during this

Answer 165

50mmol IV by rapid injection (50mL of 8.4% solution) try to give separately to CaCl as can cause a precipitate

Answer 166

Hypokalaemia itself increases the risk of SCD this risk is increased further in patients with pre-existing heart disease and in those on digoxin Tx

Answer 167

GI loss drugs renal losses endocrine disorders metabolic alkalosis Mg depletion poor dietary intake

Answer 168

U-waves T-wave flattening ST-segment changes arrhythmias (especially if on digoxin) Cardiac arrest

Answer 169

short QT interval Prolonged QRS Flat T-waves AV block Cardiac arrest

Answer 170

prolonged QT TWI Heart block Cardiac arrest

Answer 171

fluid replacement IV Furosemide 1mg/kg IV Hydrocortisone Pamidronate Tx underlying cause

Answer 172

Calcium chloride 10% 10-40mL IV 1-2g 50% Mg sulphate (4-8mmol) IV if necessary

Answer 173

prolonged PR and QT T-wave peaking AV block Cardiac arrest

Answer 174

consider when Mg >1.75 Calcium chloride10% 5-10mL IV, repeated if necessary Ventilatory support if necessary in resp. depression Saline diuresis (saline & furosemide) Haemodialysis

Answer 175

Prolonged PR and QT ST-depression TWI flattened P waves broad QRS TdP VT

Answer 176

Magnesium sulfate IV 2g 50% over different lengths of time depending on presentation

Answer 177

Up to 20x more risk than general population

Answer 178

mostly the same but also: - dialysis nurse present for HD macine - stop dialysis - fluid bolus - prompt management of any hyperkalaemia - avoid excessive potassium and volume shifts during dialysis

Answer 179

Bloods and cultures Urine output (catheter, hourly) Fluid resuscitation ABX (broad-spectrum) Lactate Oxygen, if needed

Answer 180

PPE and avoid mouth-to-mouth treat life-threatening tachyarrythmias with cardioversion try to identify toxins (relatives, friends, ambulance crews) measure temperature standard CPR if arrest occurs be prepared to continue CPR for a long time, particularly in young patients, while the poisin is excreted (consider ECLS)

Answer 181

Naloxone 400mcg IV (800mcg IM/SC) titrate up to a maximum dose of 10mg duration of action = 45-70 mins give until pt is breathing adequately and then consider need for ?ongoing infusion caution in pts with opiate dependence

Answer 182

Flumazenil (a competitive antagonist of benzos) caution in pts with benzo dependence

Answer 183

Consider sodium bicarb for treatment of TCA-induced ventricular conduction abnormalities

Answer 184

typically when a bolus of LA enters a blood vessel by mistake = severe agitation, LOC +/- tonic-clonic convulsions, sinus brady, conduction blocks, asystole, VT follow standard resuscitation measures may benefit from 20% lipid emulsion in addition to standard ALS

Answer 185

e.g. cocaine and amphetamines agitation, tachycardia, hypertensive crisis, hyperthermia, MI Tx with small doses of benzodiazepaines first-line

Answer 186

- O2 to maintain sats - salbutamol nebs - ipratropium nebs - steroids - IV Magnesium 8mmol IV over 20 mins - following senior advice, consider aminophylline in severe/near fatal asthma only - fluid and electrolyte replacement as needed - ICU input

Answer 187

follow standard ALS protocols ventilation will be difficult due to increased airway resistance, so intubate early try to avoid dynamic hyperinflation of lungs (gas trapping) always consider bilateral tension PTX in asthma

Answer 188

= systemic hypersensitivity reaction, usually rapid in onset and may cause death suspect if sudden illness develops after exposure to a trigger, with rapidly progressing skin changes and life-threatening airway and/or breathing and/or circulation problems

Answer 189

AIRWAY - airway swelling - hoarse voice - stridor BREATHING - SOB - sheeze - tiring - cyanosis - resp arrest CIRCULATION - pale, clammy - tachycardia - hypotension - reduced consciousness - myocardial ischaemia - cardiac arrest

Answer 190

can affect the skin, the mucosa, or both - erythema - urticaria - angioedema (deeper tissues - eyelids, lips, mouth, throat) Skin changes without breathing/circulation problems does not signify anaphylaxis

Answer 191

LIE PATIENT FLAT (can sit up if breathing difficulties but DO NOT STAND) Remove trigger O2 to maintain sats ADRENALINE IM - 0.5mg for adults IV fluid bolus Repeat dose after 5 mins if no response If no response --> REFRACTORY ANAPHYLAXIS GUIDELINES

Answer 192

IM is best and quickest option 0.5mg in adults anterolateral aspect of middle third of thigh

Answer 193

mast cell tryptase (will be markedly increased in anaphylaxis)

Answer 194

= a cardiac arrest at any stage of pregnancy up to 6 weeks after delivery modifications: - obtain expert help including obstetrician, paeds, anaesthetist - if risk of IVC compression, aim to establish IV/IO access above the diaphragm - left uterine displacement - prepare for emergency C-section

Answer 195

- place distressed/compromised person in left lateral position - high flow O2 to maintain sats - fluid bolus if needed - expert obstetric and anaesthetic help

Answer 196

Best done within 5 mins of maternal arrest Not done <20 weeks gestation (no risk of IVC compression) 20-23 weeks - initiate emergency delivery to permit successful resuscitation of mother gestation >24 weeks - initiate to help save the life of both mother and fetus

Answer 197

TBI hypovolaemia from massive blood loss hypoxia from respiratory arrest or airway obstruction direct injury to vital organs/major vessels tension PTX cardiac tamponade

Answer 198

= near cardiac arrest caused by blunt impact to chest wall which causes pVT/VF

Answer 199

immediate decompression of chest cavity NEEDLE DECOMPRESSION - 2nd intercostal space - 4th/5th intercostal space mid-axillary line - chest drain asap OPEN THORACOSTOMY (preferred if trained clinician available) - inciscion in chest wall (5th ICS mid-axillary line) followed by dissection into pleural space - insert chest drain following ROSC CLAMSHELL THORACOTOMY - may be required in traumatic cardiac arrest

Answer 200

correction of hypoxaemia by ventilation only is critical and may lead to ROSC

Answer 201

- attempt to rescue the drowning person without entering the water yourself - open airway and check for signs of life (agonal breathing is common) - give 5 initial ventilations (with O2 if available) - if not responded to initial ventilations, commence CPR 30:2 (avoid compression only as likely to be hypoxia driven)

Answer 202

core temp 32-35 degrees

Answer 203

core temp 28-32 degrees

Answer 204

core temp <28 degrees

Answer 205

- heart may be unresponsive to drugs until warmed - without meds until core temp >30 - once 30*C reached, double usual length of intervals between drugs - as normothermia is approached, use standard drug protocols

Answer 206

removal from cold environment remove wet clothes conscious people should mobilise full body insulation heated IV fluids

Answer 207

= rare disorder of skeletal muscle calcium homeostasis characterised by muscle contracture and life-threatening hypermetabolic crisis following exposure tof genetically predisposed individuals to halogenating anaesthetics and depolarising muscle relaxants

Answer 208

1. NON-EXERTIONAL - during high environmental temperatures 2. EXERTIONAL - during strenuous physical exercise in high environmental temperatures and/or high humidity

Answer 209

transfer to cool environment, lie flat cool to <39 (ideally lower) cold water immersion / full body conductive cooling systems cold fluids correct electrolyte abnormalities

Answer 210

stop triggering agents give O2 correct acidosis and electrolytes start active cooling DANTROLENE

Answer 211

= a measure of the amount of excess acid or base that is in the blood as a result of a metabolic derangement. A base excess that is: - more negative than -2 mmol L-1 (negative base excess) and pH less than 7.35 indicates a metabolic acidosis. - greater than +2 mmol L-1 (base excess) and pH greater than 7.45 indicates a metabolic alkalosis.

ALS Flashcards

(236 cards)