all Flashcards

1
Q

normal cardiac output

A

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

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2
Q

what 4 things affects SV

A

preload, afterload, contractility, compliance

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3
Q

cardiac index

A

CI = CO/BSA.
normal 3-4.2L/min/m2 regardless of body size.

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4
Q

what is EF

A

volume ejected vs volume remaining in LV

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5
Q

preload?

A

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)

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6
Q

MAP

A

MAP=(COxSVR)+CVP

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7
Q

SNS stim releases what

A

norepi

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8
Q

parasympathethic stim releases what

A

acetylcholine with acts on right and left vagus nerve for relaxation of HR and conduction

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9
Q

alpha adrenergic receptors stim causes what

A

arterial vasoconstriction and increased intracellular calcium

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10
Q

stim of beta1 adrenergic receptors causes what

A

(dobutamine,norepi) increased SA node, increased inotropy, chronotropy, AV conduction

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11
Q

b2 adrenergic stim causes what

A

smooth muscle relaxation, bronchodilation

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12
Q

cardiac failure

A

failure of heart to maintain CO sufficient for body metabolic demands

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13
Q

left heart failure heart sound

A

s3 heart sound

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14
Q

pulmonary vascular resistance increases in response to?

A

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

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15
Q

cvp increased or decreased in right heart failure? what about pvr?

A

both increased

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16
Q

labs in heart failure

A

dilutional changes (anemia, hyponatremia, hypocalcemia, hypoglycemia), end organ dysfx: proteinuria, increased lactate, acidsosis, increased WBC, polycythemia, BNP levels

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17
Q

meds (for heart failure)

A

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

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18
Q

dilated cardiomyopathy

A

most common type in kids.
aka congestive cardiomyopathy d/t s/s of CHF with decreased SV and EF.

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19
Q

hypertrophic cardiomyopathy

A

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.

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20
Q

restrictive cardiomyopathy

A

from fibrosis and scarring (defective endocardium). has minimal contraction so decreased diastolic function with normal systolic. poorest prognosis.

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21
Q

Dilated cardiomyopathy tx

A

vasoactives, inotropes, diuretics, afterload reduction, ACE-I (prils-angioedema) or angiotensin II receptor blockers (sartans)

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22
Q

whatdo calcium channel blockers do? and what condition are they good for

A

afterload reduction (HTN crisis), decrease contractility, improve LV function

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23
Q

myocarditis vs endo

A

myo usually virus. endo usually bacteria

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24
Q

pericarditis heart symptom

A

cardiac tamponade, rub.

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25
fetal heart develops when?
4-7 weeks
26
dvt diagnosis
usually look at symptoms + US but sometimes asymptomatic. can also do angio with contract and venogram
27
prevent DVT
scds, turns, low molecular weight heparint
28
tx dvt
thrombectomy, once again low molecular wt heparin, observation
29
superior vena cava syndrome causes
CVC, thrombosis, mediastinal malignancy
30
SVCS dx
xray (might find mass), CTs
31
svcs tx
depends on cause - can be thrombolytic, anticoag, supportive, remove cvc
32
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
33
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)
34
PFO
l to R shunt.
35
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
36
hyperoxia test
when giving hyperoxygenation to newborn, cyanosis worsens, then they fail the test. most likely have a CHD
37
syndromes associated with CHD
t21 (avsd), t18 (edwards)-HLHS and VSD, 45x (turners)-VSD and coarc, williams, digeorge-truncus, noonan
38
acyanotic with increased PBF
PDA, VSD, ASD, AVSD
39
acyanotic with ventricular outflow obstruction
AS, CoA, PS
40
cyanotic with decreased PBF
tet, tricuspid atresia
41
cyanotic with increased PBF
transposition of great arteries, truncus arteriosus, total anomalous pulmonary venous return, HLHS
42
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
43
requires PDA
AS, CoA, can be TGA, HLHS
44
postop coarc repair monitor for what?
HTN
45
tet
PS with RVH, overriding aorta (sits over both ventricles), large VSD more severe the PS, more severe the cyanosis
46
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
47
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
48
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.
49
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).
50
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
51
TAPVR
pulm veins drain into systemic veins or RA instead of LA. total (all 4 veins) or partial. needs immediate surgical repair.
52
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
53
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.
54
digoxin adverse effects and considerations
55
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.
56
septal surgeries rhythm disturbance
heart block, conduction delay
57
what does high RAP or CVP mean
RV failure or PHTN
58
what does low lAP mean
hypovolemiaw
59
hat does high LAP mean
LV failure or high LV afterload
60
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.
61
cardiopulmonary bypass postop
may need 50% maintenance x24h, sodium restriction or free water restriction, electrolyte monitoring, glucose monitoring, renal function monitoring and UOP monitoring
62
postop neonatalheart procedure monitor for?
monitor babies for NEC. NEC can also be associated with umbilical lines
63
64
Therapeutic digoxin serum level
1.1-2.2ng/ml
65
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
66
Restrictive cardiomyopathy tx
Tx: CHF management, diuretics, digitalis, vasodilators, antiarrhythmics, transplant
67
cardiac cath complications other than hematoma
arrhythmias, air emboli, MI, perforation, infection
68
inotropes do what
work through alpha and beta receptors to vasodilate, vasoconstrict, and/or enhance contractility
69
chronotropes work by what
change HR by affecting nerves controlling the heart, or by changing rhythm from the SA node (pacemaker of heart)
69
what to cholinergic drugs stimulate
(acetylcholine, bethanacol) pns
69
what do beta adrenergic drugs stimulate
SNS
69
what do anticholinergic drugs stimulate
(clozapine, quetiapine, atropine, oxybutynin, robinul, ipratropium, promethazine, noritriptyline): SNS anticholinergic drugs = CQ PARONI
70
what do beta blockers stimulate
PNS
71
what do type 1 epithelial cells do
gas exchange
71
what do type 2 epithelial cells do
produce surfactant
72
are lungs more or less compliant when youre younger
less
73
when are fetal lungs capable of gas exchange
22-24 wks (when alveoli develop)
74
where are co2 sensors / o2 sensors
brainstem o2 sensors: carotid bodies
75
is cyanosis an early or late sign of hypoxemia
late
76
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
77
what does a WNL RR for a sick/injured child indicate
impending respiratory arrest
78
what age are kids obligatory nose breathers
until 6 mos of age (NG can impair breathing up to this point)
79
normal VQ ratio
0.8 (slightly more blood flow than aeration)
80
what is alveolar dead space
areas of alveoli that are seeing ventilation but not perfusion
81
what is an intrapulmonary shunt? examples?
when alveoli are not ventilated but are perfused. asthma, atelectasis, ARDS, pleural effusion
82
how do you determine presence of an intrapulmonary shunt?
normally pao2/fio2 should be >286, if this number is decreased you have a shunt.
83
what does PEEP do
increases alevolar volume, increases FRC, moves pulmonary water (edema) out
84
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
85
what is 2,3 DPG
an intracellular RBC factor that determines hgb affinity for o2
86
acut respiratory failure definition
inability of resp system to meet demands of o2 ORRR also inability to provide adequate co2 elimination causing resp acidosis
87
acute respiratory failure causes (other than the lungs)
CNS issues, upper airway disorder, CV or heme disorders
88
what can trigger apnea of prematurity
ambient temp changes, vagal stimualtion (suction, gagging)
89
transient tachypnea of newborn
from c section or precipitous delivery (lung fluid not squezed out as in normal vag delivery)
90
choanal atresia
openings from nasal cavity occluded - manifests in delivery rm(obligate nose breather)-dyspnea worsens with mouth closure. OPA / intubate until surgery
91
where should tip of ETT end
no lower than 1-2cm above carina, no higher than 1st rib
92
determine appropriate ETT size
(age in yrs/4) + 4 so 16 yr old gets size 8
93
what to avoid when leading up to extubation
no PO intake or CPT 2-4hrs prior to and post extubation (aspiration)
94
upper airway edema tx post extubation
steroids, rac epi, neb saline, heliox
95
what do increased PIPs on vent mean?
ARDS, decreased compliance, pneumo, secretions, kinked tubing
96
nutrition while on MV
low carbs (to avoid increasing co2), low triglycerides, high fat for calories
97
cons of PEEP
low CO from impaired venous return and high ICP from impaired cerebral venous return
98
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
99
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
100
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
101
PNA causes and diagnosis
viral, bacterial. dx: CXR, secretions, blood cx, bronchoalveolar lavage, lung biopsy if severe, pleural fluid
102
hydrocarbon PNA aspiration
gas, nail polish, solvent, propellants. treat aggressively. necrosis of tissue can occur. similar to ARDS
103
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
104
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
105
croup diagnosis
A/P CXR with steeple sign(narrow glottis and subglottic airway). lateral XR with normal epiglottis
106
croup tx
heliox, rac epi, cool humidified o2, steroids, antipyretics, enteral feeds, hydration, minimize agitation
107
epiglottitis prevalence, cause
2-6yr old usually h flu (Hib vaccine). can be bacterial. acute infxn can resolve in 24-72hrs
108
epiglottitis s/s
four ds and s: drooling, dysphagia, dysphonia, distress, stridor. abrupt onset. fever, sore throat, tripoding.
109
epiglottitis dx
lateral neck XR thumb sign (thickened epiglottis)
110
bronchiolitis peak incidence and cause
mid winter-early spring usually RSV but can be flu, hmpv
111
bronchiolitis tx
o2, intubate if needed, albuterol, terbutaline, aminophylline, hydration, ribovirin if RSV
112
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)
113
pneumo tx
chest tube. tension pneumo: needle decompress then chest tubein
114
sucking chest wound
open pneumo, air in and out. flail chest. tx with PPV, cover with occlusive drssing, place chest tube.
115
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.
116
goal of status asthma tx
goal to restore airway patency, reverse bronchospasm, control inflammatory response, and decrase secretions/plugs.
117
vent settings for an asthmatic
permissive hypercarbia, prolonged expiratory time, conservative PEEP, watch for pneumo!
118
pulsus paradoxus
n exaggerated fall in a patient's blood pressure during inspiration by greater than 10 mm Hg.
119
beta 2 agonists
alb, levalb, terbutaline (systemic), metaproterenol,salmeterol
120
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
121
pts at risk for PE
sickle cell, nephrotic syndrome, cancer, chemo, hypercoaguable state (inherited), vasculitis
122
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
123
PHTN mean pulm artery pressure? what kind of shunt?
>25mmHg at rest. right to left shunt
124
preductal/postductal sats in PHTN
preductal pao2> postductal
125
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
126
BPD pts are sensitive to?
overhydration
127
bpd comes with?+s/s
PHTN > right heart failure, FTT, barrel chest, bronchospasms (LS can be crackly, wheezy, rales)
128
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
129
CDH babies present as
full term full birth weight infant who soon develops severe resp distress
130
CDH comes with
PHTN d/t lung hypoplasia, increased pulm vascular resistance.
131
CDH s/s
scaphoid abd, PMI shift, WOB, decreased/absent LS, increased chest diameter, PHTN
132
CDH CXR
gas filled bowel loops in thorax
133
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)
134
CDH postop chest tube
on affected side without suction (gradual reexpansion). position onto the affected side to expand the good lung
135
TEF most common type
type c: esophageal atresia with distal TEF
136
TEF hx
prenatal polyhydramnios
137
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
138
respiratory alkalosis causes
CNS injury, ASA ingestion, Reye's, hepatic encephalopathyrespi
139
where is CSF produced
choroid plexus: lateral, 3rd, 4th ventricles.
139
where is csf absorbed
flows freely thru subarachnoid space then absorbed by arachnoid villi
140
corpus callosum
connects brain hemispheres with nerves
141
basal ganglia purpose
controls motor function (deep in gray matter of hemispheres)
142
thalamus function
pain center, temp, tactile sensation
143
hypothalamus function
secrete ADH, Oxytocin, body temp, sweat, salivary
144
cerebellum function
balance, coordination
145
brain stem function
respiratory center
146
meninges
pia mater (inner, vascular), arachnoid (middle, feathery), dura mater (outer, tough)
147
anterior fontanelle closes at
16-18 mos
148
posterior font closes at
2 mos
149
normal ICP
5-15 (<15)
150
cushing's triad
late ominous sign of high ICP. bradycardia, htn with wide PP, irreg resps that become apnea
151
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
152
gold standard icp monitoring
intraventricular
153
zero EVD where
with external auditory meatus which approximates the level of foramen of monroe
154
what does the brain stem include
pons, midbrain, medulla
155
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
156
communicating vs noncommunicating hydrocephalus
comm: arachnoid villi unable to reabsorb CSF (ie meningitis) noncomm: obstruction to flow (ie tumor, cyst, inflammation)
157
encephalopathy: what is, causes
general disturbance in brain cellular metabolism causing ALOC. from HIE, lead poisoning, HTN, metabolic dx
158
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
159
moya moya
rare. blood vessels of internal carotids are narrowed, brain creates collaterals
160
stroke imaging
noncontrast head CT differentiates ischemic vs hemorrhagic stroke. CTA evaluates intracranial and extracranial circulation. MRI (echo to r/o cardiac embolus)
161
stroke tx
control HTN, Fever, glucose o2/ventilation heparin, tPA ASA to prevent future strokes
162
AVM tx
not all are operable. surgery total excision, embolization, sterotactic radiosurgery, and supportive care
163
goal for TBI Tx
maintain CPP, prevent secondary injury, symptom management
164
concussion
blow to head without radiographic findings: can last months.
165
brain contusion
bruise on brain: may have ICPs/szs
166
coup, contrecoup
Coup: injury to side of head that was struck Contrecoup: injury to opposite side of brain
167
signs of basilar skull fx
racoon eyes, battle sign behind ear. no NGT! look for CSF/rhinorrhea/otorrhea
168
diffuse axonal injury
accel-deceleration injury from MVA, abuse. poor neuro exam with a normal CT
169
epidural hematoma
ARTERIAL bleed in middle meningeal artery, more in older kids. lucid > LOC often associated with skull fracture
170
subdural hematoma
VENOUS bleed. more in infants. from birth trauma, falls, intentional
171
when do u start assessing for brain death
24h after injury or resus
172
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).
173
brain death tests
1. no cortex function, in coma (flaccid, no movement, no response to stimuli) 2. 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 3. apnea when co2 goes up
174
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)
175
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.
176
if some parts of brain death exam cant be compelted?
ancillary tests: can do 4 vessel cerebral angio, radionuclide CBF, EEG
177
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
178
acute SCI tx
stabilize (traction, fixation), supportive. steroids no longer recommended. if neuro shock, give volume and norepi
179
viral meningitis CSF
slight increase WBC, normal/slight increase protein, normal glucose. negative gram stain, negative culture
180
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
181
kernig sign
for meningitis pain with extension of legs
182
brudzinski sign
for meningitis flexion of neck causes involuntary bending of hip and flexion of knee
183
monitor what in meningitis?
lytes: watching for SIADH/DI
184
febrile sz age
6 mos - 6 yrs
185
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
186
arnold chiari malformation
spinal cord travels into skull, causes hydrocephalus, may need shunt
187
severe sepsis definition
sepsis plus 2 or more organ systems dysfunctioning
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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
189
septic shock first hour goals
maintain airway/o2/ventilation, restore/maintain circulation and perfusion, give ABX, normal VS, normal mental status
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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
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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
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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
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why check cortisol in septic shock
cortisol regulates catecholamine synthesis, responsiveness of adrenergic receptors, and cell membrane stability
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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
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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
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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
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Warm shock s/s
high CO, low SVR, warm/drye xtremities, flushed, cap refill flash <2sec, tachycardia, bounding pulses, wide PP
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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
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SIRS Tx
recognize before it becomes sepsis/septic shock. stop the insult. manage s/s
200
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
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kidneys role in acid base
they can secrete hydrogen into urine (make body more alkalotic) and reabsorb bicarb from urine
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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
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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
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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.
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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)
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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
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intentional burns
clear line. creases may be spared from child flexing when being dunked in. donut demarcation if put in buttocks first.
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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.
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PICS
new or worsening impairment after discharge in physical, cognitive, mental health prevent by giving anticipatory guidance
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PTSD
after exposure to a traumatic event, has persistent recollections/reminders of event and increased arousal
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5 p's of compartment syndrome
pain, pallor, pulseless, paresthesia, paralysis absent pulse is late sign
212
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
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compartment syndrome
excess pressure in muscle compartment until no capillary perfusion, more in lower extremities. true surgical emergency
214
causes of compartment syndrome
bleeding into muscle compartment, IV infiltrate, burn and crush injuries, external forces (cast, dressing)
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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
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rhabdo causes
crush, electrical burn, burn, snake venom, long sz, malignant hyperthermia, reperfusion to damaged cells after fasciotomy
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rhabdo tx
IVF: enhance clearance tx underlying cause correct lytes (esp hyperK) monitor labs +/- RRT
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stage 1 PI
Non blanchable erythema and edema
219
stage 2 PI
partial thickness loss. partial loss of dermis with red pink wound bed withOUT slough
220
stage 3 PI
full thickness skin loss, may see subQ fat but bone/tendon/muscle not exposed
221
stage 4 PI
full thickness tissue loss, will see bone, tendon, muscle. slough/eschar may be there. often with undermining/tunneling
222
unstageable PI
full thickness tissue loss, depth of wound unknown tho because covered by slough/eschar
223
DTI
purple maroon local area of discolored but intact skin. or blood filled blister from underlying damaged soft tissue from pressure/shear
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skin failure
blood shunts away from skin in critical illness > hypoperfusion of skin > skin and underlying structures begin to fail. may not be preventable.
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what Ab can cross placenta
igG
225
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
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t cells
responsible for autoimmune dsiease, organ transplant rejection
227
HIV CD4
CD4<200 means AIDS, very weak immune system
228
what do B cells become
antibodies
229
when to give FFP
deficit of coag factors, plasma volume expansion with all coagulation factors
230
when to give cryo
decreased fibrinogen, Hemophilia A, factor XIII deficit, von Willebrand
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when to give granulocytes
adjunct to infection measures in high risk pts/neonates (watch for fever)
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acute hemolytic rxn
occurs with ABO incompatible blood → hemolyzes RBCs → fever, hypotension, lumbar pain (classic sign), chest pain, anxiety, shock
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nonhemolytic transfsn rxn
response to leukocytes in the blood; may benefit from premeds in future and may need leukocyte reduced blood in future
234
TACO
pulm edema from lot volume excess from transfusion
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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)
236
DIC causes
infection shock trauma malignancies vascular abnormalities snakebite transfusion reaction heatstroke Sepsis OB emergencies Head injury
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DIC lab findings
thrombocytopenia prolonged PT, PTT decreased fibrinogen increased D dimer increased fibrin degradation products decreased coagulation factors (Protein C, S)
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DIC Tx
underlying cause blood products ffp/cryo organ supportive care from ischemic injury of blocked microvasculature
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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.
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tumor lysis
triad: hyperuricemia, hyperkalemia, hyperphosphatemia. hypocalcemia secondary to hyperphos.
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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.
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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
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ITP tx
often self limited. can give steroids, IVIG, monoclonal antibodies, splenectomy, PLT transfsn
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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
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hyperleukocytosis tx
goal: decrease leuks initiate antilekemic therapy. avoid prbcs (viscosity), leukapharesis or exchange transfsn. prevent/manage tumor lysis. control complications.
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what is vasoocclusive pain crisis
any organ system (spleen, lungs, brain) where small arterioles are obstructed by sickle cells causing ischemia, pain, organ dysfunction.
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what triggers vasoocclusive crisis
infxn, fever, dehydration, trauma, cold, stress
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vasoocclusive crisis tx
1-1.5xMIVF, o2, ABX if infxn, pain control
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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.
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most common abd trauma injuries
spleen and liver (pancreas less frequent)
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peds considerations that worsen abd trauma
less subq fat, more anterior organs, less blood volume >> rapid hypovolemia
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liver injury has what kind of pain
RUQ pain radiating to R shoulder
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what kind of pain is spleen
LUQ pain, also can radiate to shoulder
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pancreas pain
deep epigastric pain radiating to back
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cullen's sign
bruising around umbilicus
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kehr's sign
acute pain in shoulder when laying down with legs elevated d/t blood or other irritants in peritoneal cavity
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what does FAST scan look for
blood (esp blood in abd)
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what kind of pain is bowel infarct/obsturction/perf
acute sudden onset of pain/tenderness in abd
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what does upper GI perf lead to
hydrochloric acid and giestive enzymes and bile leak, causing peritonitis
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what does lower GI perf cause
fecal material and bacteria leak causing sepsis
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what doesbowel infarction cause
sepsis because of dead bowel
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what does bowel obstruction present with
distention, absent bowel sounds, vomiting (probs bilious), fever
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what does bowel perf present with
resp distress, acidosis, sepsis
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what does peritonitis present with
pain, guarding, rebound tenderness
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upper vs lower GIB
upper: proximal to upper ligament of trites (which connects to lower parts of duodenum)
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what labs for GI hemorrhage
ABG-check for met acidosis CBC T/S coags lytes LFTs pancreatic enzymes
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what access for GI hemorrhage
2 large bore IVs
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GI hemorrhage management
support ABCs fluids, blood NGT room temp saline lavage vaso octreotide endoscopic management
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s/s of liver failure
hepatosplenomegaly varices, ascites malnutrition pruritus telangiectasis (spider veins) jaundice hepatic encephalopathy renal failure cogaulopathy
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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 )
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postop liver transplant care
pulm toilet treat HTN monitor drain output correct coagulopathies
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what is intusussception preceded by
gastroenteritis
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why is intusussception bad
intestinal segments fold over and telescope on themselves. venous then arterial obstruction > perf, infarct, shock
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s/s of intusussception
paroxysmal severe abd pain bloody currant jelly stools sausage mass in RUQ bilious emesis abd distention
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intussusception tx
NPO, IVF barium enema then surgery
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NEC s/s
temp instability, feeding intolerance, abd distention, guaiac pos stools, apnea, brady late: met acidosis, thrombocytopenia, coagulopathy, shock
277
NEC diagnostics
abd xray: pneumatosis intestinalis, dilated bowel loops, pneumoperitoneum abd us: intraabd free fluid
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NEC tx
NPO, IVF (monitor lytes) gastric decompression ABX surgery for perf, peritonitis, or deterioration 30-45% mortality
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where does filtration occur in kidney
functional unit of kidney: glomerulus
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normal UOPs by age
infant: 2ml/kg/hr child: 1ml/kg/hr adolescent: 0.5ml/kg/hr
281
prerenal AKI causes
decreased preload: altered heart fx/heart failure, vasodilation, altered vascular volume
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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
283
prerenal AKI tx
dc K in fluids bolus for dehydration diuretics to differentiate btwn prerenal and renal failure avoid nephrotoxics
284
renal AKI causes
immune (glomerulonephritis, lupus) vascular (HUS, DIC, TTP) interstitial nephritis trauma nephrotoxins (ABX, contrast)
285
renal AKI s/s
aka intrarenal/intrinsic/ATN oliguric phase diuretic phase recovery phase
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postrenal aki s/s
abd / flank pain palpable mass obstruction failure to thrive
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overall for AKI, want to avoid and prevent what?
infections!
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common electrolyte imbalances of AKI
hyperkalemia hyperphosphatemia hyponatremia hypocalcemia hypo or hyper magnesemia
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hyperkalemia s/s
muscle weakness confusion ascending paralysis nausea diarrhea tall peaked T waves > wide QRS long PRI > ventricular dysrhythmias, cardiac arrest
290
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
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hyponatremia s/s
muscle twitching tremors weakness abd cramps n/v lethargy disorientation seizures coma
292
hyponatremia tx
underlying cause 3% saline if Na<120 or if symptomatic frequent neuro assessments and Na monitoring
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hypocalcemia caused by what
increased phosphate decreased production of vitamin D hypoalbuminemia
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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
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hypocalcemia tx
cause tx hyperphosphatemia EKG iv calcium monitor serum Mag since hypomagnesemia can also affect correction of hypocalcemia
296
CKD tx
anemia tx prevent bone loss (meds) meds for growth diuretics diet restrictions dialysis transplant (ESRD)
297
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
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HUS causes
e coli, salmonella, shigella, strep pneumoniae, or atypical hereditary HUS
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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.
300
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
301
ADH is aka
vasopressin (which is why its used in resus events-also has vasoconstrictor effects)
302
where is ADH from
made in hypothalamus, released by posterior pituitary (problem in either of these areas can cause ADH imbalances)
303
how does ADH affect water balance
increases renal collecting ducts' permeability to water --> decreased UOP, body holds onto water --> increased intravascular volume
304
what stimulates production/release of ADH
serum osmo, extracellular fluid volume, changes in arterial BP
305
adh is secreted in SIADH despite
despite serum hypo-osmolality, hyponatremia, euvolemia
306
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
307
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
308
SIADH labs
Na<135 serum osmo<227 BUN<10 urine osmo>200 urine SG>1.020
309
normal serum osmo
270-290
310
SIADH primary tx, goal
MIVF restriction/fluid restriction to 75% maintenance main goal to normalize serum sodium, osmo, and prevent or correct neuro sequelae
311
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
312
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
313
DI s/s
AMS, seizures, coma, weakness, twitching, THIRST, UOP>4ml/kg/hr, dilute urine, hypovolemia s/s (hypovolemic shock posisble if not tx)
314
DI labs
serum osmo>300 Na>145 urine osmo<200 urine spec grav <1.005 imaging studies
315
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
316
5 hormones for energy production/glucose homeostasis
insulin glucagon epi cortisol growth hormone
317
insulin is what kind of hormone
anabolic hormone
318
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
319
glucagon secreted where and why
by pancreas in response to low serum glucose to stimulate glycogenolysis and gluconeogenesis
320
what can neonatal sepsis present as in terms of glucose
hypoglycemia, hyperglycemia, and glucosuria
321
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
322
hypoglycemia tx
0.5-1g/kg of D25
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how to decrease PaCo2
increase rate or TV increase PIP decrease PEEP
324
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
325
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
326
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
327
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
328
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
329
galactosemia
no milk even breast milk. may heave jaundice, diarrhea, hepatosplenomegaly, lethargy, hypotonia, cataracts lactose free soy formula
330
croup sounds
upper airway sounds: dyspnea, stridor, hoarse, barky cough. no crackles/rales tho (thatd be distal lung disease)
331
normal serum aminophyllin
10-20mcg/ml
332
aerosol asthma meds
epi, albuterol, terb, isoproterenol, atropine, isoetharine, metaproterenol
333
bronchiolitis also has air trapping t/f
true: with low fever, WOB, nonproductive cough, etc
334
BPD pts have increased risk for?
bronchiolitis with air trapping
335
normal mixed venous po2
35-40
336
normal mixed venous sat svo2
60-80
337
DI priority tx
restore fluid. THEN ddavp
338
half life IV insulin
3-5min
339
transplant rejection PPX meds
tacro, azathioprine, cyclosporin (dont use too soon postop-can cause htn and hUS), methylpred, FK506
340
what is calcium inverse with
po4 (maybe also mag)
341
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
342
normal WBC, hgb, hct
WBC: 4.5-17 hgb: 11.5-14.5 hct: 33-43%
343
how to increase paco2
decrease PIP increase PEEP decrease rate
344
how to decrease pao2
decrease PIP decrease PEEP decrease I/E ratio
345
how to increase pao2
increase PIP increase PEEP no change to rate, does not affect increase I/E ratio
346
normal LAP
2-15
347
normal RAP
2-8
348
normal pulmonary artery pressure
<2/3 SBP
349
RDS is from?
decreased surfactant
350
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
351
when might cervical SCI result in chronic ventilation
3rd-5th vertebrae
352
meningococcemia
this is sepsis cause by n meningitidis. classically comes with purpura fulminans: petechial purpuric rash from coagulation of microvasculature
353
stroke to imaging time
30 mins from door to CT noncontrast CT, CT angio, and MRI
354
goal aPTT on heparin infusion (only for stroke goal?)
60-85seconds
355
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)
356
where do u zero art line to
right atrium using mid axillary, 4th intercostal space (nipple line)
357
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
358
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
359
hypokalemia EKG findings
flat/inverted T, increased P wave amplitude, prolonged PRI, U waves, PVCs
360
tricyclic antidepressant OD
depressed LOC, sz, vent arrhythmias, acidosis, dry mouth (anticholinergics), dilated pupils, blurry vision -amitriptyline, noritriptyline, doxepin, clomipramine (fluoxetine is SSRI)
361
metoclopramide
treats GERD (normally treats gerd by stimulating gut motility aka prokinetic), gastroparesis, n/v
362
carbamazepine OD
dizzy, diplopia, drowsy, blurred vision, headache, ataxia, n/v, hyponatremia, resp depression, prolonged PT/PTT
363
PHB OD
CNS depression, sedation, rash, paradoxical excitement, hyperactivity
364
clonidine OD
sedation, dry mouth, drowsiness, headache, bradycardia
365
theophylline OD
GIB, sz, palpitations
366
class 1 drugs
sodium channel blockers: procainamide, lidocaine, quinidine. decrease automaticity and conduction velocity.
367
class 2 drugs
beta blockers
368
class 3 drugs
potassium channel blockers: sotalol delays repolarization and increases refractory time
369
class 4 drugs
calcium channel blockers: amlodipine, nicardipine, diltiazem, verapamil treat SVT but not ventricular arrhtyhmias. contraindicated in WolffParkinson White.
370
status epilepticus
1st line benzos like rectal diazepam. if continue, then fospheny/pheny
371
what does ventricular preexcitation show as on EKG
initial portion of QRS is prolonged with initial slurring. appears as delta waves
372
acute esophageal bleeding varices tx
octreotide, vasopressin
373
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)
374
autonomic dysreflexia s/s
happens below level of injury, something uncomfortable HTN, bradycardia, flushing, sweating, headache, nasal congestion
375
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)
376
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
377
Dopamine vs dobutamine
Dopamine for perfusion and can help renal perfusion. Dobutamine for better cardiac output and heart perfusion
378
Phenylephrine used for?
Hypercyanotic spells in: tet, SVT, severe hypotension
379
Digoxin can worsen what
Outflow tract obstructions so use with caution for things like tet