acls course 2011 welcome(1) - resuscitation...website. we expect the 2010 materials to be available...

ACLS 2010 1

Cour Mark Mensour, MD CCFP EM ANAES FCFP Medical Director [email protected] Dear Course Participant: Welcome to the ACLS Course. This letter describes the course, the required materials, and how to prepare. You will know exactly what to expect from the course prior to arriving. Please arrive on time. Course Content and Structure The ACLS Course is offered in a learner-centered, relaxed environment where you have an opportunity to learn from your instructors and your peers. The morning begins with a short introduction to the new guidelines, followed by small group sessions and two large group discussions on acute coronary syndromes and acute pulmonary edema. Throughout the day you will participate in a series of structured learning stations where we work through a variety of resuscitations. Each participant will be a team leader and take their team through a ~ 6 minute scenario while the instructor provides feedback for improvement. You will cover all algorithms listed below and be expected to perform more independently as the day progresses. The strength of this course rests with the hands on time component. The more scenarios we get through in this course, the better prepared you will be when you encounter these scenarios in real life. Evaluation is a continuous process. There will be no written examination but there will be a practical examination in the form of an audience response system and a team scenario at the end of the day. These are closed book. Preparation Materials You will receive an ACLS information package written by Mark Mensour and Andrew Healey, which is the most important of the resources. There currently exists a 2005 guideline textbook and handbook which may be used as a resource for the course, though neither is required for this course. These are available through the laerdal website. We expect the 2010 materials to be available in the first half of 2011. The ACLS information package is copyrighted and photocopying is prohibited. This will be emailed to the email address you have provided. Preparing for the Course Participants must come to the course having memorized the following algorithms: (1) Pulseless VT/VF (2) PEA/Asystole (3) Bradycardia (4) Stable/Unstable Tachycardia As well, you will need to review the information on acute coronary syndromes, acute pulmonary edema and procedural sedation and analgesia. The rule for this course is that if you must perform a procedure in ACLS that requires sedation, you must have an approach to sedating the patient. You must have also memorized the following from the ACLS Information package (ACLS Guidelines 2010 Healey/Mensour): (1) Hs and Ts and their respective treatments (2) ACLS Made Simple Algorithm

A Weight to the Evidence – NNT The evidence supporting the care of our patients will be presented for the various treatment options in a way that helps clinicians place a weight or importance on a treatment modality. The statistic used to describe interventions in the course is one known as number needed to treat (NNT). If we use words to describe a NNT of 15 for ASA in acute coronary syndromes, we would say: We must treat 15 patients with aspirin to save one life at 30 days after the therapy in STEMI. The lower this number, the better the therapy. The lowest this number can be is 1.0. That means that every patient who receives the treatment gets benefit, and none of those that receive the control (sometimes placebo) obtain benefit. Your course package is designed to include the evidence that supports the new guidelines (NNTs) and the practical implications for those therapies as discussed. In terms of providing a weight to how important an intervention is, NNT can be helpful. For example, in acute coronary syndromes aspirin has an NNT of 15 and beta blockers in the first six hours an NNT of 31. These are essential interventions. Nitroglycerin has no NNT and morphine may have a number needed to harm (NNH) and so these interventions are far less important. We hope you find this approach helpful and useful as we progress through the course.

We look forward to seeing you at the course. Enjoy preparing for the course and if you have any questions, please don’t hesitate to contact me – [email protected] . Kindest regards, Mark Mensour Medical Director

Sara Tumber ACLS Instructor


ACLS Guidelines 2010 “Executive Summary” There is no definitive clinical evidence that early intubation or drug therapy improves neurologically intact survival to hospital discharge.

Circulation C-A-B is the order with BCLS. Lay people can now do hands only CPR until help arrives. Chest compressions (CC) are poorly done and we must do better – it changes outcome

Continuous, uninterrupted chest compressions essential with optimal rate (100+ per min) Short time from last compression to shock improves defibrillation success 30 compressions:2 ventilations until secure airway, then continuous CC, 1 breath / 6-8 secs Change compressors frequently (q 2 minutes) and change < 10 secs PETCO2 is now used to monitor CPR quality (if ETCO2 is low – improve CPR) and for ROSC

Breathing Hyperoxia and hypoxia are harmful so in presence of a pulse keep SpO2 > 94 and < 100 Hyperventilation is harmful

increased intrathoracic pressure decreased cerebral perfusion poor venous return decreased coronary perfusion

gastric distention hyperventilation

Airway Intubation low priority in setting of successful ventilation Jaw thrust is the method of choice for opening the airway LMA/King LT is a reasonable substitute for endotracheal intubation and potentially safer “Number needed to learn” = Laryngoscopy = 47, LMA = 1–3, Trachlight = ~20. PETCO2 to confirm airway placement. If low PETCO2 and ETT in the correct place, very poor prognostic indicator If PETCO2 is < 10 mmHg then improve chest compressions to improve circulation PETCO2 can monitor for ROSC with abrupt increase – usually >40 mmHg Intubation does not impart a survival advantage. Interruption of CC is harmful.

Defibrillation One shock, then immediate CPR (rhythm check after 2 min of CC, not after shock) Energy levels, waveforms, Fixed vs escalating, Pads vs paddles = no differences

Pacing As per usual, pace if unstable bradycardia or bradycardia related to coronary ischemia Dopamine and Epinephrine are substitute for transcutaneous pacing while prep for transvenous

Guidelines recommend no pacing for asystole

Drugs No drugs have ever been demonstrated to improve survival to hospital discharge though they have shown improvement to hospital admission

Endotracheal route of administration no longer recommended Intraosseous access now the second option

Consider ultrasound guided emergency line placement Most experts now state that epinephrine is reasonable, vasopressin offers no advantage Atropine no longer part of PEA/Asystole algorhythm

Amiodarone is the antiarrhythmic of choice with no evidence to support survival advantage Magnesium should be given if Torsades de Pointes


Phases of Resuscitation 0–5 minute “Electrical phase” Susceptible to early, rapid defibrillation 5–15 minutes “Mechanical phase” Requires CPR to optimize defibrillation attempts >15 minutes “Metabolic phase” Extraordinary measures necessary for resuscitation

(consider cardiopulmonary bypass, ECMO)

Post Resuscitation Therapeutic hypothermia post out of hospital VF arrest with persistent GCS < 10 recommended Some suggest therapeutic hypothermia if any alteration of mental status and no contraindication

Therapeutic hypothermia for all other types of arrests ought to be considered More recent evidence supporting PEA/asystole survivors Avoid Hypoxia and Hyperoxia keep SaO2 > 94% and <100% (80<PaO2<300) Among hospital survivors, patients with hyperoxia had a significantly lower proportion of discharges from the hospital as functionally independent compared with patients with normoxia. NNT (normoxia) = 10 (95% CI 8-14). NNH = 6 (95% CI 5-7) for hyperoxia vs normoxia post arrest NNH = 17 (95% CI 11-37) for hyperoxia vs hypoxia; hyperoxia is worse than hypoxia Kilgannon JH, Jones AE, Shapiro NI, et al. JAMA. 2010;303:2165-2171.

No neuroprognostication for >72 hrs after the event. Do not call it too early. No useful marker of true prognosis in the first 72 hours on examination.

ACS If SaO2> 94% on room air – do NOT give O2. MONA is dead. Aspirin is still the most important treatment PEA ASYSTOLE

In absence of reversible causes, these patients are dead Diligent, careful and rapid look for the Hs and Ts in a systematic way Consider – “Do I start resuscitation?” Consider – Stopping early.

Hs and Ts

Hypovolemia Hypoxia H ion - acidosis Hyper- / hypokalemia Hypoglycemia Hypothermia

Toxins Tamponade Tension pneumothorax Thrombosis - coronary Thrombosis - pulmonary Trauma


BCLS Guidelines 2010 “Executive Summary”

Maneuver ADULT Adolescent and older

CHILD 1 year to adolescent

INFANT Under 1 year of age

Airway Jaw thrust

Breathing Initial 2 breaths at 1 sec/breath 2 effective breaths at 1 sec/breath

Rescue breathing without CC 10-12 breaths / min 12-20 breaths / minute

Rescue breaths for CPR with advanced airway 8-10 breaths / minute

Conscious patient, Foreign-body airway obstruction

Heimlich maneuver (abdominal thrusts) Back blows and chest thrusts

Unconscious patient, Foreign-body airway obstruction

Begin CPR sequence. After chest compressions, check airway for object.

Circulation Pulse check (< 10 sec) Carotid Brachial

Compression landmarks Lower half of the sternum, between nipples Just below nipple line (lower half of the sternum)

Compression method Push hard, push fast Allow complete chest recoil

Heel of one hand, other hand on top

Heel of one hand or as for adults

2 or 3 fingers; 2 person: thumbs

encircling technique

Compression depth At least 2 inches At least one third AP diameter or 1.5 inches in infants and 2 inches in children

Compression rate At least 100 / minute

Compression-ventilation ratio 30:2 (one or two rescuers) 30:2 (single rescuer)

15:2 (2 rescuers)

Defibrillation (AED)

Use adult pads Do not use child pads

Prepare AED while doing CPR (attach when ready). Use pediatric system for child 1 to 8 years, for infants use

manual defibrillator and if unavailable use pediatric system; if unavailable, use adult pads.

For sudden collapse out of hospital or in-hospital arrest, use AED as soon as possible


ACLS That Matters

PULSE PRESENT?

STABLE?ADEQUATE PERFUSION?

IMMEDIATEUNINTERUPTEDEFFECTIVE CPR

RHYTHM?

De!brillateEpi/Amio

Hs and TsEpinephrine

Rate ControlDiltiazemOR MetoprololConsider CV < 48 hrs

Sedation + AdenosineSedation + Sync CV

Sinus tachycardiaAtrial !utter

Atrial "brillation

Sedate + Sync CVAmiodaroneConsider Mg

REGULAR

RATE?

QRS? Observe

RATE?

SedateCardiovert

Sedate + AnalgesiaPace

UNSTABLE = ELECTRICITY

FAST SLOW

WIDE NARROW

YES NO

FAST SLOW

VF/VT PEAASYSTOLE

YES NO

YES NO

VTach

Consider airway / PETCO2

ACLS Made Simple© 2010 Mensour Healey


Cardiac arrest, unwitnessed = Good compressions, ventilate with 30:2 when available. Cardiac arrest, witnessed = Electrical therapy at earliest moment

Rhythm checks are rhythm checks only without pulse check until an organized rhythm is visible. One shock as opposed to three because resumption of CPR more beneficial than subsequent shocks No rhythm check after defibrillation, because: – resumption of CPR of greater benefit than the potential harm of interruption of CPR – CPR unlikely to harm beating heart (no reported cases of harm) – even if rhythm is converted to perfusing rhythm, often takes 60-90 seconds prior to perfusing BP

Chest compressions while charging because the increasing duration of interruption prior to defibrillation decreases success.

– Careful communication with appropriate position No epinephrine until after second shock as this allows a rhythm check after most successful shock – 1st shock This minimizes risk of giving epinephrine to beating heart

Remember - we are probably doing this as most epi stays in the arm until perfusion restored then surge


Hs and Ts for Unstable Patients / PEA

Hs and Ts of Cardiac Arrest - Helpful Notes

Condition Features of ECG Hx / PE Management

Hypovolemia Narrow complex, rapid rate Flat neck veins Bleeding, V+D

Volume infusion – Crystalloid or blood not colloids

Hypoxia Rapid rate then slow rate Ventricular dysrhythmias in adults

Cyanosis, SpO2 Blood gasses, LOC

Oxygenate, Ventilate

H ion (Acidosis) Low voltage QRS complexes or Normal DKA, Pre-existing acidosis, Renal failure

Intubate/Ventilate Tx cause Consider NaHCO3

Hypokalemia T waves flatten > Prominent U waves > QRS widens > QT prolongs > Wide complex tachycardia (+/- TdP)

Loss of potassium Diuretic use Vomiting

Rapid, controlled correction Consider magnesium

Hyperkalemia T waves tall, peaked > P waves flatten > QRS widens Sine-wave PEA

Renal failure, DM Missed dialysis, Shunts/fistulas/line Meds, Poisoning

Ventolin neb Calcium chloride D50 + Humulin R 10 U NaHCO3 Kayexalate Dialysis

Hypoglycemia Normal or narrow complex, rapid rate DM, Altered LOC IV Glucose, IV Glucagon

Hypothermia Narrow complex tachycardia or bradycardia J or Osborne waves

Exposure history Core body temp (probe)

Tx based on Mild/Mod/Sev

Toxins - TCA Rapid heart rate, narrow initially Wide complex tachycardia

History of exposure Antichol toxidrome Altered LOC

I + V NaHCO3 IV push until QRS complex narrows and stops seizing

Tx seizures > benzos, etc.

Toxins - ⊂Rx Β-blocker Ca ch blocker Digoxin

Bradycardia, Conduction blockade Slow atrial fib

History Toxidrome

Glucagon (∃) Calcium (if no DIG) Digibind (if DIG) Fluids, Pressors Insulin + Glucose

Note if Dig + [K = Digibind (no Calcium)

Tamponade

Narrow complex, rapid rate Fast PEA

No pulse with CPR Distended neck veins

Pericardiocentesis ? US guided if poss Else ECG / blind

Tension pneumothorax

No pulse with CPR Distended neck veins Unequal breath sounds Crepitus Difficulty ventilating

Needle decompression 2nd ICS, MCL Large bore angiocath

Thrombosis, Pulmonary Embolism

No pulse with CPR Risk factors History of DVT/VTE

Volume resuscitation Hemodynamically unstable = Lysis

Thrombosis, ACS See Acute Myocardial Infarction section below

Trauma Narrow complex, rapid rate Fast PEA

Trauma history VOLUME + Blood R/o obstruction (tensionpneumo, tamponade)

Early Operating Room FAST Scan


Acute Myocardial Infarction and Acute Coronary Syndromes Goals of Therapy (1) Reduce mortality (2) Early reperfusion of the infarct-related artery (thrombolytics, PCI (cath)) (3) Prevent death, re-infarction, need for urgent revascularization, and congestive heart failure (4) Treat complications: cardiac arrest, symptomatic bradycardias, unstable tachycardias. Live better electrically.

Evidence-Based Therapy for ST Elevation Myocardial Infarction

Pearls for Investigations

20-30% of acute STEMI have normal ECGs on presentation. Serial ECGs are extremely important to providing therapy. CXR is not necessary except to rule out other disease.

Some entertain CXR to R/O aortic dissection. If you think that is the disease, need much more.

Troponins are not helpful in the very early management of ACS however they may help rule out disease that has a low pre-test probably of being cardiac in origin. 15-Lead ECGs (and R sided ECGs in some circumstances) are an important addition.

Oxygen Class I intervention if hypoxic. Provide 4 L NP if SpO2 < 94%. Otherwise no O2 for ACS.

Aspirin NNT = 19 (15-25) save one life at 30 days1. Contraindication: Anaphylactic allergy (then consider Clopidogrel)

Beta Blockers NNT = 31 to save one life at 90 days2. Reduces mortality by reducing myocardial work, ventricular dysrhythmias, and myocardial rupture. New guidelines say PO metoprolol for all with ACS (Class I). IV if Htn or Tachydysrhythmias (IIa). Contraindications Acute CHF, Heart block, HR < 50, Hypotension, Shock, Bronchospasm. In those with severe asthma, use caution but most times still give it.

Clopidogrel STEMI with LYSIS COMMIT3 - all age groups(dose 75 mg) NNT = 184 (mortality, day 8)NNT = 303 (recurrent MI, day 8) CLARITY4 (dose 300 mg then 75 mg) NNT = 15 (TIMI Flow 0 or 1, Recurrent MI, Death) Weight of the evidence suggests the dose is Clopidogrel 75 mg.

CLARITY used disease-oriented outcomes (ie angiographic flow); death and recurrent MI were not statistically significantly different between the two groups (placebo vs clopidogrel).

High Risk UA/NSTEMI CURE5 (dose 300 mg then 75 mg) NNT = 47 (CV death, nonfatal MI, stroke)

NNH = 99 (major bleeding) NNH = 24 (bleeding complications)

Weight of the evidence suggests there is large potential for harm. Probably should reserve clopidogrel for high risk unstable angina (ie ECG changes) or NSTEMI (ie positive cardiac biomarkers).

PCI Evidence for 600 mg PO for Primary PCI if age. Dosage varies based upon consultant opinion.

PCI (cath) vs Lytics Guidelines 2010

Duration of Symptoms PCI Delay Preferred Therapy

< 3 hours Immediate PCI

Not immediate Fibrinolysis (Class I < 12 hrs)

> 3 hours < 12 hrs

< 60 - 110 min PCI (Class I)

> 60 - 110 min Fibrinolysis


Thrombolytics Indications: New LBBB, STE ≥ 1 mm in two anatomically contiguous leads If ST depression anteriorly, look for STE posteriorly: 15 lead ECG.

Contraindications: Wrong diagnosis Active bleeding non-compressible site Brain ‘stuff’ = CVA in last X months, ICH any time in their life, Intracranial neoplasm;

The benefit of thrombolytics is time-dependant. Early presenters where there will be a delay to PCI need lysis if there is no contraindication. In late presenters it may be acceptable to delay lysis for a short period while arranging PCI. The risk of thrombolytics is bleeding and the most life threatening of these are intracranial bleeding and GI bleeding. ICH occurs about 1-2% of the time with new generation lytics (tPA, TNK). In either case, the other mortality altering therapies should be given rapidly.

Region of Infarction NNT Fractional Risk7

Cumulative (add to baseline risk of 0.5%)

Anterior 276 Age: > 65 = 0.5% | > 75 = 0.5% | > 80 = 0.5% | > 85 = 0.5%

New LBBB 376 Blood pressure: SBP > 160 = 0.5% | SBP > 180 = 0.5%

Inferior 1256 Weight < 70 kg = 0.5% || tPA/TNK = 0.5% || Any prev stroke = 2 - 4%

Heparins for Acute Coronary Syndromes (STEMI, NSTEMI, UA)

Age > 75, STEMI + Thrombolysis Fondaparinux 2.5 mg SC OD Or Enoxaparin 0.75 mg/kg SC BID

Age <75 STEMI + Thrombolysis Fondaparinux 2.5 mg SC OD

Or Enoxaparin 30 mg IV then 1 mg/kg SC BID STEMI + Primary PCI UFH 60 IU/kg bolus (max 4000 IU) then 12 IU/kg/hr NSTEMI / High Risk UA Fondaparinux 2.5 mg SC OD

Crt > 220: Enoxaparin converts to OD not BID

The Evidence All STEMI8 STEMI Lysis9 High Risk UA/NSTEMI10

High Risk UA/NSTEMI11

Treatment Fondaparinux Enoxaparin LMWH Fondaparinux

Control UFH UFH UFH Enoxaparin

Time Period 30 d 30 d 3-14 d 30 d

NNT for outcome

64 49 43 No difference

death or reinfarction death or nonfatal MI death, MI, recurrent angina, urgent revasc

death, MI, refractory ischemia

NNH for outcome

No harm* 140 No harm 55 (Enox)

severe hemorrhage major bleeding severe hemorrhage major bleeding

LHH -- 2.9 -- --

Comments

N = 12 092 pts 2867 pts no reperfusion therapy; changed inclusion criteria halfway; otherwise tx better than standard; guidewire thrombosis higher in PCI.

N = 20 506 pts Not as much plavix as used now, else treated similarly

N = 11 128 pts NNT (enox) = 212 to prevent one case of thrombocytopenia)

N = 20 078 pts, Inclusion: Biomarkers and ECG changes Fondaparinux NNT 172 for death NNH Cath Rel Complications = 209


Thrombolytics Indications: New LBBB, STE ≥ 1 mm in two anatomically contiguous leads If ST depression anteriorly, look for STE posteriorly: 15 lead ECG.

Contraindications: Wrong diagnosis Active bleeding non-compressible site Brain ‘stuff’ = CVA in last X months, ICH any time in their life, Intracranial neoplasm;

The benefit of thrombolytics is time-dependant. Early presenters where there will be a delay to PCI need lysis if there is no contraindication. In late presenters it may be acceptable to delay lysis for a short period while arranging PCI. The risk of thrombolytics is bleeding and the most life threatening of these are intracranial bleeding and GI bleeding. ICH occurs about 1-2% of the time with new generation lytics (tPA, TNK). In either case, the other mortality altering therapies should be given rapidly.

Other Interventions Nitroglycerin Provide relief from ischemic pain; No mortality benefit ever demonstrated. Morphine Good analgesic. No mortality benefit; small trials suggest may be harmful12. Gp IIb/IIIa inhibitors Beneficial for those undergoing percutaneous intervention (Cardiac Cath)

Can be given by interventionalist at time of Cath.

ACE Inhibitor Needs to be given within the first 24 hours. NNT = 21013 to save one life. Given by 24 hours. Outcome measured at 30 days.

Statins Initial high dose statin (atorvastatin 80 mg) resulted in better combined outcome, NNT= 3914 Combined outcome death, nonfatal AMI, cardiac arrest with resuscitation, recurrent symptomatic myocardial ischemia with objective evidence requiring emergent rehospitalization at 16 weeks. Almost all of the difference came from recurrent ischemia component of end point.

Right Ventricular and Posterior MI

Indications for a 15-Lead ECG = Abnormal 12-lead ECG Purpose ->Pick up RV and posterior MI. RV MIs are pre-load dependent. Interventions that reduce preload include morphine and nitroglycerin = hypotension

References 1 ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial

infarction: ISIS-2. Lancet 1988; 2:349-60. 2 Hjalmarson A, Herlitz J, Holmberg S, et al. The Goteborg metoprolol trial. Effects on mortality and morbidity in acute myocardial infarction. Circulation 1983; 67(6 Pt 2):I26-32. 3 COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Addition of clopidogrel to aspirin in 45 852 patients with acute myocardial infarction: randomised placebo-controlled

trial. Lancet 2005; 366:1607–21. 4 Sabatine MS, Cannon CP, Gibson M for the CLARITY-TIMI 28 Investigators. Addition of Clopidogrel to Aspirin and Fibrinolytic Therapy for Myocardial Infarction with ST-Segment Elevation. NEJM 2005;

352:1179-89. 5 The CURE Trial Investigators. Effects of Clopidogrel in Addition to Aspirin in Patients with Acute Coronary Syndromes without ST-Segment Elevation. NEJM 2001; 345:494-502. 6 Letovsky E, Allen T. The MI Letter 1999; 7:2. 7 Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from

all randomised trials of more than 1000 patients. Lancet 1994; 343:311-322. 8 The OASIS-6 Trial Group. Effects of Fondaparinux on Mortality and Reinfarction in Patients with Acute ST-Segment Elevation Myocardial Infarction. JAMA 2006; 295:1519-30. 9 Antman EM, Morrow DA, McCabe CH, et al. for the EXTRACT-TIMI 25 Investigators. Enoxaparin versus Unfractionated Heparin with Fibrinolysis for ST-Elevation Myocardial Infarction. NEJM 2006;

354:1477-88. 10 Magee KD, Sevcik W, Moher D, Rowe BH. Low molecular weight heparins versus unfractionated heparin for acute coronary syndromes. The Cochrane Database of Systematic Reviews 2003, Issue 1. Art.

No.: CD002132. DOI: 10.1002/14651858.CD002132. 11 The Fifth Organization to Assess Strategies in Acute Ischemic Syndromes (OASIS-5) Investigators. Comparison of Fondaparinux and Enoxaparin in Acute Coronary Syndromes. NEJM 2006; 354:1464-76. 12 Meine TJ, Roe M, Chen AY, et al. for the CRUSADE Investigators Durham. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality

Improvement Initiative. Am Heart J 2005; 149:1043-9. 13 ACE Inhibitor Myocardial Infarction Collaborative Group. Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in

randomized trials. Circulation 1998; 97:2202-12.

14 Schwartz GG, Olsson AG, Ezekowitz MD, et al. for the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study Investigators. Effects of atorvastatin early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA 2001; 285:1711-8.


Acute Pulmonary Edema Goals of Therapy Important Messages

(1) Reduce mortality and morbidity (1) Resuscitation speed, mobilize resources (2) Reduce complications (2) Be ready with BiPAP and Intubation EARLY (3) Rapidly identify reversible causes (3) Drugs given in a stepwise fashion (4) In cardiogenic shock, rapidly transport for PCI (4) Early consideration for reversible causes

Evidence-Based Therapy for Acute Pulmonary Edema

Oxygen Hypoxia predominates. Apply high concentrations of O2.

BiPAP/CPAP Non-invasive ventilation (CPAP, BiPAP) has been shown to decrease intubation rates and mortality rates1.

NNT = 6 (95% CI 4-8) to prevent one intubation compared to standard medical therapy1. NNT = 11 (95% CI 7-25) to prevent one death compared to standard medical therapy1.

BiPAP in those patients with chest pain is high risk and probably ill-advised2. Patients having a myocardial infarction and acute pulmonary edema should be treated as if they are in cardiogenic shock. Rapidly secure airway, remove work of breathing. Treat MI, transfer to PCI without delay.

Studies have all been small. More research is needed.

Nitroglycerin* (MOST IMPORTANT)

Early and aggressive nitrates allow rapid reduction in preload. Route is not important, however transdermal nitroglycerin is not effective (perfusion is poor). Sublingual nitrates should be given aggressively prior to initiation of IV nitroglycerin therapy. Titrate to decreased SOB and SBP ~ 100 mmHg. Start as big as BP will allow (10-20-30 + mcg/min) and titrate up very quickly (to over 100 mcg if possible). Rapid improvement is typically seen but patients must be monitored closely for deterioration.

Aspirin Indicated especially if believe that CHF is related to an ischemic event.

ACE Inhibitor Consider early use of 12.5 mg - 25 mg PO Captopril. Attacks pulmonary edema at a different pathophysiological mechanism. Most of the trials regarding this therapy use insufficient doses of nitroglycerin. (Refs availabile)

Furosemide (Lasix) If volume overloaded, reduce volume with diuretics. Not primary treatment for pulmonary edema. Tx for chronic CHF. Note: This is not an emergency.

Intubation Be ready. These patients are hypoxic, and can’t be well preoxygenated. They desaturate quickly. Most experienced and most skilled intubator should be available in the room. Well pre-oxygenate. Back up method of ventilation +/- intubation ready.

Vasopressors As needed for hypotension. Consider volume replacement as most often intravascularly deplete. If hypotensive, dobutamine although theoretically preferred, will drop BP farther. Consider dopamine / norepinephrine (levophed) in addition to dobutamine in this circumstance. For cardiogenic shock Norepinephrine is preferred over dopamine (De Baker – NEJM 362;779-789)

Morphine Advocated for acute pulmonary edema. However not usually needed if enough nitrates. Some data to suggest may be harmful3. Also the ADHERE database suggests harm Use with caution and in small doses. Vasodilatory effects have been suggested from small studies with invasive monitors in place.

Look for Reversible Causes Arrhythmia - bradycardia = pace; tachycardia = cardioversion.(unless sinus) Myocardial infarction - intubation, ventilation if increased WOB, early PCI for cardiogenic shock. Medication non-compliance Pulmonary embolism - if unstable, consider thrombolysis. Pneumonia - often these two diseases present together. Treat both if unsure or suspect.

Cardiogenic shock is a different entity although acute pulmonary edema may progress to cardiogenic shock. This disease requires intubation and ventilation, +/- use of vasopressors.

References 1 Masip J, Roque M, Sanchez B, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema - systematic review and meta-analysis. JAMA 2005; 294:3124-3130.

2 Mehta S, Jay G, Woolard R, et al. Randomized, prospective trial of bilevel vs continuous positive airway pressure in acute pulmonary edema. Crit Care Med 1997; 25:620-628.

3 Meine TJ, Roe M, Chen AY, et al. for the CRUSADE Investigators Durham. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J 2005; 149:1043-9.


Rapid Sequence Intubation

Rapid sequence intubation is the virtually simultaneous administration, after preoxygenation, of a potent sedative agent and a rapidly acting neuromuscular blocking agent to facilitate rapid tracheal intubation without interposed mechanical ventilation. RSI is the cornerstone of emergency airway management. RSI is superior in terms of success rates, complication rates, and control of adverse effects making it the procedure of choice. Difficult intubation is not a contraindication to RSI; rather, it indicates to the MD that a careful pre-intubation plan must be made with a particular emphasis on the ability to ventilate the patient. The cardinal principle in assessing the patient with a difficult airway for RSI is the determination of whether the patient is likely to be adequately ventilated with a bag and mask; then, if ventilation is felt ensured, the decision to proceed with an attempt is guided by the likelihood of successful oral intubation. The old recommendation that an intubator should hold his or her breath during the laryngoscopy to determine the maximal time that the patient should be without ventilation predated pulse oximetry and has no place in modern airway management.

Preparation Monitoring (SpO2, ECG, BP, EtCO2 ready), IV access

Preoxygenation 8 VC breaths or 5 minutes of maximum oxygenation Recognize those at risk of desaturating quickly (obese, peds) If preoxygenate well, almost never require bagging. There are subsets of patients who you can’t pre-oxygenate well.

Pretreatment Lidocaine - Elevated ICP, Reactive airways disease Opiod - Elevated ICP, IHD, ICH, Vascular dissection Atropine - Children < 10 (controversial) Defasiculation - elevated ICP > 5 yo / 20 kg; open globe injuries.

Paralysis AFTER Induction KEY DETERMINANT: Skill level No bagging unless SpO2 < 90%. Apnea ≠ BVM

Protection + Positioning NO Sellick’s maneuver (cricoid) (may decrease success); Sniffing position. No bagging unless SpO2 < 90%!!!!

Placement with Proof Early ETCO2 (purple Δ yellow); Listen for AE bilaterally/epigastrium.

Post-Intubation Management Sedation +/- paralysis Hemodynamic and oxygen monitoring Appropriate ventilator settings

Data from tens of thousands of intubations have demonstrated the safety and superiority of RSI in the emergency department. Fewer studies have demonstrated its safety outside of the critical care environments of the ED, ICU and OR. In the hands of a skilled operator in the right setting, RSI is the technique of choice in the “baggable” patient.

Difficult Airway Assessment

Difficult Mask Ventilation Difficult Laryngoscopy Difficult Cricothyrotomy

Mask seal Obese (BMI > 26 kg/m2) Age > 55 yo No teeth Stiff lungs (eg. asthma, CHF)

Look at head and neck Evaluate 3-3-2 rule Mallampati Obstruction Neck mobility

Surgery, previous Hematoma or infection Obese Radiation Tumor

Although these are commonly cited methods for assessing difficulty with mask ventilation, laryngoscopy, cricothyrotomy, no decision aid perfectly predicts the ability to perform any three of these skills. As a consequence, there are two key considerations when performing RSI: (1) I must understand no tool is perfect; (2) I must always have a plan A, B, C... etc.

Walls, Murphy, Luten, Schneider (2004). Manual of Emergency Airway Management, 2nd Edition.


Rapid Sequence Intubation, continued

Evidence-Based Airway Management - Rapid Sequence Intubation

Drug Dose Onset Duration of Action

Adverse Effects Remarks

INDUCTION AGENTS

Propofol 1.5 mg/kg 60 s 8 +/- 4 mins Hypotension

Crystalloid 12 ml/kg prior to induction optimizes preload and avoids hypotension.

Etomidate 0.3 mg/kg 45 s 5 +/- 3 mins Myoclonus Masseter spasm Vomiting

Indicated hemodynamically unstable patients. Avoids hypotension

Ketamine 2 mg/kg 60 s 20 mins Hypersalivation Bronchial SM relaxation Laryngospasm Myoclonus Tachycardia Hypertension Emesis

Midazolam 0.3 mg/kg 1-5 mins variable Ineffective Paradoxical excitation Awareness

Unpredictably ineffective Variable degrees of bioavailability.

PARALYTIC AGENTS

Succinylcholine 1.5 mg/kg 45 s 8-10 mins Hyperkalemia Malignant hyperthermia

Primarily contraindicated in at risk of hyperK: History of MH Burns > 5 days - complete healing Crush > 5 days - complete healing Denervation UMN, LMN > 5 days to 6 mos Neuromuscular disease, myopathies Intra-abdominal sepsis > 5 days - resolved Prepare to treat hyperK when QRS wide. Prepare to treat MH with dantrolene.

Rocuronium 1 mg/kg 45-60 s 20 mins Recurarization

MAINTENANCE

Propofol 50-100 mcg/kg/min

infusion Use for no longer than 36 hours HPB warning: Propofol infusion syndrome Add Rocuronium 0.3 mg/kg prn

Lorazepam 0.05 mg/kg 6 – 12 hrs Add Rocuronium 0.3 mg/kg prn

Midazolam 0.15 mg/kg variable Add Rocuronium 0.3 mg/kg prn


Procedural Sedation and Analgesia Patients often present to the emergency department requiring painful or unpleasant procedures. Procedural sedation and analgesia is often required for these procedures and is becoming standard of care. Emergency physicians are called upon to perform this skill daily and have many pharmacological options at their disposal, including midazolam, propofol, etomidate, ketamine and others.

Evidence-Based Sedation – Pharmacology

Drug Dose Onset Duration of Action

Adverse Effects Remarks

Propofol Age < 65

1 mg/kg TTE*

60 sec 8 +/- 4min Hypotension Apnea Airway obstruction

Excellent sedative - amnestic Jaw thrust will be required for snoring = airway obstruction Can use in hypotensive patients if procedure will reverse cause of hypotension (eg. Dysrhythmia – but not Atrial Fibrillation)

Propofol Age > 65

0.5 mg/kg TTE*

90 sec 12 +/- 4min

Ketamine 1 mg/kg (IV)

4 mg/kg

(IM)

IV - 60 sec IM - 5 mins

IV 20 mins IM 30 mins

Hypersalivation Bronchial SM relaxation Laryngospasm Myoclonus Tachycardia Hypertension Emesis

Add 0.05 mg/kg midazolam + 0.02 mg/kg Atropine in same IM syringe if using the IM method. Maintains airway reflexes/respirations in most patients. Safety data is excellent. TTE if using the IV route with 0.5 mg/kg aliquots.

Etomidate 0.1 mg/kg 60 sec 5 +/- 3 mins Vomiting Myoclonus Masseter spasm

Hemodynamically stable add In non-paralyzed patients, encounter more adverse events.

Midazolam 0.1 mg/kg 1-3 min 45-60 min Respiratory depression Paradoxical excitation

Unpredictably ineffective Variable degrees of bioavailability.

Fentanyl 1 - 5 mcg/kg

60 sec 20 mins Respiratory depression Chest rigidity (rare)

Caution combining fentanyl with other sedatives re: resp depression Vasodilatation can cause hypotension

*TTE = Titrate to effect

Evidence-Based Sedation – Potential Approaches for Sedation in Commonly Encountered Scenarios

Urgent cardioversion Propofol

Emergent Cardioversion, hypotensive Low dose Propofol or Ketamine

Emergent Cardioversion, not hypotensive Propofol

Transcutaneous pacing Versed + Fentanyl or Ketamine

Scenarios where help is required Use your judgment


2010 Guideline Update - Quick Points direct from AHA Guidelines 2010 Documents The routine use of cricoid pressure in cardiac arrest is not recommended (Class III, LOE C).

Continuous waveform capnography is recommended in addition to clinical assessment as the most reliable method of confirming and monitoring correct placement of an endotracheal tube (Class I, LOE A).

Frequent experience or frequent retraining is recommended for providers who perform endotracheal intubation (Class I, LOE B).

The endotracheal tube should be secured with tape or a commercial device (Class I, LOE C).

Performing CPR while a defibrillator is readied is strongly recommended for all patients in cardiac arrest (Class I, LOE B). If the tachycardic patient is unstable with severe signs and symptoms related to a suspected arrhythmia (eg, acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock), immediate cardioversion should be performed (with prior sedation in the conscious patient) (Class I, LOE B).

Special Circumstance - Arterial Line If the arterial relaxation “diastolic” pressure is less than 20 mm Hg, it is reasonable to consider trying to improve quality of CPR by optimizing chest compression parameters or giving a vasopressor or both (Class IIb, LOE C).

Special Circumstance - SCVO2 Monitor in Place When in place before cardiac arrest, it is reasonable to consider using continuous ScvO2 measurement to monitor quality of CPR, optimize chest compressions, and detect ROSC during chest compressions or when rhythm check reveals an organized rhythm (Class IIb, LOE C). If SCVO2 is less than 30%, it is reasonable to consider trying to improve the quality of CPR by optimizing chest compression parameters (Class IIb, LOE C).

There is no definitive clinical evidence that early intubation or drug therapy improves neurologically intact survival to hospital discharge. In

other words, vascular access, drug delivery, and advanced airway placement should not cause significant interruptions in chest

compression or delay defibrillation. CLASS III RECCOMENDATIONS - AVOID / DO NOT DO / MAY BE HARMFUL

Routine administration of magnesium sulfate in cardiac arrest is not recommended (Class III, LOE A) unless torsades de pointes is present.

Available evidence suggests that routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit (Class IIb, LOE B). For this reason atropine has been removed from the cardiac arrest algorithm. Routine use of sodium bicarbonate is not recommended for patients in cardiac arrest (Class III, LOE B). Routine administration of calcium for treatment of in-hospital and out-of-hospital cardiac arrest is not recommended (Class III, LOE B). Fibrinolytic therapy should not be routinely used in cardiac arrest (Class III, LOE B). When pulmonary embolism is presumed or known to be the cause of cardiac arrest, empirical fibrinolytic therapy can be considered (Class IIa, LOE B; see Part 12). Electric pacing is not recommended for routine use in cardiac arrest (Class III, LOE B).


Acronyms ACS Acute Coronary Syndrome AED Automatic external defibrillator AMI Acute Myocardial Infarction Amio Amiodarone CC Chest Compressions CHF Congested Heart Failure CI Conference Interval CPR Cardiopulmonary Resuscitation Crt Creatinine CV Cardioversion Sync CV Synchronized Cardioversion DKA Diabetic Ketoacidosis DM Diabetes Mellitus DVT Deep Vein Thrombosis EtC02 End-Tidal Carbon Dioxide ETT Endotracheal Tube FAST Focused Abdominal Sonography in Trauma Hypovol Hypovolemia HR Heart Rate ICH Intracranial Haemorrhage ICS Intracostal Space ICP Intracranial Pressure Inc ICP Increased Intracranial pressure IHD Ischemic Heart Disease K+ Potassium LBBB Left Bundle Branch Block LOC Level/Loss of Consciousness LHH Likelihood of Helping vs Harming LMA Laryngeal Mask Airway LMN Lower Motor Neuron LMWH Low Molecular Weight Heparin MCL Mid-Clavicular Line Mg Magnesium MH Malignant Hyperthermia NaHCO3 Sodium Bicarbonate NNH Number Needed to Harm NNT Number Needed to Treat NSTEMI Non-ST Elevation Myocardial Infarct PCI Percutaneous Coronary Intervention PE Pulmonary Embolism PEA Pulseless Electrical Activity RSI Rapid Sequence Induction/Intubation RV Right Ventricular STEMI ST Elevation Myocardial Infarct STE ST Elevation TCA Tricyclic Antidepressants TTE Titrate To Effect Tx Treatment UA Unstable Angina UFH Unfractionated Heparin

UMN Upper Motor Neuron US Ultrasound V+D Vomiting and Diarrhea VC Vital Capacity VF Ventricular Fibrillation VT Ventricular Tachycardia VTE Venous Thromboembolism WOB Work of Breathing

ACLS Rhythm Evaluation - Nov 2001 Developed by Grant MacEwan College - Edmonton, Alberta, Canada

ADVANCED CARDIOVASCULAR LIFE SUPPORT

RHYTHM INTERPRETATION REVIEW Analyse each rhythm strip presented below. An answer key is provided. Knowledge of rhythm interpretation is a prerequisite for Advanced Cardiovascular Life Support courses.

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ANSWER KEY TO RHYTHM INTERPRETATION REVIEW

1 Ventricular Fibrillation

2 Sinus Rhythm with PJC's

3 2nd Degree Heart Block Mobitz Type I

4 Atrial Fibrillation

5 Sinus Rhythm with Multifocal PVC's

7 Sinus Rhythm with Unifocal PVCs

6 1st Degree Heart Block

8 Sinus Rhythm with PAC's

9 Accelerated Junctional Rhythm

10 Asystole

11 Junctional Escape Rhythm

12 Normal Sinus Rhythm

13 Ventricular Tachycardia

14 Sinus Bradycardia

15 Ventricular Bigeminy

16 Sinus Tachycardia

17 3rd Degree Heart Block (complete)

18 Idioventricular Rhythm

19 Atrial Flutter

20 2nd Degree Heart Block Mobitz Type II