Stages of Anesthesia Analgesia without amnesia Stage I: Analgesia Nausea, vomiting, hyperreactivity, irregular respiration Stage II: Excitement Sleep, normal respiration and blood pressure Stage III: Surgical Anesthesia Depression of vasomotor and respiratory centers – coma and death Stage IV: Medullary Depression

WHAT ARE COMMON CAUSES OF PERIOP CARDIAC ARREST?

Anesthestic-related Cardiac Arrest and Its Mortality: A Report Covering 72,959 Anesthetics over 10 Years from a US Teaching Hospital 72,959 anesthetics over 10 year study 144 cardiac arrests (19.7 per 10,000 95% CI) 15 anesthesia attributable and contributory 129 patient disease condition or surgery medication-related in 40%, complications associated with central venous access in 20%, airway-related complications in 20%, unknown or possible vagal reaction in 13%, and perioperative myocardial infarction in a single case Newland MC, Ellis SJ, Lydiatt CA, Peters KR, Tinker JH, Romberger DJ, Ullrich FA, Anderson JR (2002) Anesthesiology 97:108–15

Crisis management during anesthesia: cardiac arrest ECG rhythm at the time of the arrest was reported in 86 cases (67%). – sinus bradycardia (23%) – asystole (22%) – Tach/v tach/v-fib (14%); – Pulseless electrical activity (7%) 29 reports in which details of oxygen sat were included – 11 of the 29 were associated with hypoxaemia and the rest were associated with other causes, mostly direct drug effects and autonomic stimulation W B Runciman, R W Morris, L M Watterson, J A Williamson and A D Paix Qual. Saf. Health Care 2005;14;e14 doi: /qshc

WHAT TO DO SHOULD CARDIAC ARREST OCCUR PERIOPERATIVELY?

Classification Arrest V-fib Pulseless VTPEAAsystole Pre-arrest TachycardiaBradycardia Afib/Flutter

Ventricular Fibrillation / Tachycardia most common cause of sudden cardiac arrests – ends in death within minutes unless corrective measures are promptly taken. useless quivering of heart  no blood flow Tx: only one therapy works  defibrillation Defibrillation success: chances drop every minute

Ventricular Fibrillation / Tachycardia Survival reduced 7-10%/min (without CPR) Rapid defibrillation is key CPR prolongs VF, slows deterioration Minutes: collapse to 1st shock Eisemberg JAMA 1979; 241:

SCREAM! SShock360J monophasic, 1st and subsequent shocks. CCPRAfter shock, immediately begin chest compressions followed by respirations (30:2 ratio) for 2 minutes. RRhythmRhythm check after 2 minutes of CPR (and after every 2 minutes of CPR thereafter) and shock again if indicated. Check pulse only if an organized or non-shockable rhythm is present. EEpi- nephrine 1 mg IV/IO q3-5 min. Or vasopressin 40 U IV/IO, once, in place of the 1st or 2nd dose of epi. AM AM Anti- arrhythmic Meds Consider antiarrhythmics. Amiodarone 300mg IV/IO, may repeat once at 150mg in 3-5 min. if VF/PVT persists or Lidocaine (if amiodarone unavailable) mg/kg IV/IO, may repeat X 2, q5-10 min. at mg/kg, (3mg/kg max. loading dose) if VF/PVT persists,or Magnesium Sulfate1-2 g IV/IO diluted in 10mL D5W (5-20 min. push) for torsades de pointes or suspected/ known hypomagnesemia.

EPINEPHRINE

Alpha Adrenoreceptor Review a1 Receptors - Stimulation leads to Constriction of Vascular Smooth Muscle – Increases Peripheral Vascular Resistance (PVR). a2 Receptors – Stimulation Inhibits NE Release

Beta Adrenoreceptor Review ß1 Receptors - Stimulation Results in Increased Heart Rate, Conduction Velocity and Contractility ß2 Receptors - Relaxation of Vascular Smooth Muscle, Skeletal Muscle and Bronchial Smooth Muscle

Epinephrine Stimulates a and ß Adrenergic Receptors – Low Doses - ß Effects predominate – High doses, a effects predominate. Increases Heart Rate, Increased Contractility. – Net Effect - Increase in Cardiac Output due to effect of ß1 Receptor Constricts Arterioles of Skin, Mucous Membranes, and Viscera. – Net Effect – Increase in PVR due to effect of a1 Receptor

Epinephrine Indications – Increases: Heart rate Force of contraction Conduction velocity – Peripheral vasoconstriction – Bronchial dilation

Epinephrine Dosing – 1 mg IV push; may repeat every 3 to 5 minutes – May use higher doses (0.2 mg/kg) if lower dose is not effective – Endotracheal Route 2.0 to 2.5 mg diluted in 10 mL normal saline

Epinephrine Precautions – Raising blood pressure and increasing heart rate may cause myocardial ischemia, angina, and increased myocardial oxygen demand

VASOPRESSIN

Vasopressin In Vivo – released from posterior pituitary in response to decreased ECF volume Very powerful vasoconstrictor Indications – Used to “clamp” down on vessels – No direct effects on heart

Vasopressin Dosing – One time dose of 40 units only – May be substituted for epinephrine – If no response in minutes resume epinephirne, do nor repeat doses of vasopressin Not supported by human data – May be given down the endotracheal tube DO NOT double the dose Dilute in 10 mL of NS

Vasopressin Precautions – May result in an initial increase in blood pressure immediately following return of pulse – Myocardial ischemia and angina Increased peripheral vascular resistance

ANTI-ARRYTHMICS

Antiarrhythmics Interact with Electrolyte Channels in Atrial Muscle and/or Ventricular Muscle and/or SA Node and/or AV Node and/or Purkinjie Fibers – Class I – Sodium Channel Blockers: Procainamide, Lidocaine, Flecainide, Propafenone – Class II – ß Blockers – Class III – K Channel Blockers: Amiodarone, Sotalol, Ibutilide. – Class IV – Calcium Channel Blockers: Non Dihydropyridines. – Other – Adenosine, Digoxin, Magnesium Sulfate

Amiodarone MOA: – delays repolarization (prolongs refractory period) – Blocks a and b adrenergic receptors – Affects sodium, potassium and calcium channels. Indications – For refractory V Fib and Sustained V Tachycardia – Antiarrhythmic of 1 st Choice – Powerful antiarrhythmic with substantial toxicity, especially in the long term

Amiodarone Dosing – Should be diluted in 20 to 30 mL of D5W 300 mg bolus after first Epinephrine dose Repeat doses at 150 mg

Amiodarone Precautions – May produce vasodilation & shock (hypotension, dizziness) – May have negative inotropic effects (bradycardia and heart block) – Terminal elimination Half-life lasts up to 40 days

Lidocaine MOA: – Depresses automaticity – Depresses excitability – Raises ventricular fibrillation threshold – Decreases ventricular irritability

Lidocaine Dosing – Initial dose: 1.0 to 1.5 mg/kg IV For refractory VF may repeat 1.0 to 1.5 mg/kg IV in 3 to 5 minutes; maximum total dose, 3 mg/kg A single dose of 1.5 mg/kg IV in cardiac arrest is acceptable Endotracheal administration: 2 to 2.5 mg/kg diluted in 10 mL of NS

Lidocaine Precautions – Bradycardia, hypotension, heart block, sinus node depression

Magnesium Sulfate Indications – Cardiac arrest associated with torsades de pointes or suspected hypomagnesemic state Dosing – 1 to 2 g diluted in 10 mL of D5W IV push Precautions – Occasional fall in blood pressure with rapid administration – Use with caution if renal failure is present

Procainamide Indications – Depresses automaticity – Depresses excitability – Raises ventricular fibrillation threshold – Decreases ventricular irritability

Procainamide Dosing – 30 mg/min IV infusion – May push at 50 mg/min in cardiac arrest – In refractory VF/VT, 100 mg IV push doses given every 5 minutes are acceptable – Maximum total dose: 17 mg/kg

Procainamide Precautions – If cardiac or renal dysfunction is present, reduce maximum total dose to 12 mg/kg and maintenance infusion to 1 to 2 mg/min

Asystole / Pulseless Electrical Activity Asystole: lack of ventricular electrical activity & lack of ventricular mechanical activity PEA: presence of organized ventricular electrical activity but not accompanied by meaningful ventricular mechanical activity (sufficient to generate a palpable pulse)

PEA! P Problem search E Epinephrine 1 mg IV/IO q3-5 min. Or vasopressin 40 U IV/IO, once, in place of the 1st or 2nd dose of epi. A Atropine 1 mg IV/IO q3-5 min. (3mg max.) HypovolemiaTablets HypoxiaTamponade, Cardiac Hydrogen Ion (Acidosis)Tension Pneumothorax Hyper-/HypokalemiaThrombosis, coronary (ACS) Hypothermia Thrombosis, pulmonary (embolism) HypoglycemiaTrauma

Acetylcholine Overview and Effects Heart – Decrease in Heart Rate by Reducing the Firing Rate of the SA node and Increasing Conduction Time through the AV node. Blood Vessels – Cause Mild Dilatation of Blood Vessels

Cholinergic Antagonists - Atropine Atropine – Blocks Muscarinic Receptors – Post- Ganglionic Receptors in Parasympathetic Transmission – SA Node Effects - Increase Firing Rate – AV Node Effects – Decrease Conduction Time – Overall – Increased Heart Rate, Minimal BP Effect Reference: Grauer Page 78

Atropine Sulfate Dosing – 1 mg IV push – Repeat every 3 to 5 minutes – May give via ET tube (2 to 2.5 mg) diluted in 10 mL of NS – Maximum Dose: 0.04 mg/kg

Atropine Sulfate Precautions – Increases myocardial oxygen demand – May result in unwanted tachycardia or dysrhythmia

ADDITIONAL

Tracheal administration of medications Doses: 2 – 3 times iv dose Dilute in 10cc distilled H 2 O or NS N N aloxone A A tropine V asopressin V asopressin E E pinephrine L L idocaine