Shock!
Oxygen delivery is dependent on what two things?
Cardiac output and Arterial oxygen content
DO2= CO x CaO2
What is the antidote for Acetaminophen intoxication?
N-Acetylcysteine 140mg/kg PO or IV
What components entail stroke volume?
Preload, Afterload, Contractility
-Minimize interruptions in compressions
- Change compressor every 2 minutes or sooner if fatigued
- If no advanced airway, 15:2 compressions:ventilation ratio
- If advanced airway, provide continuous compressions and give breath every 2-3 sec
You have a new-onset DKA. You just started insulin drip at 0.1 units/kg/hr. How quickly should the patients blood glucose be allowed to drop?
Typically 50-100 dL/hr
Name 5 types of shock
Hypovolemic, Cardiogenic, Distributive, Obstructive, Dissociative
15 yo F ingested a substance in a suicide attempt. She presents with temperature of 100.6, HR: 120, BP: 140/90, RR: 25. She is agitated and hallucinating. On exam she has dry flushed skin and dilated pupils. She has not made any urine yet. What is the likely toxidrome?
This patient ingested Benadryl.
This could be any Antihistamines, TCAs, atropine, scopolamine, or antispasmodics
Pulmonary Stenosis
Right ventricular outflow tract obstruction
Overriding Aorta
VSD
Name at least 5 reversible causes of cardiac arrest.
Hypovolemia, Hypoxia, Hydrogen Ion (Acidosis), Hypoglycemia, Hypo-hyperkalemia, hypothermia
Tension ptx, tamponade, toxins, thrombosis (pulmonary), thrombosis (coronary)
ADH has what two functions?
Retain water in the body
Constrict blood vessels
What are the four causes of Hypoxemia?
Hypoventiation
V/Q mismatch
Shunting
Diffusion restriction
17 yo M comes to the ER for chest pain. He ingested unknown substance at a party earlier today. He is sweating and febrile, HR: 140, RR: 25. He is tremulous and suddenly has a seizure in front of you. What is the likely toxidrome?
Cocaine, amphetamines, pseudoepherdine
What are the treatments of SVT if a patient does not show cardiopulmonary compromise? What if the patient does show cardiopulmonary compromise?
SVT: P waves absent/abnormal, RR interval is not variable, infant rate usu > 220, child rate usu > 180/min, history of abrupt change
Vagal maneuvers if pt stable
Adenosine if not stable: First dose 0.1 mg/kg rapid bolus (max 6mg), Second dose 0.2 mg/kg rapid bolus (max 12 mg)
What is code dose epinephrine?
IV/IO: 0.01mg/kg or 0.1 ml/kg of 1:10,000
ETT: 0.1 mg/kg or 0.1 ml/kg of 1:1000
A TBI patient has systolic hypertension, bradycardia, and slow respirations. What is this?
Cushings triad - a late sign of advanced increased intracranial pressure
Besides your clinical bedside assessment, name other tools we can use in the PICU that may help to diagnose and manage shock.
Labs: Mixed venous Oxygen Sat, Lactate, inflammatory markers or other labs that may be associated with the diagnosis of shock (troponin, D-dimer, etc)
Monitoring: Near-infrared Spectroscopy (NIRS), Pulse ox, Central venous pressure monitoring, CO monitor, arterial line
Imaging: Echo, POC ultrasound/lung ultrasound, CXR
2 yo M, presents with unknown history. Pt is hypothermic, bradycardic, and hypotensive. Pupils are constricted on exam and RR: 3 breaths per minute. What is the likely ingested substance and what is the treatment?
Like Opioid ingestion: heroin, morphine, methadone, dilaudid, fentanyl, etc
Naloxone 0.1 mg/kg IV/IM/ETT
At the cellular level, the cardiac myocyte includes tropomyosin and troponin which work together to block the myosin binding site on actin during relaxation. What happens during ATP mediated contraction?
Calcium binds to troponin, which causes tropomysin to move and exposes myosin binding sites on the actin filament allowing ATP mediated contraction to occur.
During a bath, your patient has lost a pulse and CPR is initiated. Bag mask ventilation with oxygen has started. The bedside nurse attaches the monitor and ventricular tachycardia is present at the pulse check. There is still no pulse. What is the next step?
First shock 2 J/kg
Second shock 4 J/kg
Subsequent shocks >4 J/K to max of 10 J/Kg or adult dose
Decadron/Dexamethasone- a glucocorticosteroid with predominant anti-inflammatory properties. Glucocorticoids have been shown to inhibit the production of factors involved in inflammation including vasoactive and chemoattractant factors, as well as the secretion of lipolytic and proteolytic enzymes and to decrease migration of leukocytes to areas of injury.
Name 3 Vasoactive agents, their receptors, and their actions
Epi : a-1 agonist, B1 agonist, B2 agonist-inc CO, HR, MAP, SVR
Dopa: B1 agonist, a1 agonist- inc CO, HR, MAP, SVR
Dobuta: B1 agonist, B2 agonist- inc CO, HR
NE: A1 agonist > B1 agonist- Inc MAP, SVR, PVR
Vaso: V1 receptor agonist - Inc MAP, SVR
Phenylephrine: a1 agonist- inc MAP, SVR
Malignant Hyperthermia is a rare pharmacogenetic disease that is triggered by inhaled anesthetics. What are some of the signs and symptoms?
Bonus: A mutation in what autosomal dominant receptor is responsible for this?
Caused by Inhaled anesthesia agents (except NO) or Depolarizing neuromuscular blockers (succinylcholine)
Typically occurs after 3+ exposures. Begins 30 min to 24 hrs from exposure. Very high temps >42, pupils normal, Extreme rigidity "rigor mortis like", HYPOreflexia, sweaty, hypercarbia, tx with Dantrolene and aggressive cooling
Bonus: ryanodine receptor
Your patient arrives to the PICU with a blood pressure that is >95th percentile (based on gender, age, and height) of 3 different individual readings. The patient is complaining of headache, nausea, with lab work showing increase in renal function and liver function tests. What is the diagnosis and how do you treat?
Hypertensive emergency: severe increase in BP accompanied by life-threatening symptoms and/or acute organ damage
Decrease BP by 20-25% of overall goal over 24-48 hours. Dropping BP rapidly may worsen end-organ damage
First line medications: Nitroprusside: Breaks down NO, nonselective vasodilator, Nicardipine: CCB, smooth muscle relaxation and vasodilation, Labetalol: A1 and beta blocker, dihydropyridine: smooth muscle relaxation and vasodilation
Your patient has a heart rate of 240. EKG reads Wide QRS complex (>0.09 sec). Your patient has now become hypotensive, with poor capillary refill and is showing signs of altered mental status. What is the most likely heart rhythm and how do you treat it?
Possible ventricular tachycardia
Treated with synchronized cardioversion: Begin with 0.5 - 1 J/kg, if not effective, increase to 2J/kg. Sedate if needed but do not delay cardioversion.
How do you calculate anion gap and name the causes of elevated anion gap.
AG = Na - (Cl + HCO3)
MUDPILES
Methanol, Uremia, DKA, Propylene glycol/Paraldehyde, Isoniazide, Lactic acidosis, Ethylene glycoll, Salicylates