Adult Resus

EpidemiologyIncidence 1:1000/yr; accounts for 15-20% deaths; witnessed in 50%; bystander CPR occurs in 20%; bystander CPR significantly improves survival; 7% survival 70-79yrs, 3% survival >80yrs; permanent brain damage in 10-30%Ventilation does improve neurological outcome in children with non-cardiac causes of arrest; 1% survival from PEA; <1% survival from asystole

Patho-physiology

Chest compressions: approx 50% of flow is regurgitant across valves Decreases LV size and enables easier defibrillation Cerebral blood flow 25% normal when CPR <1min from arrest (15% @ 3mins, 5% @ 5mins) Blood flow to myocardium 20-50% of normal Significant ROSC if hands off interval >15secs ETCO2 correlates well with coronary perfusion pressure and survival from cardiac arrest (if <10, survival unlikely) No evidence of improved outcome with: abdo compression, rapid compression, simultaneous compression-ventilation Cough CPR: thoracic pump mechanism, only in conscious monitored patients Open chest CPR: better CO but no improvement of outcome if started >20mins after sustained CPR, improves initial resus success but not long term survival Active compression-decompression CPR: no better in survival to discharge; small benefit at 1hr in pre- hospital settingBreathing: exhaled air has FiO2 0.16

Differences between old

and new guidelines

Recently updated in 2010; emphasises interventions proven to work (ie. Chest compressions, early defib, post-resus cooling); simplerKey messages: early chest compressions; push hard; push fast; minimise interruptions; defib ASAP; if ROSC, cool early and avoid over-oxygenationBLS: no finger sweep unless FB seen no longer do pulse check if lay person (maybe if health care provider) – instead look for “signs of circulation”: start resus if not responding and not breathing normally Chest compressions only: OK if out of hospital, shockable rhythm, <4mins since arrest (just over 1 compression/sec) – increasing evidence that ventilation does little to change outcome in out of hospital 1Y cardiac arrest, and may be harmful if attempts interrupt CPR Do chest compressions first – no longer do rescue breaths (except in children) Place hand over “centre of chest” (2 fingers below nipple line if <1yr) AED now considered BLS skill

BLS / ALS (cntd)

Continue until: moves purposefully / breathes normally / opens eyes / impossible to continue / professional help arrives / AED arrives

CPR first (with 2-5 rescue breaths), help fast (after 1 min): only applies to non-laypersons; if suspect non-cardiac cause

1) In child (unless witnessed collapse / known heart problem)2) Drowning / choking / hanging (?still in recommendation)

A Guedel: centre of incisors to angle of jaw or angle of mouth to tragus

BLS / ALS

Aim: to provide effective oxygenation of vital organs through artificial circulation of oxygenated blood until restoration of normal COMove victim if: unsafe, need to for CPR, need to control severe bleeding

Danger?Responsive? – shake, sternal rub, moving, unconsciousHelp: do 1st always in adults; ask if AED availableA: turn on side if drowning; no finger sweep unless solid FB seenB: look, listen, feel 10 secs; move FB if visible; no rescue breaths 8 breaths/min, 0.8-1.2L, 1 sec long RR 6-10 once ETT (every 15 compressions)C: if not breathing normally and no signs of life (professional can

do pulse check); start CPR, no rescue breaths: 30:2 Pauses should be <10secs; swap providers Q2min; depth 1/3 AP diameter (5cm in adults); “centre of chest”; 100-120/min; duty cycle 50%; 5 cycles/2mins; rhythm check every 2mins (only check pulse if perfusable rhythm) Attach AED ASAP

C

Intraosseous access: BIG, EZ-IO Child: 2cm below medial tibial tuberosity Adult: medial malleolus, distal femur, sternum (FAST 1), humeral head, ileum Contraindications: proximal ipsilateral fracture, ipsilateral vascular injury, osteoporosis, osteogenesis imperfecta

Precordial thump: de-emphasised; indicated if witnessed / monitored cardiac arrest, high voltage electrocutionProlonged CPR if: poisoning, asthma, hypothermia, pregnancy if plan postmortem CSShock: 200J biphasic; maximum available if monophasic Single shock only Commence CPR immediately after shock; check rhythm at 2mins if compatible with pulse, check pulseDrugs: no evidence that any drugs alter rate of hospital discharge; dose 3-10x if via ETT (LEAN)Adrenaline: 1mg (1ml 1:1000, 10ml 1:10,000) adrenaline after 2nd shock every 2nd cycle 0.1-1mcg/kg/min infusion can be used ROSC, arrival to hospital, short term survival no evidence survival to discharge / neurological outcomeAmiodarone: 300mg amiodarone after 3rd shock (ie. Refractory to shock and adrenaline) can consider repeat dose of 150mg 15mg/kg/day infusion ROSC, arrival to hospital, short term survival, response to shock no evidence of long term benefit

C

Lignocaine: 1mg/kg consider 0.5mg/kg additional dose after 10mins Indicated in situations where amiodarone contraindicated; “probably harmful”NaHCO3: 1mmol/kg over 2-3mins Indicated if hyperkalaemia, metabolic acidosis, tricyclic antidepressant OD (1st line), cardiac arrest >15minsMgSO4: 5mmol bolus rpt x1 INF 20mmol/4hrs no in ROSC / survival indicated in torsade de pointes (1st line), digitoxicity, hypokalaemia, hypomagnesaemia, profound hypothermia (1st line)K: 5mmol KCl IV bolus Indicated in hypokalaemiaCa Gluconate: 5-10mls 10% indicated if hyperkalaemia, hypocalcaemia, calcium channel blocker OD

VT

BrugadaCriteria

1) Absent RS in any V1-6 (nearly 100% sensitivity) (ie. R wave only, or S wave only)2) RS >100 (>95% specificity) 3) AV dissociation: (all of below absent if baseline rhythm is AF) Notching of QRS at different positions (40% sensitivity; less in paeds; >75% spec) Fusion beats: QRS with features of narrow atrial and wide ventricular Capture beats: normal QRS amongst broad complexes4) Absence of typical LBBB / RBBB morphology in V1 and V6 If dominant R waves in V1 = RBBB like in V1: VT if smooth monophasic peak / taller L rabbit ear (taller on R suggests RBBB; most specific) / qR present in V6: VT if QS present (ie. Monophasic negative peak) / rS ratio <1 (ie. Tiny R wave, large S wave) If dominant S wave in V1 = LBBB like in V1: VT if R wave >30-40ms / RS interval 60-70ms / Notching of S wave In V6: VT if QS present / qR ratio small (ie. Tiny Q wave, large R wave)Others: taller L rabbit ear in aVR (taller R rabbit ear in TCA OD); QRS >140 (>100 in children); Precordial QRS concordance (20% sensitivity, 90% specificity); QRS / RS in V1 (50% VT, 2% SVT); LAD/RAD (VT>SVT); Axis change compared to sinus; Notching near nadir of S wave

Suggestive of SVT with aberrancy: RSR / QS in V1 (85% SVT, 10% VT); slows with carotid massage; varying BBB

VT

Pathophysiology: re-entrant (most common in 1st 30mins after MI) and automaticity (most common >12hrs after MI due to denervation hypersensitivity to norepinephrine and epinephrine in area beyond infarct)Causes: MI, HOCM, mitral valve prolapse, drugs (digoxin, Ia antiarrhythmics, sympathomimetics)Classification: monomorphic (more common in structural heart disease / IHD); polymorphic (more common in poisoning); fascicular tachycardia (rare; can occur without underlying heart disease; looks like SVT with aberrant conduction with relatively narrow QRS, RBBB, LAD)Assessment of patient: hypotension common; canon a waves on JVP (AV dissociation), variable intensity of S1; VT more likely if >35yrs, active angina, previous MI

Management: Electrical cardioversion: synchronised unless pulseless; indicated if severe chest pain / APO, hypotension; 90% success rate; use 50J biphasicOverdrive pacingDrugs: Amiodarone: 150mg IV over 5-10mins repeat over 10-20mins if needed 600mg/24hrs 30% effective in 1hr; best if poor LV function Procainamide: 100mg IV 50mg/min IV until reversion (max 500mg) Most effective (75%); but contraindicated if MI / LV dysfunction due to negative inotrope Sotalol: 1.5mg/kg over 5mins 65% effective; contraindicated if cardiovascular compromise (ie. Poor LV function) or long QTc Lignocaine: 1-1.5mg/kg IV Q5mins (max 300mg/hr) 50mg bolus if needed Use if ischaemic VT; less effective than procainamide/sotalol (20% with intiial bolus; further 10% with 2nd) otherwise Chloral hydrate toxicity beta-blockers Na channel blocker (eg. TCA) NaHCO3

Stimulants alpha and beta-blockers

VF

Chaotic broad complex rhythmRate 300-600; initially coarse (more likely to cardiovert) amplitude over time asystole after 1-3minsManagement: non-synchronised DC cardioversion; use drugs only if DC shock fails (see above)

H’s HypoxiaHypovolaemiaHypo / hyperkalaemiaHypothermia

ThrombosisTamponadeToxinsTension pneumothorax

T’s

Post-Resuscitation Management

Aims: continue respiratory support; maintain cerebral perfusion; treat/prevent cardiac arrhythmia; determine/treat cause of arrestB: aim SaO2 94-98% (hyperoxaemia may be harmful); aim PaCO2 35-40 (hypoCO2 may be harmful)C: aim patient’s normal BP or SBP >100; can give 50-100mcg adrenaline boluses or infusion (0.1- 1mcg/kg/min); no specific evidence to suggest use of IVF; insufficient evidence to support vasopressors, inotropes or mechanical balloon pumps etc…; no studies showed benefit of ongoing antiarrhythmics, but may be reasonable to continue drug that cardioverted patient; if STEMI / new LBBB immediate angiography and PCID: BSL associated with mortality, treat BSL >10; no evidence for ongoing sedation / antiepileptics / paralysis

Therapeutic Hypothermia

Mechanism of action: Only shown to be of benefit post VT/VF in out of hospital cardiac arrest (theoretically maybe in PEA/asystole; not supported yet post-HI, but prevention of hyperthermia is); cerebral metabolic function and O2 demand, glutamate levels, prevention of free-radical induced damage, reperfusion injury, calcium shifts, intracranial pressure

HACA (Hypothermia after Cardiac Arrest, European, NEJM 2002): for 24hrs- At 6/12, favourable neuro: 55% hypoT : 40% normoT, NNT 6 15% improvement- At 6/12, death: 40% hypoT : 55% normoT, NNT 7- No significant difference in complication rates (but trend to sepsis, bleeding and pneumonia in hypoT group)- severe disability and death by 15% at 6/12

Melbourne study, Bernard et al, NEJM 2002: for 12hrs- Good outcome: 50% hypoT : 25% normoT (improved by 20-25%)- No significant difference in mortality (? 50% in hypoT, 68% in normoT)

ILCOR recommendations, 2002: Criteria: unconscious adults whose initial rhythm was VF, with out of hospital ROSC (ROSC <60mins after onset of resus + persistent absence of response to verbal commands on other recommendations); GCS <6; motor <4 Contraindications: severe cardiogenic shock, malignant arrhythmias, pregnancy, 1Y coagulopathy, cardiac arrest 2Y to another disease process (eg. Trauma); children; sepsis Technique: cool to 32-34°C ASAP maintain for 12-24hrs from time at which reaches 32-34°C passive rewarming over 8hrs; Keep room temp 20°C; keep head slightly elevated; aim MAP >90 Requires sedation (propofol 1-3mg/kg/hr, morphine 2-5mg/hr) and paralysis (panc/vec 4mg/hr); Initiate ASAP after ROSC (may have benefit up to 4-6hrs) Can do using: EXTERNAL: air circulation blanket; If rate of cooling <1°C /hr then add others: surface fan, ice packs (keep L axilla free of ice to prevent risk if defib; put on both groin, R axilla and head; oil skin with paraffin prior to putting packs) INTERNAL: 30ml/kg 4°C N saline over 30mins (av. 2L); Peritoneal / pleural lavage; ECMOTo rewarm: slowly at 0.25 – 0.5°C /hr (over 8hrs); aim T 37°C; stop sedation and paralysis at 36°C to allow assessment; beware hypotension; prevent shivering; do passively, but add bear hugger if takes >8hrsStop if: significant bleeding, cardiovascular instability, arrhythmiaComplications: arrhythmia (VF, AF, extreme bradycardia); cardiovascular instability; coagulopathy, infection, hyperglycaemia, K / phos / Mg, diuresis

Complications

Abdominal organ perforation; penile erection, lower limb venous engorgement, abdominal distension unrelieved by NGT insert intraperitoneal trochar and NGT

Contra-indications

Unsuccessful pre-hospital ACLS, known terminal illness not in immediate post-operative period, obviously unsurvivable injury, advance directive, rescuers at riskPre-hospital termination: non-witnessed, no bystander CPR, no pre-hospital defib, no ROSCHospital termination: 20 mins CPR without reversible cause + non-shockable rhythm + no ROSC before ED transportation + non-witnessed arrest

Prognosis

Time to CPR/defib: strongest determinants of survival no CPR no long term survival post-8mins CPR no long term survival post-12mins (defib must occur within 12mins to affect outcome) CPR <3mins and ALS <6mins 70% survival in VF CPR >3mins and ALS <6mins 40% survival in VFLocation: out of hospital: 35% survival to hospital arrival (15% if VF, 2% if asystole) 5% survival to hospital discharge (10% if VF/VT (15% if witnessed), 0.1% if asystole) in hospital: average 40% survival at 1 month, 5% at 2 years in ward: even worse prognosis than out of hospital (MET have had no effect) in ED/CCU: 70% survival (lower in ICU as severe underlying disease)Duration of CPR: survival unlikely if long enough for drugs to be givenCause: better prognosis if drugs / arrhythmiaEcho findings: absence of cardiac kinetic activity = <5% probability of ROSC Cardiac kinetic activity = 80% chance of ROSC