ABCs William Beaumont Hospital Department of Emergency Medicine

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Presentation transcript:

ABCs William Beaumont Hospital Department of Emergency Medicine Resuscitation ABCs William Beaumont Hospital Department of Emergency Medicine

What we are covering in a nutshell… Airway Breathing Circulation and Shock

Airway: Decision to Intubate Failure to maintain or protect airway Reposition the patient and apply the jaw thrust or chin lift maneuver to open the airway Failure to ventilate or oxygenate Hypoxemia not responding to above maneuvers or application of external O2 Fatigue or tiring out secondary to tachypnea, excessive work of breathing Anticipate the need for intubation Status epilepticus, OD, multiple trauma, sepsis…

Sniffing Position The sniffing position is achieved by A) Extending the head while B) Simultaneously flexing the neck Neck flexion is maintained by placing padding behind the head Contraindicated: potential C-spine injury

Difficult Intubation: Physical Characteristics Anatomically abnormal facies Neck Trauma Prominent Incisors Receding Mandible or Small Jaw C-spine immobilization Short and thick neck Large tongue

Difficult BVM Characteristics Edentulous Obesity History of snoring Beards or facial hair Facial or neck trauma Obstructive airway disease or bronchospasm 3rd trimester pregnancy

Mallampati Signs for Difficult Intubation I – entire tonsillar pillars seen; 2- upper tonsils seen 3; hard and soft palate seen; 4; only hard palate seen

Comparing Pediatric and Adult Airways Anatomic differences Small mouth plus proportionately larger soft tissues and structures (tongue and tonsils) Airway location and vocal cords are higher and more anterior in children Most narrow portion of the airway in kids is at the cricoid cartilage – therefore uncuffed ET tubes should be used (adults most narrow below the cricoid at the vocal cords) Pediatric cricothyroid membrane is small, difficult to palpate, and incise so cricothyroidotomy is contraindicated < 8 y/o

Comparing Pediatric and Adult Airways Anatomic Differences cont… Pediatric trachea is shorter so is more prone to R mainstem intubation and tube dislodgement Larger occiput causes passive flexion of the c-spine and buckling of the airway -> sniffing position to open the airway and align the axis of the oropharynx/larynx/vocal cords

Pediatric Airway Estimating ET tube size Broselow tape (age+16)/4 ETT size estimation based upon the width of the child’s fifth fingernail

Endotracheal Intubation Purpose – to achieve definitive airway control (LMA and combitube are NOT) Indications Respiratory failure Airway protection in an unconscious patient Decrease the work of breathing Therapeutic interventions such as hyperventilation for HI or to protect the airway during diagnostic studies

Straight vs Curved Blades Straight Blade Preferred in infants and kids < 8 yo tip of the blade passes over the epiglottis and tongue to physically lift them out of the way Curved Blade Fits into the vallecula between the tongue and epiglottis to lift the palate and soft tissues anteriorly Mechanically difficult to use in obese adults and children with lots of floppy soft tissue structures

RSI = Rapid Sequence Intubation Definition = systematic protocol using sedatives and paralytics to increase chances of successful intubation and decrease the risk of aspiration (hopefully) Indications – airway control or compromise, shock, head injury, impending respiratory arrest Contraindications – physically obstructed airway, severe mid facial fractures, neck or throat surgery or trauma When to think twice – short, fat bull neck, c spine trauma, oral abscess or masses, ludwig’s angina, facial burns

The 6 P’s of RSI 1. Prepare 2. Pre Oxygenate Equipment – suction, blade, ETT, monitor, nursing staff, drugs 2. Pre Oxygenate Provides a period of time after the patient becomes apneic in which they will remain adequately oxygenated BVM or 100% O2 for 3-5 minutes

The 6 P’s of RSI 3. Pre Treatment Sedation – opioids, benzos, ketamine, etomidate Head Injury or Increased ICP – lidocaine, fentanyl, defasciculating dose of paralytic Atropine for Kids prior to intubation to prevent vagal induced bradycarida 4. Paralysis Depolarizing Agents = Succinylcholine Nondepolarizing Agents = pancuronium, vecuronium, but mostly ROCURONIUM

Succinylcholine Mimics Ach at the neuromuscular junction Onset of action is 20-30 seconds Duration is 90-120 seconds Dose 1-1.5mg/kg for adults and 1.5-2mg/kg for kids (remember to pre treat with atropine) Side Effects histamine release causing hypotension rise in ICP Release of K from cells – precaution in burn patients, diabetics, patients found down (rhabdo)

Nondepolarizing Agents – Rocuronium Reversible, competitive antagonist of Ach at the neuromuscular junction Slower onset of action but longer acting Can be reversed (rarely) with edrophonium Onset is 45-60 seconds Duration is 30 minutes Dose is 0.6-1.0 mg/kg for adults and kids

The 6 P’s of RSI 5. Pass the Tube Assess the depth of paralysis through degree of relaxation of the jaw muscle or eye lids Apply cricoid pressure = Sellick Maneuver to prevent aspiration (not maneuvering the trachea) Visualize the cords Pass the tube into the trachea

The 6 P’s of RSI 6. Position Check See the tube pass through the cords Check for symmetric chest wall rise and fall with bagging Check for equal bilateral breath sounds End tidal CO2 detection (color change) CXR for position of ETT Normal tube position 22-24 cm at the teeth (tube size x 3)

The 6 P’s of RSI Pitfalls – OK this is 7, we made this one up Not preparing and checking your equipment Forgetting cricoid pressure Over aggressively BVM causing gastric distension and increased risk of aspiration

Cricothyroidotomy Creation of an opening in the cricothyroid membrane for placement of a trach tube when oral intubation fails or is contraindicated Incidence – 1% of all ED intubations Contraindications (relative) distorted neck anatomy pre existing infection coagulopathy children < 10 years old

Cricothyroidotomy Locate cricothyroid cartilage 3-4 cm vertical skin incision Horizontal stab thru cricothyroid membrane Insert hemostat & dilate opening horizontally then vertically Insert #4 Shiley trach tube or 5 mm ET tube (cut short) & verify position Inflate balloon & secure tube

Questions? Let’s move on to circulation

Circulation Shock – a pathologic state that initiates a sequence of stress responses in the body designed to preserve flow to vital organs 4 Types of Shock Hypovolemic - hemorrhagic, nonhemorrhagic Distributive – septic, anaphylactic, neurogenic Cardiogenic – arrhythmias, other – AMI, cardiomyopathy, OD Obstructive – tension pneumothorax, cardiac tamponade, pulmonary embolus, ductal dependent

Septic Shock Septic shock – patient with sepsis who remains hypotensive (SBP < 90) despite adequate fluid resuscitation Sepsis – patient with presumed or known infection plus 2 or more SIRS criteria SIRS criteria – systemic inflammatory response syndrome 1) temp > 38*C or < 36*C 2) HR > 90 bpm 3) RR > 20/ min or PaCo2 < 34 4) WBC > 12,000 or < 4,000

Septic Shock Pathophysiology a focus of infection causes release of large amount of toxin the body reacts by releasing mediators and humoral defenses such as complement, cytokines , and platelet activating factor Clinical Features hot flushed skin, hyperthermia or hypothermia, tachycardia, tachypnea, wide pulse pressure, mental status changes

Septic Shock Therapy Attention to ABC’s – assess ventilation and oxygenation Aggressive fluid administration – Normal saline fluid boluses of 20cc/kg may need to repeat 2-3 times until SBP>90 Empiric antibiotics – cover Gm + and Gm – Lab evaluation – CBC, BMP, U/A, urine & blood cultures, CXR, lactic acid

Septic Shock Pressors Norepinephrine - first line drug 2-20 mcg/kg/min Dopamine – may add to norepinephrine or change to this based on clinical response 5-20 mcg/kg/min Vasopressin – should not be sole agent Phenylephrine – used in patients with excessive tachycardia from pressors Consider steroids sepsis associated with adrenal insufficiency hydrocortisone 100mg IVP or dexamethazone 4 mg IVP

Hemorrhagic Shock Defined – blood loss of significant magnitude to overcome normal physiologic compensatory response and compromise tissue perfusion Blood loss triggers increased cardiac rate & force of contraction To maintain BP, redistribution of blood flow occurs to preserve vital organ function, conserve water and sodium, and control blood loss. Baroreceptors sense fall in BP and release norepinephrine. Norepinephrine increases CO and stimulates renin secretion (increasing Na & H2O reabsorption)

Hemorrhagic Shock Norepinephrine causes vasoconstriction especially in the splanchnic blood vessels which can increase circulating blood volume by 20-30% Acute hemorrhage also causes local activation of the clotting cascade so blood vessels contract and plateletes adhere to damaged vessels.

Hemorrhagic Shock Skin cool, clammy, mottled Tachycardia, narrow pulse pressure RR > 22 PaCo2 < 32 Site of hemorrhage not always obvious Treatment Control hemorrhage Rapid infusion of several liters NS in adults or successive 20cc/kg boluses in kids If still hypotensive after aggressive fluid resuscitation, then transfuse 5-10 ml/kg PRBC type specific If uncontrolled hemorrhage, then use uncrossmatched blood (type O neg)

Hemorrhagic Shock Class 1 – 15% loss – mild tachycardia only, rapid response to fluids Class 2 – 15-30% loss –PP (DBP and PVR), subtle MS changes, cap refill > 2 s Class 3 – 30-40% loss – SBP, marked MS changes, transient response to IVF Class 4 - > 2 L loss – obtunded, clammy, marked hypotension, narrow PP, minimal or no response to IVF – needs blood

CARDIOGENIC SHOCK Clinical Definition: results when >40% myocardial necrosis from ischemia, inflammation or toxins Primary cause – pump failure Cardiogenic shock produces same circulatory and metabolic alterations as hemorrhagic shock Clinical distended neck veins imply CHF, PE, tamponade muffled heart tones think tamponade fever & new murmur – endocarditis loud machine like murmur – papillary muscle rupture asymmetric breath sounds – pneumothorax Beck’s triad (pericardial tamponade)– JVD, hypotension, muffled heart tones

CARDIOGENIC SHOCK TREATMENT O2, PEEP for CHF, intubate for impending respiratory failure Inotropic support - dobutamine, dopamine Treat underlying cause – AMI, PE Inamrinone (Inocor) for refractory hypotension, may improve CO by increasing cAMP, no tachyphylaxis and no increased myocardial O2 consumption Consider aortic balloon pump – improves diastolic coronary perfusion and cardiac output by 30%

ANAPHYLACTIC SHOCK Results from IgE mediated systemic response to an allergen IgE causes mast cells to release histamine resulting in vasodilation, bronchoconstriction, capillary leak into interstitial space Clinical – the quicker the symptoms manifest, the more severe the reaction Symptoms - flushing, warmth, urticaria, pruritis, dyspnea, wheezing, angioedema, tachycardia, tachypnea, hypotension

Anaphylactic Shock Therapy Benadryl/Cimetadine – H1 H2 blockers prevent urticaria, reduce bronchoconstriction, reduce fluid transudation Corticosteroids Nebulized B2 agonist – reduce bronchospasm Epinephrine alpha agonist – reverses hypotension by vasoconstriction beta agonist – bronchodilation, positive ionotrope and chronotrope stop T cell and mast cell activation reduce bronchial inflammation

CENTRAL NEUROGENIC SHOCK Definition – loss of neurologic function and autonomic tone below the level of the spinal cord lesion Hypotension from spinal shock is a diagnosis of exclusion in the trauma patient. It is caused by loss of vasomotor tone and lack of reflex tachycardia from disruption of autonomic ganglia. Clinical – flaccid paralysis, loss of DTR’s, loss of bladder tone, bradycardia, hypotension, hypothermia, skin warm & dry, good urine output

Central Neurogenic Shock Treatment Adequate fluid replacement Atropine – treat vagal mediated bradycardia Ephedrine/Phenylephrine – promote vasoconstriction and promote cord perfusion Methylprednisolone - given w/in 8 hrs of injury shown to improve neurologic recovery

BURNS Fluid Resuscitation Rule of Nines Parkland Formula for Burns 4ml/kg x (% BSA burned) give ½ of fluid in first 8 hours Rule of Nines Technique for estimating the extent of body surface area burned The difference between the BSA of an adult and an infant reflects the size of the infant’s head which is proportionately larger than an adult.

RULE OF NINES Diagram #5                                            

PEDIATRIC RESUSCITATION DOSES Defibrillation 2J/kg then 4J/kg, 4J/kg Epinephrine .01mg/kg (1:10,000) Atropine .01mg/kg Glucose D10 2-4ml/kg (not D50) Fluid 20-40 ml/kg NS bolus Drugs you can give thru an ET tube (NAVEL) Narcan Atropine Valium Epi Lidocaine

HYPERKALEMIA K level EKG changes 5.6 – 6.0 tall peaked T waves 6.0 – 7.0 long PR & QT decreased P waves ST segment depression 7.0 – 8.0 idioventricular rhythm wide QRS 10.0 and up sine wave

HYPERKALEMIA

TREATMENT OF HYPERKALEMIA Kayexalate ion exchange resin given po or pr each gram exchanges with & eliminates 1mEq K Insulin/Glucose/HCO3 – use if EKG changes or unstable glucose enters cells & pulls K with it dose: Insulin 10 U IV, Glucose 1 amp D50, 1 amp HCO3 Ca gluconate/ Ca Cl – use if hypotension, CP, SOB, lethargy, coma 10ml of 10% Ca Cl (1 amp) slowly over 10-20 min if patient on Digoxin, be very cautious – Calcium potentiates toxic effects of digoxin on the heart

THE END