all Flashcards
normal cardiac output
cardiac output is blood ejected from LV in 1 minute.
it is SVxHR. normal is 200ml/kg/min in neonate to 100ml/kg/min in adolescence
what 4 things affects SV
preload, afterload, contractility, compliance
cardiac index
CI = CO/BSA.
normal 3-4.2L/min/m2 regardless of body size.
what is EF
volume ejected vs volume remaining in LV
preload?
blood in ventricles at end of diastole and prior to contraction
determined by cardiac fiber length/stretch and volume returned from systemic and pulm circulation. most accurately determined by PAWP (cath lab or OR)
MAP
MAP=(COxSVR)+CVP
SNS stim releases what
norepi
parasympathethic stim releases what
acetylcholine with acts on right and left vagus nerve for relaxation of HR and conduction
alpha adrenergic receptors stim causes what
arterial vasoconstriction and increased intracellular calcium
stim of beta1 adrenergic receptors causes what
(dobutamine,norepi) increased SA node, increased inotropy, chronotropy, AV conduction
b2 adrenergic stim causes what
smooth muscle relaxation, bronchodilation
cardiac failure
failure of heart to maintain CO sufficient for body metabolic demands
left heart failure heart sound
s3 heart sound
pulmonary vascular resistance increases in response to?
decreased o2. so right heart failure can result from PHTN but also potentiates it because then u have less CO therefore less o2 resulting in more pulm vasoconstriction
cvp increased or decreased in right heart failure? what about pvr?
both increased
labs in heart failure
dilutional changes (anemia, hyponatremia, hypocalcemia, hypoglycemia), end organ dysfx: proteinuria, increased lactate, acidsosis, increased WBC, polycythemia, BNP levels
meds (for heart failure)
Improve contractility: b blockers, digoxin, dobutamine, dopamine, epi, vaso, calcium chloride, milrinone
Optimize preload: diuretics, sodium/fluid restriction
Decrease afterload: nitroprusside, ACE I, ARB, iNO
Anxiolytics, pain meds
dilated cardiomyopathy
most common type in kids.
aka congestive cardiomyopathy d/t s/s of CHF with decreased SV and EF.
hypertrophic cardiomyopathy
leads to left ventricular outflow track obstruction. things that increase HR/contractility can worsen.
thats why its most common cause of young sudden cardiac death in athletes.
restrictive cardiomyopathy
from fibrosis and scarring (defective endocardium). has minimal contraction so decreased diastolic function with normal systolic. poorest prognosis.
Dilated cardiomyopathy tx
vasoactives, inotropes, diuretics, afterload reduction, ACE-I (prils-angioedema) or angiotensin II receptor blockers (sartans)
whatdo calcium channel blockers do? and what condition are they good for
afterload reduction (HTN crisis), decrease contractility, improve LV function
myocarditis vs endo
myo usually virus. endo usually bacteria
pericarditis heart symptom
cardiac tamponade, rub.
fetal heart develops when?
4-7 weeks
dvt diagnosis
usually look at symptoms + US but sometimes asymptomatic.
can also do angio with contract and venogram
prevent DVT
scds, turns, low molecular weight heparint
tx dvt
thrombectomy, once again low molecular wt heparin, observation
superior vena cava syndrome causes
CVC, thrombosis, mediastinal malignancy
SVCS dx
xray (might find mass), CTs
svcs tx
depends on cause - can be thrombolytic, anticoag, supportive, remove cvc
fetal vs neonatal circulation
fetal: has intracardiac shunts, high PVR, low SVR, low CO, gas exchange in placenta.
neonate: no shunts, low PVR, high SVR, high CO, gas exchange in lungs
PDA
L to R of oxygenated blood. close with indomethacin or surgical ligation.
aortic blood goes to pulmonary artery back to lungs again ( in fetus its the opposite)
PFO
l to R shunt.
when to be concerned for CHD in newborn
murmur WITH cyanosis (suggests r to l shunt), esp if cyanosis worsens with crying
failed hyperoxia, etc
hyperoxia test
when giving hyperoxygenation to newborn, cyanosis worsens, then they fail the test. most likely have a CHD
syndromes associated with CHD
t21 (avsd), t18 (edwards)-HLHS and VSD, 45x (turners)-VSD and coarc, williams, digeorge-truncus, noonan
acyanotic with increased PBF
PDA, VSD, ASD, AVSD
acyanotic with ventricular outflow obstruction
AS, CoA, PS
cyanotic with decreased PBF
tet, tricuspid atresia
cyanotic with increased PBF
transposition of great arteries, truncus arteriosus, total anomalous pulmonary venous return, HLHS
avsd (av canal defect),what is it commonly seen with, what can happen postop
with t21.
firstly: deformed tricuspid and mitral valve - has common AV valve between atria and ventricles instead of two separate valves. allows blood to leak back into atria.
also: ASD and VSD.
need surgery in infancy with patches and valve repairs.
can develop PHTN and heart blocks
requires PDA
AS, CoA, can be TGA, HLHS
postop coarc repair monitor for what?
HTN
tet
PS with RVH, overriding aorta (sits over both ventricles), large VSD
more severe the PS, more severe the cyanosis
postop tet repair
commonly postop RV failure so treat that and minimize o2 demands.
commonly have AV asynchrony: dysrhythmias.
watch for bleeding!
make sure pt has adequate preload, low pulmonary vascular pressures
tricuspid atresia-description, surgery
tricuspid is not patent. must have PFO OR ASD! (may still require PGE.). usually also has hypoplastic RV with RVOO. so blood has to go RA>LA>LV>some to aorta, some to pulm artery
surgery in first week of life
tet spell description and treatment
starts with hypoxia, irritability, hyperpnea, then prolonged intense cyanosis leading to syncope (or cardiac arrest).
tx: comfort, knee chest, morphine, o2, NS bolus, sodium bicarb, propanolol (decrease hearts response), phenylephrine (to increase SVR and therefore decrease the R TO L shunt). if severe, intubate.
TGA description, surgery
aorta and pulm artieries switched. needs PDA, ASD, or pFO. so needs PGE.
preop needs baloon septostomy to maintain the type of ASD. then they can do arterial switch with cardiopulmonary bypass (postop will have myocardial dysfunction needing vasoactives).
truncus arteriosus
pulm artery and aorta dont split in utero. so theres a single valve vessel over the ventricles with a very large VSD.
DiGeorge syndrome.
surgery one of the most extensive neonatal cardiac surgeries-very complicated postop. theyll need more surgeries as they grow
TAPVR
pulm veins drain into systemic veins or RA instead of LA. total (all 4 veins) or partial.
needs immediate surgical repair.
HLHS
mitral valve and aortic valve are stenosed or atresia. LV hypoplastic or nonexistent. ascending aorta tiny or can be well formed.
can be diagnosed in utero.
at birth: PGE until repair
HLHS surgeries
after PGE
stage 1: improves condition, but not repair (norwood palliation): creates conduit to replace PDA and stop PGE. also creates common atria and new aorta. so still ductal dependent but not through a real PDA
stage 2 palliation at 6 mos age: SVC is connected to pulm artery so blood can bypass right heart. shunt made in first surgery can be removed now. now volume load is reduced on the RV.
stage 3 palliation: IVC goes directly to pulm artery.
now blood from body goes to pulm artery, to lungs, oxygenate, return to pulm vein, to common atria, thru tricuspid, to RV, to new aorta.
still causes wear and tear on RV over time; monitor RV function and may need heart transplant still.
digoxin adverse effects and considerations
chest tube drainage postop cath,s/s of tamponade
typically decreases rapidly over the first few postop hours. BE WORRIED if more than 3ml/kg/hr for >3hrs, or 5-10ml/kg/hr in one hour. do coag studies, can be r/t inadequate heparin reversal.
if drainage stops, MIGHT BE TAMPONADE: acute increase in filling pressures like RAP, LAP, CVP or equalization of LAP AND RAP (lap should be higher). vein distention, hypotension, narrow PP.
septal surgeries rhythm disturbance
heart block, conduction delay
what does high RAP or CVP mean
RV failure or PHTN
what does low lAP mean
hypovolemiaw
hat does high LAP mean
LV failure or high LV afterload
postop heart surgery oxygenation/ventilation considerations
use volume or pressure contorl venitlation.
be very careful with suction-dont wanna stress the heart.
be careful with supplemental o2 especially with single ventricle: pulmonary dilation effects of o2 can be bad for them and flood the lungs.
cardiopulmonary bypass postop
may need 50% maintenance x24h, sodium restriction or free water restriction, electrolyte monitoring, glucose monitoring, renal function monitoring and UOP monitoring
postop neonatalheart procedure monitor for?
monitor babies for NEC. NEC can also be associated with umbilical lines
Therapeutic digoxin serum level
1.1-2.2ng/ml
Hypertrophic cardiomyopathy tx
Tx: B adrenergic agonists, calcium channel blockers (provide afterload reduction, decrease contractility, and improve LV diastolic function), diuretics and inotropes with caution (these pts don’t tolerate dehydration), ICD/pacing, surgical resection
Restrictive cardiomyopathy tx
Tx: CHF management, diuretics, digitalis, vasodilators, antiarrhythmics, transplant
cardiac cath complications other than hematoma
arrhythmias, air emboli, MI, perforation, infection
inotropes do what
work through alpha and beta receptors to vasodilate, vasoconstrict, and/or enhance contractility
chronotropes work by what
change HR by affecting nerves controlling the heart, or by changing rhythm from the SA node (pacemaker of heart)
what to cholinergic drugs stimulate
(acetylcholine, bethanacol) pns
what do beta adrenergic drugs stimulate
SNS
what do anticholinergic drugs stimulate
(clozapine, quetiapine, atropine, oxybutynin, robinul, ipratropium, promethazine, noritriptyline): SNS
anticholinergic drugs = CQ PARONI
what do beta blockers stimulate
PNS
what do type 1 epithelial cells do
gas exchange
what do type 2 epithelial cells do
produce surfactant
are lungs more or less compliant when youre younger
less
when are fetal lungs capable of gas exchange
22-24 wks (when alveoli develop)
where are co2 sensors / o2 sensors
brainstem
o2 sensors: carotid bodies
is cyanosis an early or late sign of hypoxemia
late
should pco2 be higher or lower in head injury pts? why?
lower (ie low 30s).
because hypercarbia causes cerebral vasodilation for increased CBF also causes increased ICP
what does a WNL RR for a sick/injured child indicate
impending respiratory arrest
what age are kids obligatory nose breathers
until 6 mos of age (NG can impair breathing up to this point)
normal VQ ratio
0.8 (slightly more blood flow than aeration)
what is alveolar dead space
areas of alveoli that are seeing ventilation but not perfusion
what is an intrapulmonary shunt? examples?
when alveoli are not ventilated but are perfused.
asthma, atelectasis, ARDS, pleural effusion
how do you determine presence of an intrapulmonary shunt?
normally pao2/fio2 should be >286, if this number is decreased you have a shunt.
what does PEEP do
increases alevolar volume, increases FRC, moves pulmonary water (edema) out
oxyhgb dissociation curve:
left vs right shift?
what causes left shift? right shift?
left latches on, right releases.
left shift increases binding of o2 to hgb, but makes it harder to release it to tissues. causes: hypothermia, alkalosis, hypocapnia, low DPG, CO poisoning
right shift has decreased affinity for o2, harder to bind o2 at the alveoli and also easier to release it to tissues. causes: hyperthermia, acidosis, hypercapnia, high DPG
what is 2,3 DPG
an intracellular RBC factor that determines hgb affinity for o2
acut respiratory failure definition
inability of resp system to meet demands of o2 ORRR also inability to provide adequate co2 elimination causing resp acidosis
acute respiratory failure causes (other than the lungs)
CNS issues, upper airway disorder, CV or heme disorders
what can trigger apnea of prematurity
ambient temp changes, vagal stimualtion (suction, gagging)
transient tachypnea of newborn
from c section or precipitous delivery (lung fluid not squezed out as in normal vag delivery)
choanal atresia
openings from nasal cavity occluded - manifests in delivery rm(obligate nose breather)-dyspnea worsens with mouth closure. OPA / intubate until surgery
where should tip of ETT end
no lower than 1-2cm above carina, no higher than 1st rib
determine appropriate ETT size
(age in yrs/4) + 4
so 16 yr old gets size 8
what to avoid when leading up to extubation
no PO intake or CPT 2-4hrs prior to and post extubation (aspiration)
upper airway edema tx post extubation
steroids, rac epi, neb saline, heliox
what do increased PIPs on vent mean?
ARDS, decreased compliance, pneumo, secretions, kinked tubing
nutrition while on MV
low carbs (to avoid increasing co2), low triglycerides, high fat for calories
cons of PEEP
low CO from impaired venous return and high ICP from impaired cerebral venous return
inadvertent intrinsic peep
lung overdistention from flow obstruction and too short exhalation time.
s/s: rising CO2, poor chest wall movement
especially seen with bronchiolitis, CLD
ARDS patho
systemic stress response leading to increased alveolar capillary membrane permeability (pulm edema) and bronchoconstriction. PTHN develops. decreased perfusion to alevolar cells (especially type 2 pneumocytes) reduces FRC and compliance
ARDS general management
intubate (PEEP); volume control or pressure control.
permissive hypercapnea if with normal o2 and ph>7.2 and no cerebral effects.
also HFOV/ECMO
ensure normal preload, reduce afterload, support heart contractility, fluid boluses, transfuse for low hgb, epi.
decrease activity, paralysis, sedation, comfort, normothermia.
increased protein needs(hypermetabolic state), early enteral feeds.
iNO if PHTN.
proning
PNA causes and diagnosis
viral, bacterial.
dx: CXR, secretions, blood cx, bronchoalveolar lavage, lung biopsy if severe, pleural fluid
hydrocarbon PNA aspiration
gas, nail polish, solvent, propellants.
treat aggressively. necrosis of tissue can occur. similar to ARDS
foreign body upper vs lower airway and post extraction
larynx or tracheal: stridor, retractions, cough, inability to make sounds
bronchi: cough, wheezing, cyanosis, air trapping, decreased breath sounds.
post extraction watch for developing edema obstruction
croup s/s, prevalence, cause, season
barky cough worse at night, hoarseness + low grade fever and other URI symptoms.
prevalent 3mos-3yrs with a tendency to recur.
can be viral or bacterial.
happens late autumn/early winter
croup diagnosis
A/P CXR with steeple sign(narrow glottis and subglottic airway).
lateral XR with normal epiglottis
croup tx
heliox, rac epi, cool humidified o2, steroids, antipyretics, enteral feeds, hydration, minimize agitation
epiglottitis prevalence, cause
2-6yr old
usually h flu (Hib vaccine). can be bacterial.
acute infxn can resolve in 24-72hrs
epiglottitis s/s
four ds and s:
drooling, dysphagia, dysphonia, distress, stridor.
abrupt onset.
fever, sore throat, tripoding.
epiglottitis dx
lateral neck XR thumb sign (thickened epiglottis)
bronchiolitis peak incidence and cause
mid winter-early spring
usually RSV but can be flu, hmpv
bronchiolitis tx
o2, intubate if needed, albuterol, terbutaline, aminophylline, hydration, ribovirin if RSV
CXR appearance in pneumo
absent pulm vascular markings, uniformly translucent area without lung markings, free pleural air in nondependent portions of chest, subq air along mediastinum, bronchi, deviated trachea/heart, flat diaphragm (tension pneumo)
pneumo tx
chest tube.
tension pneumo: needle decompress then chest tubein
sucking chest wound
open pneumo, air in and out. flail chest.
tx with PPV, cover with occlusive drssing, place chest tube.
chest tube management
either to water seal or suction.
give pain management.
bubbling in water seal = air evacuation
fluctuations in water seal synced with RR = normal.
monitor for crepitus.
goal of status asthma tx
goal to restore airway patency, reverse bronchospasm, control inflammatory response, and decrase secretions/plugs.
vent settings for an asthmatic
permissive hypercarbia, prolonged expiratory time, conservative PEEP, watch for pneumo!
pulsus paradoxus
n exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg.
beta 2 agonists
alb, levalb, terbutaline (systemic), metaproterenol,salmeterol
status asthmaticus tx
intubate if absolutely needed, ECMO if not effective, inhaled b2 agonists, systemic b2 agonists (loading then gtt), anticholinergics (atrovent) to block PNS, steroids, mag sulfate (calcium antagonist to promote bronchodilation), ketamine to bronchodilate, may need inhaled anesthetic like isoflurane
pts at risk for PE
sickle cell, nephrotic syndrome, cancer, chemo, hypercoaguable state (inherited), vasculitis
PE tx
o2/intubate, LMW heparin, thrombolytic, supportive CV care (potential for right heart failure and obstructive shock), ABX if infectious emboli, embolectomy if massive
PHTN mean pulm artery pressure? what kind of shunt?
> 25mmHg at rest. right to left shunt
preductal/postductal sats in PHTN
preductal pao2> postductal
PHTN tx
goal: achieve/sustain pulm artery dilation and increase pao2.
hyperventilation for hypocapnic alkalosis, NaHco3, IV vasodilators (prostacyclins, flolan, epoprostenol, remodulin), HFOV, iNO, ECMO, maximize cardiac output, nutrition
BPD pts are sensitive to?
overhydration
bpd comes with?+s/s
PHTN > right heart failure, FTT, barrel chest, bronchospasms (LS can be crackly, wheezy, rales)
BPD tx
supp o2, permissive hypercapnia, slow wean off MV (+/- trach after 6-8 wks), bronchodilators, steroids, diuretics (Watch electrolytes), may need GT to optimize nutrition and prevent reflux, minimize agitation, promote neurodevelopment, pulm toilet, prevent infections
CDH babies present as
full term full birth weight infant who soon develops severe resp distress
CDH comes with
PHTN d/t lung hypoplasia, increased pulm vascular resistance.
CDH s/s
scaphoid abd, PMI shift, WOB, decreased/absent LS, increased chest diameter, PHTN
CDH CXR
gas filled bowel loops in thorax
CDH tx
upright positioning
get baby stable so acidosis/hypoxia/hypotension resolved then OR: immediatley intubate with high RR and low PIPs to prevent pneumo, decompress stomach, use iNO (avoid barotrauma), cluster care
may need chest tube preop (pneumo common for these kids)
CDH postop chest tube
on affected side without suction (gradual reexpansion). position onto the affected side to expand the good lung
TEF most common type
type c: esophageal atresia with distal TEF
TEF hx
prenatal polyhydramnios
TEF tx/management/considerations
abx (asp pna), will need surgery.
carefully place OG or NG to remove secretions from proximal pouch. no paci. prone with HOB up (asp). fluid/electrolytes. neutral thermal.
OR: may need staged repair. may need. G tube.
may need PPN/TPN for a while
respiratory alkalosis causes
CNS injury, ASA ingestion, Reye’s, hepatic encephalopathyrespi
where is CSF produced
choroid plexus: lateral, 3rd, 4th ventricles.
where is csf absorbed
flows freely thru subarachnoid space then absorbed by arachnoid villi
corpus callosum
connects brain hemispheres with nerves
basal ganglia purpose
controls motor function (deep in gray matter of hemispheres)
thalamus function
pain center, temp, tactile sensation
hypothalamus function
secrete ADH, Oxytocin, body temp, sweat, salivary
cerebellum function
balance, coordination
brain stem function
respiratory center
meninges
pia mater (inner, vascular), arachnoid (middle, feathery), dura mater (outer, tough)
anterior fontanelle closes at
16-18 mos
posterior font closes at
2 mos
normal ICP
5-15 (<15)
cushing’s triad
late ominous sign of high ICP.
bradycardia, htn with wide PP, irreg resps that become apnea
tx high ICP
analgesia, sedation, hyperosmolars, mild hyperventilation to promote cerebral vasoconstriction to reduce ICP, temp regulation, sz management, barbiturates, HOB up midline, hydration/nutrition, low stim
gold standard icp monitoring
intraventricular
zero EVD where
with external auditory meatus which approximates the level of foramen of monroe
what does the brain stem include
pons, midbrain, medulla
PNS vs SNS
PNS: eyes constrict/dry, watery mouth, slow HR and RR, bronchoconstriction, peristalsis, bladder contraction
SNS: eyes dilate/watery, mouth dry, sweating, HR up, RR up, bronchodilation, digestion stops, bladder relaxes
communicating vs noncommunicating hydrocephalus
comm: arachnoid villi unable to reabsorb CSF (ie meningitis)
noncomm: obstruction to flow (ie tumor, cyst, inflammation)
encephalopathy: what is, causes
general disturbance in brain cellular metabolism causing ALOC. from HIE, lead poisoning, HTN, metabolic dx
risks for stroke
cardiac issues (should do echo and r/o cardiac embolus as cause), sickle cell, CNS infection, head/neck trauma, moya moya, vasculopathy, birth control
moya moya
rare. blood vessels of internal carotids are narrowed, brain creates collaterals
stroke imaging
noncontrast head CT differentiates ischemic vs hemorrhagic stroke.
CTA evaluates intracranial and extracranial circulation.
MRI
(echo to r/o cardiac embolus)
stroke tx
control HTN, Fever, glucose
o2/ventilation
heparin, tPA
ASA to prevent future strokes
AVM tx
not all are operable.
surgery total excision, embolization, sterotactic radiosurgery, and supportive care
goal for TBI Tx
maintain CPP, prevent secondary injury, symptom management
concussion
blow to head without radiographic findings: can last months.
brain contusion
bruise on brain: may have ICPs/szs
coup, contrecoup
Coup: injury to side of head that was struck
Contrecoup: injury to opposite side of brain
signs of basilar skull fx
racoon eyes, battle sign behind ear.
no NGT!
look for CSF/rhinorrhea/otorrhea
diffuse axonal injury
accel-deceleration injury from MVA, abuse. poor neuro exam with a normal CT
epidural hematoma
ARTERIAL bleed in middle meningeal artery, more in older kids.
lucid > LOC
often associated with skull fracture
subdural hematoma
VENOUS bleed. more in infants. from birth trauma, falls, intentional
when do u start assessing for brain death
24h after injury or resus
requirements to do brain death testing
need 2 exams, 2 diff providers with observation period in between.
must exclude reversible causes (hypothermia, drug toxicity, etc).
brain death tests
- no cortex function, in coma (flaccid, no movement, no response to stimuli)
- no brainstem fx: dilated midposition pupils that do not respond to light, no face/tongue movement, no gag/cough/suck/rooting, no corneal reflex, no induced eye movement on oculocephalic or oculovestibular
- apnea when co2 goes up
oculocephalic test
Dolls eyes test
hold eyelids open, move head rapidly side to side: if brain dead, eyes always point in direction of nose without lagging and moving. (cannot do if pt has cervical spine injury)
oculovestibular cold calorics
irrigate each ear with ice water.
only do if tympanic membrane intact.
elevate HOB to 30deg and inject water deep into canal.
if brain stem intact, CN 3 and 6 are stimmed and there will be slow horizontal nystagmus toward stimulus then rapidly away.
if brain stem not intact, eyes will remain fixed.
if some parts of brain death exam cant be compelted?
ancillary tests: can do 4 vessel cerebral angio, radionuclide CBF, EEG
complete vs incomplete acute spinal cord injury
Complete: complete loss of motor/sensory function below level of injury (quadriplegia, paraplegia)
Incomplete: some loss of motor/sensory with some spared function below injury
acute SCI tx
stabilize (traction, fixation), supportive.
steroids no longer recommended.
if neuro shock, give volume and norepi
viral meningitis CSF
slight increase WBC, normal/slight increase protein, normal glucose.
negative gram stain, negative culture
bacterial meningitis CSF and cause
increased WBC, increased protein, low glucose, positive gram stain and culture
newborns: e coli, GBS
>2mos: n meningitidis, GBS, strep pneumoniae, haemophilus influenzae
kernig sign
for meningitis
pain with extension of legs
brudzinski sign
for meningitis
flexion of neck causes involuntary bending of hip and flexion of knee
monitor what in meningitis?
lytes: watching for SIADH/DI
febrile sz age
6 mos - 6 yrs
meningocele vs myelomeningocele
meningo: cystic CSF cavity protrudes thru a bony defect
myelo: spinal cord+roots protrude thru bony defect (most severe neural cord defect). requires surgery. may have tethered cord so as child grows and it stretches, they have issues with bowel/bladder
arnold chiari malformation
spinal cord travels into skull, causes hydrocephalus, may need shunt
severe sepsis definition
sepsis plus 2 or more organ systems dysfunctioning
septic shock definition
sepsis plus cardiovascular dysfunction with persistent abnormal perfusion (not only hypotension)
–> because kids can maintain their BP longer than adults and hypotension would be a late septic shock finding
septic shock first hour goals
maintain airway/o2/ventilation, restore/maintain circulation and perfusion, give ABX, normal VS, normal mental status
first 15 mins of septic shock
high flow o2(mask, cpap, bipap, intubate)
establish IO/IV access
20ml/kg bolus isotonic saline IVP - repeat up to 60ml/kg. (stop for rales, crackles, hepatomegaly).
correct hypoglycemia, hypocalcemia.
give ABX. want bcx first but dont delay ABX for culture
first 15-60min of septic shock tx
fluid refractory shock. inotropes
epi 0.05-3mcg/kg/min cold shock
norepi 0.05mcg/kg/min warm shock
dopamine if epi/norepi unavailable
first 60 mins septic shock tx
catecholamine resistant shock.
goal normal MAP, PP, SVO2<70, CI 3.3-6
give stress dose hydrocort, obtain cortisol level first if possible
why check cortisol in septic shock
cortisol regulates catecholamine synthesis, responsiveness of adrenergic receptors, and cell membrane stability
septic shock still not improving after adrenal insufficiency has been addressed?
persistent catecholamine resistant shock
-r/o and correct pericardial effusion, pneumo, increased intraabd pressure.
consider ECMO
cold shock vs warm shock pressors
cold shock with a normal BP (low CO and high SVR) needs epi, dopamine, milrinone.
cold shock with a low bp (low CO, low SVR) needs epi, dopamine, then norepi or dobutamine.
warm shock (low bp with high co and low svr) needs norepi, dopamine, and then vaso or epi or dobutamine
cold shock s/s
low CO, low OR high SVR, cool/cold clammy extremities, mottled, cap refill >2sec, diminished pulses, tachycardia (brady if neonate), narrow PP
Warm shock s/s
high CO, low SVR, warm/drye xtremities, flushed, cap refill flash <2sec, tachycardia, bounding pulses, wide PP
SIRS diagnosis
TWO must be present, and one MUST BE temp or wbc:
temp >38.5 or <36
high or low leukocytes (or bandemia)
tachycardia
tachypnea
SIRS Tx
recognize before it becomes sepsis/septic shock. stop the insult. manage s/s
BP is not a good indicator of altered perfusion in peds since they maintain their BP so long. so what is?
mental status, cap refill, pulses, pulse pressure, extremity temp, skin color, UOP, acidosis, lactic acid level
kidneys role in acid base
they can secrete hydrogen into urine (make body more alkalotic) and reabsorb bicarb from urine
when is a foley indicated?
acute urinary retention/bladder outlet obstruction, accurate measurements for critically ill kids, periop use, healing of open perineal/sacral wounds if incontinent, prolonged immobilization, comfort for end of life
ventilator associated event: what is and prevention
4 days of MV: 2 days of stability with deterioration after.
bundle: hand hygiene, elevate HOB, oral care, daily ERT
toxin management
ocular/dermal: irrigation
GI: NO ipecac. gastric lavage, whole bowel irrigation, activated charcoal, cathartics
supportive care
antidotes:
-acetaminophen gets n acetylcysteine
-digoxin gets digoxin fab antibodies
-opioids get naloxone
-asa gets ion trapping drugs to rapidly eliminate in alkaline environment
-benzo gets flumazenil
HD may be needed. but consult poison control.
submersion tx
fluid resuscitation, intubation, CV support, supportive care, rewarming (remove wet stuff, warm blankets, heat lamp, forced warm air blanket, warmed fluids and o2)
unintentional vs intentional abd trauma
intentional usually has multiple organs affected with inconsistent history. unintentional is usually only one organ with a consistent history. both may or may not have abd bruising
intentional burns
clear line. creases may be spared from child flexing when being dunked in. donut demarcation if put in buttocks first.
abusive head trauma and what can mimic it
leading cause of death from NAT.
comes with subdural hematoma, retinal hemorrhage, rib fracture, torn frenulum, APNEA!! note glutaric aciduria t1 can cause subdural and retinal hemorrhages.
PICS
new or worsening impairment after discharge in physical, cognitive, mental health
prevent by giving anticipatory guidance
PTSD
after exposure to a traumatic event, has persistent recollections/reminders of event and increased arousal
5 p’s of compartment syndrome
pain, pallor, pulseless, paresthesia, paralysis
absent pulse is late sign
pelvic fx
will need external fixation device and prolonged bed rest (prevent skin breakdown and continue pulm toilet like IS to prevent atelectasis)
high risk for hemorrhage, neuro injury, sacral fx
compartment syndrome
excess pressure in muscle compartment until no capillary perfusion, more in lower extremities. true surgical emergency
causes of compartment syndrome
bleeding into muscle compartment, IV infiltrate, burn and crush injuries, external forces (cast, dressing)
rhabdo physiologic manifestations
lyte disturbances from muscle cell content release as theyre destroyed: hyperkalemia, hyperphosphatemia, metabolic acidosis, hyperuricemia
high CK (higher it is, more likely the AKI), tea urine, myalgia, weak, tachy, low UOP, n/v, fever, agitation, confusion, acidosis
rhabdo causes
crush, electrical burn, burn, snake venom, long sz, malignant hyperthermia, reperfusion to damaged cells after fasciotomy
rhabdo tx
IVF: enhance clearance
tx underlying cause
correct lytes (esp hyperK)
monitor labs
+/- RRT
stage 1 PI
Non blanchable erythema and edema
stage 2 PI
partial thickness loss. partial loss of dermis with red pink wound bed withOUT slough
stage 3 PI
full thickness skin loss, may see subQ fat but bone/tendon/muscle not exposed
stage 4 PI
full thickness tissue loss, will see bone, tendon, muscle. slough/eschar may be there. often with undermining/tunneling
unstageable PI
full thickness tissue loss, depth of wound unknown tho because covered by slough/eschar
DTI
purple maroon local area of discolored but intact skin. or blood filled blister from underlying damaged soft tissue from pressure/shear
skin failure
blood shunts away from skin in critical illness > hypoperfusion of skin > skin and underlying structures begin to fail.
may not be preventable.
what Ab can cross placenta
igG
iGg role, IgM, A, E
igG: bacteria, virus, protozoa, toxins
M: nonself ABO types, bacteria
A: from milk. only coats GI tract. kills viruses
E: allergy, parasites
t cells
responsible for autoimmune dsiease, organ transplant rejection
HIV CD4
CD4<200 means AIDS, very weak immune system
what do B cells become
antibodies
when to give FFP
deficit of coag factors, plasma volume expansion with all coagulation factors
when to give cryo
decreased fibrinogen, Hemophilia A, factor XIII deficit, von Willebrand
when to give granulocytes
adjunct to infection measures in high risk pts/neonates (watch for fever)
acute hemolytic rxn
occurs with ABO incompatible blood → hemolyzes RBCs → fever, hypotension, lumbar pain (classic sign), chest pain, anxiety, shock
nonhemolytic transfsn rxn
response to leukocytes in the blood; may benefit from premeds in future and may need leukocyte reduced blood in future
TACO
pulm edema from lot volume excess from transfusion
TRALI
immune response where alveolar capillary membrane is injured because of the antibodies and then there’s an accumulation of pro-inflammatory molecules (acute onset hypoxemia, pulmonary edema; may need aggressive respiratory support)
DIC causes
infection
shock
trauma
malignancies
vascular abnormalities
snakebite
transfusion reaction
heatstroke
Sepsis
OB emergencies
Head injury
DIC lab findings
thrombocytopenia
prolonged PT, PTT
decreased fibrinogen
increased D dimer
increased fibrin degradation products
decreased coagulation factors (Protein C, S)
DIC Tx
underlying cause
blood products
ffp/cryo
organ supportive care from ischemic injury of blocked microvasculature
ITP - what is it? s/s? labs?
antibodies against own plts (immune disorder).
exact cause unknown. normal bone marrow.
previously healthy kid with recent viral illness.
has bruises, petechiae.
low PLT but NORMAL PT/PTT.
tumor lysis
triad: hyperuricemia, hyperkalemia, hyperphosphatemia.
hypocalcemia secondary to hyperphos.
hyperleukocytosis
leuks >100k.
poor prognostic if with metabolic, resp, hemorrhagic complications.
the high viscosity causes thrombi in microvasculature–>dyspnea, hypoxia, focal neuro deficits, ataxia, agitation, confusion, delirium, stupor.
sickle cell
mutated Hgb gene.
RBCs sickle in response to deoxygenation. further sickled by acidosis, hypoxemia, dehydration, hypothermia, hyperthermia.
sickled cells increase blood viscosity, occlude vessels» thrombosis , ischemia, infarction
ITP tx
often self limited.
can give steroids, IVIG, monoclonal antibodies, splenectomy, PLT transfsn
tumor lysis PPX
limit K and phos intake, hydration 2xMIVF to maximize excretion, alkalinization with NaHCO3 in MIVF for urine pH 7-8, allopurinol, EKG monitoring (hyperk)
if emergent tx, treat lytes +/- HD
hyperleukocytosis tx
goal: decrease leuks
initiate antilekemic therapy. avoid prbcs (viscosity), leukapharesis or exchange transfsn. prevent/manage tumor lysis. control complications.
what is vasoocclusive pain crisis
any organ system (spleen, lungs, brain) where small arterioles are obstructed by sickle cells causing ischemia, pain, organ dysfunction.
what triggers vasoocclusive crisis
infxn, fever, dehydration, trauma, cold, stress
vasoocclusive crisis tx
1-1.5xMIVF, o2, ABX if infxn, pain control
acute chest syndrome
severe lung related complication of sickle cell. creates PNA like illness with fever and WOB and wheezing and pain. creates lung infiltrates. leading cause of morbidity/death in sickle cell.
tx same as vasoocclusive crisis.
most common abd trauma injuries
spleen and liver (pancreas less frequent)
peds considerations that worsen abd trauma
less subq fat, more anterior organs, less blood volume»_space; rapid hypovolemia
liver injury has what kind of pain
RUQ pain radiating to R shoulder
what kind of pain is spleen
LUQ pain, also can radiate to shoulder
pancreas pain
deep epigastric pain radiating to back
cullen’s sign
bruising around umbilicus
kehr’s sign
acute pain in shoulder when laying down with legs elevated d/t blood or other irritants in peritoneal cavity
what does FAST scan look for
blood (esp blood in abd)
what kind of pain is bowel infarct/obsturction/perf
acute sudden onset of pain/tenderness in abd
what does upper GI perf lead to
hydrochloric acid and giestive enzymes and bile leak, causing peritonitis
what does lower GI perf cause
fecal material and bacteria leak causing sepsis
what doesbowel infarction cause
sepsis because of dead bowel
what does bowel obstruction present with
distention, absent bowel sounds, vomiting (probs bilious), fever
what does bowel perf present with
resp distress, acidosis, sepsis
what does peritonitis present with
pain, guarding, rebound tenderness
upper vs lower GIB
upper: proximal to upper ligament of trites (which connects to lower parts of duodenum)
what labs for GI hemorrhage
ABG-check for met acidosis
CBC
T/S
coags
lytes
LFTs
pancreatic enzymes
what access for GI hemorrhage
2 large bore IVs
GI hemorrhage management
support ABCs
fluids, blood
NGT room temp saline lavage
vaso
octreotide
endoscopic management
s/s of liver failure
hepatosplenomegaly
varices, ascites
malnutrition
pruritus
telangiectasis (spider veins)
jaundice
hepatic encephalopathy
renal failure
cogaulopathy
liver failure tx
restrict protein (encephalopathy)
decrease serum ammonia
monitor fluid, electrolyes (may require HD for hepatorenal syndrome)
manage portal HTN
manage coagulopathy
manage ascites
end stage-liver transplant (biliary atresia congenital defect will also need transplant )
postop liver transplant care
pulm toilet
treat HTN
monitor drain output
correct coagulopathies
what is intusussception preceded by
gastroenteritis
why is intusussception bad
intestinal segments fold over and telescope on themselves.
venous then arterial obstruction > perf, infarct, shock
s/s of intusussception
paroxysmal severe abd pain
bloody currant jelly stools
sausage mass in RUQ
bilious emesis
abd distention
intussusception tx
NPO, IVF
barium enema
then surgery
NEC s/s
temp instability, feeding intolerance, abd distention, guaiac pos stools, apnea, brady
late: met acidosis, thrombocytopenia, coagulopathy, shock
NEC diagnostics
abd xray: pneumatosis intestinalis, dilated bowel loops, pneumoperitoneum
abd us: intraabd free fluid
NEC tx
NPO, IVF (monitor lytes)
gastric decompression
ABX
surgery for perf, peritonitis, or deterioration
30-45% mortality
where does filtration occur in kidney
functional unit of kidney: glomerulus
normal UOPs by age
infant: 2ml/kg/hr
child: 1ml/kg/hr
adolescent: 0.5ml/kg/hr
prerenal AKI causes
decreased preload: altered heart fx/heart failure, vasodilation, altered vascular volume
manifestations of prerenal AKI
oliguria vs nonoliguria
unexplained metabolic acidosis
azotemia (high urea and Cr and other nitrogen wastes)
increased BUN, BUN/Cr ratio, urine SG>1.020
prerenal AKI tx
dc K in fluids
bolus for dehydration
diuretics to differentiate btwn prerenal and renal failure
avoid nephrotoxics
renal AKI causes
immune (glomerulonephritis, lupus)
vascular (HUS, DIC, TTP)
interstitial nephritis
trauma
nephrotoxins (ABX, contrast)
renal AKI s/s
aka intrarenal/intrinsic/ATN
oliguric phase
diuretic phase
recovery phase
postrenal aki s/s
abd / flank pain
palpable mass obstruction
failure to thrive
overall for AKI, want to avoid and prevent what?
infections!
common electrolyte imbalances of AKI
hyperkalemia
hyperphosphatemia
hyponatremia
hypocalcemia
hypo or hyper magnesemia
hyperkalemia s/s
muscle weakness
confusion
ascending paralysis
nausea
diarrhea
tall peaked T waves > wide QRS long PRI > ventricular dysrhythmias, cardiac arrest
most immediate hyperkalemia tx? what other tx are there?
insulin + hypertonic glucose.
but if cardiac unstable, give CaCl / calcium gluc first. but not if theyre on digoxin.
but sodium bicarb can also work to move K into cells or albuterol.
can also remove K by lasix, kayexalate (sodium polystyrene), HD
hyponatremia s/s
muscle twitching
tremors
weakness
abd cramps
n/v
lethargy
disorientation
seizures
coma
hyponatremia tx
underlying cause
3% saline if Na<120 or if symptomatic
frequent neuro assessments and Na monitoring
hypocalcemia caused by what
increased phosphate
decreased production of vitamin D
hypoalbuminemia
s/s hypocalcemia
tingling
Chvotsek’s
Trousseau’s (inflate BP cuff to 20mm above SBP and watch hand/finger for spasms)
muscle cramps
lethargy
seizures
hypotension
prolonged QT
hypocalcemia tx
cause
tx hyperphosphatemia
EKG
iv calcium
monitor serum Mag since hypomagnesemia can also affect correction of hypocalcemia
CKD tx
anemia tx
prevent bone loss (meds)
meds for growth
diuretics
diet restrictions
dialysis
transplant (ESRD)
HUS s/s
triad:
hemolytic anemia
thrombocytopenia
AKI
potential for multisystem involvement:
GI-perf, stricutre, bloody diarrhea, obstruction, intusussception
heme-thrombocytopenia, hemolytic anemia
renal-AKI, failure
necrotic lesions in: CNS, pulm, adrenal, cardiac
pale, lethargic, irritable, abd pain, bruising, petechiae, purpura, sz, oliguria/anuria, elevated bUN/Cr
HUS causes
e coli, salmonella, shigella, strep pneumoniae, or atypical hereditary HUS
HUS Patho
PLT aggregations and fibrin depositions in small vessels in kidney, gut, and CNS.
hemolytic anemia lyses RBC because of shearing of the RBC as they pass through the narrowed vessels.
HUS tx
early recognition, supportive care
may need peritoneal dialysis
tx complications
tx anemia
give PLTs if bleeding
manage szs
restrict PO intake if GI affected, give more calories from glucose than protein to minimize azotemia
goal: restore fluid/electrolyte balance
ADH is aka
vasopressin (which is why its used in resus events-also has vasoconstrictor effects)
where is ADH from
made in hypothalamus, released by posterior pituitary (problem in either of these areas can cause ADH imbalances)
how does ADH affect water balance
increases renal collecting ducts’ permeability to water –> decreased UOP, body holds onto water –> increased intravascular volume
what stimulates production/release of ADH
serum osmo, extracellular fluid volume, changes in arterial BP
adh is secreted in SIADH despite
despite serum hypo-osmolality, hyponatremia, euvolemia
SIADH causes
brain issues (including like meningitis, anesthesia, TBI, etc), lung diseases, pHTN, spinal fusion, malignancy, mitral valve repair
meds: morphine, barbiturates, antineoplastics, carbamazepine, acetylcholine, epi, norepi
siadh s/s other than low UOP
hyponatremia
n/v anorexia
abd cramping, diarrhea
mental status lethargy, disoriented
headache
seizures if Na<120 and/or cerebral edema
weight gain, pitting edema
SIADH labs
Na<135
serum osmo<227
BUN<10
urine osmo>200
urine SG>1.020
normal serum osmo
270-290
SIADH primary tx, goal
MIVF restriction/fluid restriction to 75% maintenance
main goal to normalize serum sodium, osmo, and prevent or correct neuro sequelae
siadh tx other than fluid stuff
hyper sal ifffff neuro effects with goal to raise Na by 0.5-1meq/hr, dosing 2-4mg/kg
loop diuretics like lasix 1mg/kg
DI causes
neurogenic vs nephrogenic
neurogenic: ADH deficiency from failure to sythesize, failure to secrete, or a combo.
nephrogenic: no deficiency. normal secretion. renal system is resistant to ADH’s effects.
brain tumor, TBI, neurosurgery, pituitary lesions, hypothalamic lesions
DI s/s
AMS, seizures, coma, weakness,
twitching,
THIRST,
UOP>4ml/kg/hr, dilute urine, hypovolemia s/s (hypovolemic shock posisble if not tx)
DI labs
serum osmo>300
Na>145
urine osmo<200
urine spec grav <1.005
imaging studies
DI tx/goal
goal: correct dehydration and slowly correct hypernatremia
bolus fluid
replace ongoing losses
ADH replacement: gtt titrated to a goal UOP, IM/SC, intranasal if chronic
do not decrease Na faster than 0.5-1meq/hr
monitor labs and urine and weights
5 hormones for energy production/glucose homeostasis
insulin
glucagon
epi
cortisol
growth hormone
insulin is what kind of hormone
anabolic hormone
insulin secreted where and why
by B-islet cells of pancreas in response to increased serum glucose to increase glucose uptake in cells, stimulate glycogenesis, protein synthesis, formation of adipose tissue
glucagon secreted where and why
by pancreas in response to low serum glucose to stimulate glycogenolysis and gluconeogenesis
what can neonatal sepsis present as in terms of glucose
hypoglycemia, hyperglycemia, and glucosuria
hypoglycemia threshold, s/s, causes
BG<50
seizures, tremors, jittery, ALOC, depressed cardiac function, apnea, tachy, diaphoresis, anxiety, hunger
hypoglycemia may also be caused by hypopituitarism, adrenal insufficiency, liver failure, inborn errors
hypoglycemia tx
0.5-1g/kg of D25
how to decrease PaCo2
increase rate or TV
increase PIP
decrease PEEP
patho of DKA
underproduction of insulin with rising serum glucose > alternative pathways activated > body must use fats instead of glucose > acetoacetic acids formed and converted to ketones > metabolic acids from fatty acid oxidation accumulate resulting in acidosis
lactate is also produced from alternate pathways causing acidosis
elevated serum glucose elevates serum osmo resulting in diuresis
DKA s/s and labs
polydipsia, phagia, uria
slightly elevated BUN
weight loss
glucose >200
ketonuria
ketonemia
pH<7.2, HCO3<15
hyperkalemia (r/t acidosis)
hyperphosphatemia
Hyponatremia
hyperosmolarity (from hyperglycemia) > osmotic diuresis > dehydration > hypovolemic shock
AMS/signs of high ICP
tachycardia
hypotension (may be late sign r/t hypovolemic shock)
poor peripheral perfusion
tachypnea
Kussmauls deep rapid labored breaths (trying to blow off Co2)
acetone breath
abd tenderness, n/v
concurrent infxn
DKA tx
ensure airway/breathing
volume resuscitate if in shock
otherwise cautious fluid replacement
-IV access
-bolus 20ml/kg
-replace fluid volume deficit (typically 10-20% dehydration) + maintenance fluid over 48h
insulin 0.05-0.1 u/kg/hr regular insulin IV
-don’t drop glucose by more than 50-100 per hr
-add glucose to fluids once serum levels are 250-300
correct lytes
-replace K and PO4 by adding to IVF
-avoid single doses
DKA cerebral edema
rare but significant
risks with young age, first DKA, increased BUN, decreased CO2, insulin bolus, rapid glucose correction, aggressive fluids, use of BICARB
tx like normal cerebral edema
PKU
cannot metabolize protien (amino acid phenylalanine)
major effects on CNS>retardation
Guthrie blood test (most states all newborns)
FTT, hyperactivity, vomiting
restrict phenylanine, maintain serum level 2-8, special milk substitutes
galactosemia
no milk even breast milk.
may heave jaundice, diarrhea, hepatosplenomegaly, lethargy, hypotonia, cataracts
lactose free soy formula
croup sounds
upper airway sounds: dyspnea, stridor, hoarse, barky cough. no crackles/rales tho (thatd be distal lung disease)
normal serum aminophyllin
10-20mcg/ml
aerosol asthma meds
epi, albuterol, terb, isoproterenol, atropine, isoetharine, metaproterenol
bronchiolitis also has air trapping t/f
true: with low fever, WOB, nonproductive cough, etc
BPD pts have increased risk for?
bronchiolitis with air trapping
normal mixed venous po2
35-40
normal mixed venous sat svo2
60-80
DI priority tx
restore fluid. THEN ddavp
half life IV insulin
3-5min
transplant rejection PPX meds
tacro, azathioprine, cyclosporin (dont use too soon postop-can cause htn and hUS), methylpred, FK506
what is calcium inverse with
po4 (maybe also mag)
normal Ca
K
mag
phos
Cl
bicarb
Ca:8.5-11
K: 3-5
mag: 1.5-2.5
phos: 3-5.5
cl: 102-112
bicarb: 18-29
normal WBC, hgb, hct
WBC: 4.5-17
hgb: 11.5-14.5
hct: 33-43%
how to increase paco2
decrease PIP
increase PEEP
decrease rate
how to decrease pao2
decrease PIP
decrease PEEP
decrease I/E ratio
how to increase pao2
increase PIP
increase PEEP
no change to rate, does not affect
increase I/E ratio
normal LAP
2-15
normal RAP
2-8
normal pulmonary artery pressure
<2/3 SBP
RDS is from?
decreased surfactant
BPD is?
need for o2 longer than 28days after birth
from overinflation and etelectasis
has increased pulm vascular resistance, PHTN, cor pulmonale
key: hypercarbia, hypoxemia
when might cervical SCI result in chronic ventilation
3rd-5th vertebrae
meningococcemia
this is sepsis cause by n meningitidis. classically comes with purpura fulminans: petechial purpuric rash from coagulation of microvasculature
stroke to imaging time
30 mins from door to CT
noncontrast CT, CT angio, and MRI
goal aPTT on heparin infusion (only for stroke goal?)
60-85seconds
early septic shock presentation
hyperdynamic state with elevated CO and decreased SVR with flushing, warm arms/legs, bounding pulses, wide PP (later CO falls, hypotension, worse met acidosis)
where do u zero art line to
right atrium using mid axillary, 4th intercostal space (nipple line)
heliox
lower density, promotes laminar flow in upper/lower airways. less turbulent. promotes delivery of o2 and inhaled meds through areas of obstruction.
for croup
what do a waves on icp monitoring mean
plateau waves that usually appear when already high ICP becomes critically high from hypercapnia, hypoxia, cerebral edema. call MD
hypokalemia EKG findings
flat/inverted T, increased P wave amplitude, prolonged PRI, U waves, PVCs
tricyclic antidepressant OD
depressed LOC, sz, vent arrhythmias, acidosis, dry mouth (anticholinergics), dilated pupils, blurry vision
-amitriptyline, noritriptyline, doxepin, clomipramine (fluoxetine is SSRI)
metoclopramide
treats GERD (normally treats gerd by stimulating gut motility aka prokinetic), gastroparesis, n/v
carbamazepine OD
dizzy, diplopia, drowsy, blurred vision, headache, ataxia, n/v, hyponatremia, resp depression, prolonged PT/PTT
PHB OD
CNS depression, sedation, rash, paradoxical excitement, hyperactivity
clonidine OD
sedation, dry mouth, drowsiness, headache, bradycardia
theophylline OD
GIB, sz, palpitations
class 1 drugs
sodium channel blockers: procainamide, lidocaine, quinidine.
decrease automaticity and conduction velocity.
class 2 drugs
beta blockers
class 3 drugs
potassium channel blockers: sotalol
delays repolarization and increases refractory time
class 4 drugs
calcium channel blockers: amlodipine, nicardipine, diltiazem, verapamil
treat SVT but not ventricular arrhtyhmias.
contraindicated in WolffParkinson White.
status epilepticus
1st line benzos like rectal diazepam.
if continue, then fospheny/pheny
what does ventricular preexcitation show as on EKG
initial portion of QRS is prolonged with initial slurring. appears as delta waves
acute esophageal bleeding varices tx
octreotide, vasopressin
what to check before giving digoxin and why
potassium and PRI.
hypokalemia aggravates digoxin cardiac toxicity. digoxin can cause arrhythmias and heart block. (indicated by long PRI)
autonomic dysreflexia s/s
happens below level of injury, something uncomfortable
HTN, bradycardia, flushing, sweating, headache, nasal congestion
halperidol side effects
parkinsonianism (slow, stiff, tremor, issues w balance and walking)
tardive dyskinesia (uncontrollable facial movements like lip smacking, tongue thrusting, rapid blinking)
acute dystonia (involuntary muscle contractions, abnormal movements/postures)
What does sudden increase in ETCO2 indicate?
malignant hyperthermia
or
ventilation of a previously unventilated lung.
gradual increase would be rising body temp or hypoventilation
sudden fall is equipment failure or dislodged
continuous exponential drop may be pulmonary embolus
Dopamine vs dobutamine
Dopamine for perfusion and can help renal perfusion. Dobutamine for better cardiac output and heart perfusion
Phenylephrine used for?
Hypercyanotic spells in: tet, SVT, severe hypotension
Digoxin can worsen what
Outflow tract obstructions so use with caution for things like tet
