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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
Q

fetal heart develops when?

A

4-7 weeks

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26
Q

dvt diagnosis

A

usually look at symptoms + US but sometimes asymptomatic.
can also do angio with contract and venogram

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27
Q

prevent DVT

A

scds, turns, low molecular weight heparint

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28
Q

tx dvt

A

thrombectomy, once again low molecular wt heparin, observation

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29
Q

superior vena cava syndrome causes

A

CVC, thrombosis, mediastinal malignancy

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30
Q

SVCS dx

A

xray (might find mass), CTs

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31
Q

svcs tx

A

depends on cause - can be thrombolytic, anticoag, supportive, remove cvc

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32
Q

fetal vs neonatal circulation

A

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

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33
Q

PDA

A

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)

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34
Q

PFO

A

l to R shunt.

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35
Q

when to be concerned for CHD in newborn

A

murmur WITH cyanosis (suggests r to l shunt), esp if cyanosis worsens with crying
failed hyperoxia, etc

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36
Q

hyperoxia test

A

when giving hyperoxygenation to newborn, cyanosis worsens, then they fail the test. most likely have a CHD

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37
Q

syndromes associated with CHD

A

t21 (avsd), t18 (edwards)-HLHS and VSD, 45x (turners)-VSD and coarc, williams, digeorge-truncus, noonan

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38
Q

acyanotic with increased PBF

A

PDA, VSD, ASD, AVSD

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39
Q

acyanotic with ventricular outflow obstruction

A

AS, CoA, PS

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40
Q

cyanotic with decreased PBF

A

tet, tricuspid atresia

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41
Q

cyanotic with increased PBF

A

transposition of great arteries, truncus arteriosus, total anomalous pulmonary venous return, HLHS

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42
Q

avsd (av canal defect),what is it commonly seen with, what can happen postop

A

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

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43
Q

requires PDA

A

AS, CoA, can be TGA, HLHS

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44
Q

postop coarc repair monitor for what?

A

HTN

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45
Q

tet

A

PS with RVH, overriding aorta (sits over both ventricles), large VSD

more severe the PS, more severe the cyanosis

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46
Q

postop tet repair

A

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

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47
Q

tricuspid atresia-description, surgery

A

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

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48
Q

tet spell description and treatment

A

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.

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49
Q

TGA description, surgery

A

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).

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50
Q

truncus arteriosus

A

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

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51
Q

TAPVR

A

pulm veins drain into systemic veins or RA instead of LA. total (all 4 veins) or partial.
needs immediate surgical repair.

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52
Q

HLHS

A

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

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53
Q

HLHS surgeries

A

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.

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54
Q

digoxin adverse effects and considerations

A
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55
Q

chest tube drainage postop cath,s/s of tamponade

A

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.

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56
Q

septal surgeries rhythm disturbance

A

heart block, conduction delay

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57
Q

what does high RAP or CVP mean

A

RV failure or PHTN

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58
Q

what does low lAP mean

A

hypovolemiaw

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59
Q

hat does high LAP mean

A

LV failure or high LV afterload

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60
Q

postop heart surgery oxygenation/ventilation considerations

A

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.

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61
Q

cardiopulmonary bypass postop

A

may need 50% maintenance x24h, sodium restriction or free water restriction, electrolyte monitoring, glucose monitoring, renal function monitoring and UOP monitoring

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62
Q

postop neonatalheart procedure monitor for?

A

monitor babies for NEC. NEC can also be associated with umbilical lines

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63
Q
A
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64
Q

Therapeutic digoxin serum level

A

1.1-2.2ng/ml

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65
Q

Hypertrophic cardiomyopathy tx

A

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

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66
Q

Restrictive cardiomyopathy tx

A

Tx: CHF management, diuretics, digitalis, vasodilators, antiarrhythmics, transplant

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67
Q

cardiac cath complications other than hematoma

A

arrhythmias, air emboli, MI, perforation, infection

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68
Q

inotropes do what

A

work through alpha and beta receptors to vasodilate, vasoconstrict, and/or enhance contractility

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69
Q

chronotropes work by what

A

change HR by affecting nerves controlling the heart, or by changing rhythm from the SA node (pacemaker of heart)

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69
Q

what to cholinergic drugs stimulate

A

(acetylcholine, bethanacol) pns

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69
Q

what do beta adrenergic drugs stimulate

A

SNS

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69
Q

what do anticholinergic drugs stimulate

A

(clozapine, quetiapine, atropine, oxybutynin, robinul, ipratropium, promethazine, noritriptyline): SNS

anticholinergic drugs = CQ PARONI

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70
Q

what do beta blockers stimulate

A

PNS

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71
Q

what do type 1 epithelial cells do

A

gas exchange

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71
Q

what do type 2 epithelial cells do

A

produce surfactant

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72
Q

are lungs more or less compliant when youre younger

A

less

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73
Q

when are fetal lungs capable of gas exchange

A

22-24 wks (when alveoli develop)

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74
Q

where are co2 sensors / o2 sensors

A

brainstem
o2 sensors: carotid bodies

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75
Q

is cyanosis an early or late sign of hypoxemia

A

late

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76
Q

should pco2 be higher or lower in head injury pts? why?

A

lower (ie low 30s).
because hypercarbia causes cerebral vasodilation for increased CBF also causes increased ICP

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77
Q

what does a WNL RR for a sick/injured child indicate

A

impending respiratory arrest

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78
Q

what age are kids obligatory nose breathers

A

until 6 mos of age (NG can impair breathing up to this point)

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79
Q

normal VQ ratio

A

0.8 (slightly more blood flow than aeration)

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80
Q

what is alveolar dead space

A

areas of alveoli that are seeing ventilation but not perfusion

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81
Q

what is an intrapulmonary shunt? examples?

A

when alveoli are not ventilated but are perfused.
asthma, atelectasis, ARDS, pleural effusion

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82
Q

how do you determine presence of an intrapulmonary shunt?

A

normally pao2/fio2 should be >286, if this number is decreased you have a shunt.

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83
Q

what does PEEP do

A

increases alevolar volume, increases FRC, moves pulmonary water (edema) out

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84
Q

oxyhgb dissociation curve:
left vs right shift?
what causes left shift? right shift?

A

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

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85
Q

what is 2,3 DPG

A

an intracellular RBC factor that determines hgb affinity for o2

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86
Q

acut respiratory failure definition

A

inability of resp system to meet demands of o2 ORRR also inability to provide adequate co2 elimination causing resp acidosis

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87
Q

acute respiratory failure causes (other than the lungs)

A

CNS issues, upper airway disorder, CV or heme disorders

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88
Q

what can trigger apnea of prematurity

A

ambient temp changes, vagal stimualtion (suction, gagging)

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89
Q

transient tachypnea of newborn

A

from c section or precipitous delivery (lung fluid not squezed out as in normal vag delivery)

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90
Q

choanal atresia

A

openings from nasal cavity occluded - manifests in delivery rm(obligate nose breather)-dyspnea worsens with mouth closure. OPA / intubate until surgery

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91
Q

where should tip of ETT end

A

no lower than 1-2cm above carina, no higher than 1st rib

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92
Q

determine appropriate ETT size

A

(age in yrs/4) + 4
so 16 yr old gets size 8

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93
Q

what to avoid when leading up to extubation

A

no PO intake or CPT 2-4hrs prior to and post extubation (aspiration)

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94
Q

upper airway edema tx post extubation

A

steroids, rac epi, neb saline, heliox

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95
Q

what do increased PIPs on vent mean?

A

ARDS, decreased compliance, pneumo, secretions, kinked tubing

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96
Q

nutrition while on MV

A

low carbs (to avoid increasing co2), low triglycerides, high fat for calories

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97
Q

cons of PEEP

A

low CO from impaired venous return and high ICP from impaired cerebral venous return

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98
Q

inadvertent intrinsic peep

A

lung overdistention from flow obstruction and too short exhalation time.
s/s: rising CO2, poor chest wall movement
especially seen with bronchiolitis, CLD

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99
Q

ARDS patho

A

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

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100
Q

ARDS general management

A

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

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101
Q

PNA causes and diagnosis

A

viral, bacterial.
dx: CXR, secretions, blood cx, bronchoalveolar lavage, lung biopsy if severe, pleural fluid

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102
Q

hydrocarbon PNA aspiration

A

gas, nail polish, solvent, propellants.
treat aggressively. necrosis of tissue can occur. similar to ARDS

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103
Q

foreign body upper vs lower airway and post extraction

A

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

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104
Q

croup s/s, prevalence, cause, season

A

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

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105
Q

croup diagnosis

A

A/P CXR with steeple sign(narrow glottis and subglottic airway).
lateral XR with normal epiglottis

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106
Q

croup tx

A

heliox, rac epi, cool humidified o2, steroids, antipyretics, enteral feeds, hydration, minimize agitation

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107
Q

epiglottitis prevalence, cause

A

2-6yr old
usually h flu (Hib vaccine). can be bacterial.
acute infxn can resolve in 24-72hrs

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108
Q

epiglottitis s/s

A

four ds and s:
drooling, dysphagia, dysphonia, distress, stridor.
abrupt onset.
fever, sore throat, tripoding.

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109
Q

epiglottitis dx

A

lateral neck XR thumb sign (thickened epiglottis)

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110
Q

bronchiolitis peak incidence and cause

A

mid winter-early spring
usually RSV but can be flu, hmpv

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111
Q

bronchiolitis tx

A

o2, intubate if needed, albuterol, terbutaline, aminophylline, hydration, ribovirin if RSV

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112
Q

CXR appearance in pneumo

A

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)

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113
Q

pneumo tx

A

chest tube.
tension pneumo: needle decompress then chest tubein

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114
Q

sucking chest wound

A

open pneumo, air in and out. flail chest.
tx with PPV, cover with occlusive drssing, place chest tube.

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115
Q

chest tube management

A

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.

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116
Q

goal of status asthma tx

A

goal to restore airway patency, reverse bronchospasm, control inflammatory response, and decrase secretions/plugs.

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117
Q

vent settings for an asthmatic

A

permissive hypercarbia, prolonged expiratory time, conservative PEEP, watch for pneumo!

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118
Q

pulsus paradoxus

A

n exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg.

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119
Q

beta 2 agonists

A

alb, levalb, terbutaline (systemic), metaproterenol,salmeterol

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120
Q

status asthmaticus tx

A

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

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121
Q

pts at risk for PE

A

sickle cell, nephrotic syndrome, cancer, chemo, hypercoaguable state (inherited), vasculitis

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122
Q

PE tx

A

o2/intubate, LMW heparin, thrombolytic, supportive CV care (potential for right heart failure and obstructive shock), ABX if infectious emboli, embolectomy if massive

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123
Q

PHTN mean pulm artery pressure? what kind of shunt?

A

> 25mmHg at rest. right to left shunt

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124
Q

preductal/postductal sats in PHTN

A

preductal pao2> postductal

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125
Q

PHTN tx

A

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

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126
Q

BPD pts are sensitive to?

A

overhydration

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127
Q

bpd comes with?+s/s

A

PHTN > right heart failure, FTT, barrel chest, bronchospasms (LS can be crackly, wheezy, rales)

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128
Q

BPD tx

A

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

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129
Q

CDH babies present as

A

full term full birth weight infant who soon develops severe resp distress

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130
Q

CDH comes with

A

PHTN d/t lung hypoplasia, increased pulm vascular resistance.

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131
Q

CDH s/s

A

scaphoid abd, PMI shift, WOB, decreased/absent LS, increased chest diameter, PHTN

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132
Q

CDH CXR

A

gas filled bowel loops in thorax

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133
Q

CDH tx

A

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)

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134
Q

CDH postop chest tube

A

on affected side without suction (gradual reexpansion). position onto the affected side to expand the good lung

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135
Q

TEF most common type

A

type c: esophageal atresia with distal TEF

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136
Q

TEF hx

A

prenatal polyhydramnios

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137
Q

TEF tx/management/considerations

A

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

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138
Q

respiratory alkalosis causes

A

CNS injury, ASA ingestion, Reye’s, hepatic encephalopathyrespi

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139
Q

where is CSF produced

A

choroid plexus: lateral, 3rd, 4th ventricles.

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139
Q

where is csf absorbed

A

flows freely thru subarachnoid space then absorbed by arachnoid villi

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140
Q

corpus callosum

A

connects brain hemispheres with nerves

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141
Q

basal ganglia purpose

A

controls motor function (deep in gray matter of hemispheres)

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142
Q

thalamus function

A

pain center, temp, tactile sensation

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143
Q

hypothalamus function

A

secrete ADH, Oxytocin, body temp, sweat, salivary

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144
Q

cerebellum function

A

balance, coordination

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145
Q

brain stem function

A

respiratory center

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146
Q

meninges

A

pia mater (inner, vascular), arachnoid (middle, feathery), dura mater (outer, tough)

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147
Q

anterior fontanelle closes at

A

16-18 mos

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148
Q

posterior font closes at

A

2 mos

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149
Q

normal ICP

A

5-15 (<15)

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150
Q

cushing’s triad

A

late ominous sign of high ICP.
bradycardia, htn with wide PP, irreg resps that become apnea

151
Q

tx high ICP

A

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
Q

gold standard icp monitoring

A

intraventricular

153
Q

zero EVD where

A

with external auditory meatus which approximates the level of foramen of monroe

154
Q

what does the brain stem include

A

pons, midbrain, medulla

155
Q

PNS vs SNS

A

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
Q

communicating vs noncommunicating hydrocephalus

A

comm: arachnoid villi unable to reabsorb CSF (ie meningitis)
noncomm: obstruction to flow (ie tumor, cyst, inflammation)

157
Q

encephalopathy: what is, causes

A

general disturbance in brain cellular metabolism causing ALOC. from HIE, lead poisoning, HTN, metabolic dx

158
Q

risks for stroke

A

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
Q

moya moya

A

rare. blood vessels of internal carotids are narrowed, brain creates collaterals

160
Q

stroke imaging

A

noncontrast head CT differentiates ischemic vs hemorrhagic stroke.
CTA evaluates intracranial and extracranial circulation.
MRI
(echo to r/o cardiac embolus)

161
Q

stroke tx

A

control HTN, Fever, glucose
o2/ventilation
heparin, tPA
ASA to prevent future strokes

162
Q

AVM tx

A

not all are operable.
surgery total excision, embolization, sterotactic radiosurgery, and supportive care

163
Q

goal for TBI Tx

A

maintain CPP, prevent secondary injury, symptom management

164
Q

concussion

A

blow to head without radiographic findings: can last months.

165
Q

brain contusion

A

bruise on brain: may have ICPs/szs

166
Q

coup, contrecoup

A

Coup: injury to side of head that was struck

Contrecoup: injury to opposite side of brain

167
Q

signs of basilar skull fx

A

racoon eyes, battle sign behind ear.
no NGT!
look for CSF/rhinorrhea/otorrhea

168
Q

diffuse axonal injury

A

accel-deceleration injury from MVA, abuse. poor neuro exam with a normal CT

169
Q

epidural hematoma

A

ARTERIAL bleed in middle meningeal artery, more in older kids.
lucid > LOC
often associated with skull fracture

170
Q

subdural hematoma

A

VENOUS bleed. more in infants. from birth trauma, falls, intentional

171
Q

when do u start assessing for brain death

A

24h after injury or resus

172
Q

requirements to do brain death testing

A

need 2 exams, 2 diff providers with observation period in between.
must exclude reversible causes (hypothermia, drug toxicity, etc).

173
Q

brain death tests

A
  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
Q

oculocephalic test

A

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
Q

oculovestibular cold calorics

A

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
Q

if some parts of brain death exam cant be compelted?

A

ancillary tests: can do 4 vessel cerebral angio, radionuclide CBF, EEG

177
Q

complete vs incomplete acute spinal cord injury

A

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
Q

acute SCI tx

A

stabilize (traction, fixation), supportive.
steroids no longer recommended.
if neuro shock, give volume and norepi

179
Q

viral meningitis CSF

A

slight increase WBC, normal/slight increase protein, normal glucose.
negative gram stain, negative culture

180
Q

bacterial meningitis CSF and cause

A

increased WBC, increased protein, low glucose, positive gram stain and culture
newborns: e coli, GBS
>2mos: n meningitidis, GBS, strep pneumoniae, haemophilus influenzae

181
Q

kernig sign

A

for meningitis
pain with extension of legs

182
Q

brudzinski sign

A

for meningitis
flexion of neck causes involuntary bending of hip and flexion of knee

183
Q

monitor what in meningitis?

A

lytes: watching for SIADH/DI

184
Q

febrile sz age

A

6 mos - 6 yrs

185
Q

meningocele vs myelomeningocele

A

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
Q

arnold chiari malformation

A

spinal cord travels into skull, causes hydrocephalus, may need shunt

187
Q

severe sepsis definition

A

sepsis plus 2 or more organ systems dysfunctioning

188
Q

septic shock definition

A

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
Q

septic shock first hour goals

A

maintain airway/o2/ventilation, restore/maintain circulation and perfusion, give ABX, normal VS, normal mental status

190
Q

first 15 mins of septic shock

A

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

191
Q

first 15-60min of septic shock tx

A

fluid refractory shock. inotropes
epi 0.05-3mcg/kg/min cold shock
norepi 0.05mcg/kg/min warm shock
dopamine if epi/norepi unavailable

192
Q

first 60 mins septic shock tx

A

catecholamine resistant shock.
goal normal MAP, PP, SVO2<70, CI 3.3-6
give stress dose hydrocort, obtain cortisol level first if possible

193
Q

why check cortisol in septic shock

A

cortisol regulates catecholamine synthesis, responsiveness of adrenergic receptors, and cell membrane stability

194
Q

septic shock still not improving after adrenal insufficiency has been addressed?

A

persistent catecholamine resistant shock
-r/o and correct pericardial effusion, pneumo, increased intraabd pressure.
consider ECMO

195
Q

cold shock vs warm shock pressors

A

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

196
Q

cold shock s/s

A

low CO, low OR high SVR, cool/cold clammy extremities, mottled, cap refill >2sec, diminished pulses, tachycardia (brady if neonate), narrow PP

197
Q

Warm shock s/s

A

high CO, low SVR, warm/drye xtremities, flushed, cap refill flash <2sec, tachycardia, bounding pulses, wide PP

198
Q

SIRS diagnosis

A

TWO must be present, and one MUST BE temp or wbc:
temp >38.5 or <36
high or low leukocytes (or bandemia)
tachycardia
tachypnea

199
Q

SIRS Tx

A

recognize before it becomes sepsis/septic shock. stop the insult. manage s/s

200
Q

BP is not a good indicator of altered perfusion in peds since they maintain their BP so long. so what is?

A

mental status, cap refill, pulses, pulse pressure, extremity temp, skin color, UOP, acidosis, lactic acid level

201
Q

kidneys role in acid base

A

they can secrete hydrogen into urine (make body more alkalotic) and reabsorb bicarb from urine

202
Q

when is a foley indicated?

A

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

203
Q

ventilator associated event: what is and prevention

A

4 days of MV: 2 days of stability with deterioration after.
bundle: hand hygiene, elevate HOB, oral care, daily ERT

204
Q

toxin management

A

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.

205
Q

submersion tx

A

fluid resuscitation, intubation, CV support, supportive care, rewarming (remove wet stuff, warm blankets, heat lamp, forced warm air blanket, warmed fluids and o2)

206
Q

unintentional vs intentional abd trauma

A

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

207
Q

intentional burns

A

clear line. creases may be spared from child flexing when being dunked in. donut demarcation if put in buttocks first.

208
Q

abusive head trauma and what can mimic it

A

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.

209
Q

PICS

A

new or worsening impairment after discharge in physical, cognitive, mental health
prevent by giving anticipatory guidance

210
Q

PTSD

A

after exposure to a traumatic event, has persistent recollections/reminders of event and increased arousal

211
Q

5 p’s of compartment syndrome

A

pain, pallor, pulseless, paresthesia, paralysis
absent pulse is late sign

212
Q

pelvic fx

A

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

213
Q

compartment syndrome

A

excess pressure in muscle compartment until no capillary perfusion, more in lower extremities. true surgical emergency

214
Q

causes of compartment syndrome

A

bleeding into muscle compartment, IV infiltrate, burn and crush injuries, external forces (cast, dressing)

215
Q

rhabdo physiologic manifestations

A

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

216
Q

rhabdo causes

A

crush, electrical burn, burn, snake venom, long sz, malignant hyperthermia, reperfusion to damaged cells after fasciotomy

217
Q

rhabdo tx

A

IVF: enhance clearance
tx underlying cause
correct lytes (esp hyperK)
monitor labs
+/- RRT

218
Q

stage 1 PI

A

Non blanchable erythema and edema

219
Q

stage 2 PI

A

partial thickness loss. partial loss of dermis with red pink wound bed withOUT slough

220
Q

stage 3 PI

A

full thickness skin loss, may see subQ fat but bone/tendon/muscle not exposed

221
Q

stage 4 PI

A

full thickness tissue loss, will see bone, tendon, muscle. slough/eschar may be there. often with undermining/tunneling

222
Q

unstageable PI

A

full thickness tissue loss, depth of wound unknown tho because covered by slough/eschar

223
Q

DTI

A

purple maroon local area of discolored but intact skin. or blood filled blister from underlying damaged soft tissue from pressure/shear

224
Q

skin failure

A

blood shunts away from skin in critical illness > hypoperfusion of skin > skin and underlying structures begin to fail.
may not be preventable.

225
Q

what Ab can cross placenta

A

igG

225
Q

iGg role, IgM, A, E

A

igG: bacteria, virus, protozoa, toxins
M: nonself ABO types, bacteria
A: from milk. only coats GI tract. kills viruses
E: allergy, parasites

226
Q

t cells

A

responsible for autoimmune dsiease, organ transplant rejection

227
Q

HIV CD4

A

CD4<200 means AIDS, very weak immune system

228
Q

what do B cells become

A

antibodies

229
Q

when to give FFP

A

deficit of coag factors, plasma volume expansion with all coagulation factors

230
Q

when to give cryo

A

decreased fibrinogen, Hemophilia A, factor XIII deficit, von Willebrand

231
Q

when to give granulocytes

A

adjunct to infection measures in high risk pts/neonates (watch for fever)

232
Q

acute hemolytic rxn

A

occurs with ABO incompatible blood → hemolyzes RBCs → fever, hypotension, lumbar pain (classic sign), chest pain, anxiety, shock

233
Q

nonhemolytic transfsn rxn

A

response to leukocytes in the blood; may benefit from premeds in future and may need leukocyte reduced blood in future

234
Q

TACO

A

pulm edema from lot volume excess from transfusion

235
Q

TRALI

A

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
Q

DIC causes

A

infection
shock
trauma
malignancies
vascular abnormalities
snakebite
transfusion reaction
heatstroke
Sepsis
OB emergencies
Head injury

237
Q

DIC lab findings

A

thrombocytopenia
prolonged PT, PTT
decreased fibrinogen
increased D dimer
increased fibrin degradation products
decreased coagulation factors (Protein C, S)

238
Q

DIC Tx

A

underlying cause
blood products
ffp/cryo
organ supportive care from ischemic injury of blocked microvasculature

239
Q

ITP - what is it? s/s? labs?

A

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.

240
Q

tumor lysis

A

triad: hyperuricemia, hyperkalemia, hyperphosphatemia.
hypocalcemia secondary to hyperphos.

241
Q

hyperleukocytosis

A

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.

242
Q

sickle cell

A

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

243
Q

ITP tx

A

often self limited.
can give steroids, IVIG, monoclonal antibodies, splenectomy, PLT transfsn

244
Q

tumor lysis PPX

A

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

245
Q

hyperleukocytosis tx

A

goal: decrease leuks
initiate antilekemic therapy. avoid prbcs (viscosity), leukapharesis or exchange transfsn. prevent/manage tumor lysis. control complications.

246
Q

what is vasoocclusive pain crisis

A

any organ system (spleen, lungs, brain) where small arterioles are obstructed by sickle cells causing ischemia, pain, organ dysfunction.

247
Q

what triggers vasoocclusive crisis

A

infxn, fever, dehydration, trauma, cold, stress

248
Q

vasoocclusive crisis tx

A

1-1.5xMIVF, o2, ABX if infxn, pain control

249
Q

acute chest syndrome

A

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.

250
Q

most common abd trauma injuries

A

spleen and liver (pancreas less frequent)

251
Q

peds considerations that worsen abd trauma

A

less subq fat, more anterior organs, less blood volume&raquo_space; rapid hypovolemia

252
Q

liver injury has what kind of pain

A

RUQ pain radiating to R shoulder

253
Q

what kind of pain is spleen

A

LUQ pain, also can radiate to shoulder

254
Q

pancreas pain

A

deep epigastric pain radiating to back

255
Q

cullen’s sign

A

bruising around umbilicus

256
Q

kehr’s sign

A

acute pain in shoulder when laying down with legs elevated d/t blood or other irritants in peritoneal cavity

257
Q

what does FAST scan look for

A

blood (esp blood in abd)

258
Q

what kind of pain is bowel infarct/obsturction/perf

A

acute sudden onset of pain/tenderness in abd

259
Q

what does upper GI perf lead to

A

hydrochloric acid and giestive enzymes and bile leak, causing peritonitis

260
Q

what does lower GI perf cause

A

fecal material and bacteria leak causing sepsis

261
Q

what doesbowel infarction cause

A

sepsis because of dead bowel

262
Q

what does bowel obstruction present with

A

distention, absent bowel sounds, vomiting (probs bilious), fever

263
Q

what does bowel perf present with

A

resp distress, acidosis, sepsis

264
Q

what does peritonitis present with

A

pain, guarding, rebound tenderness

265
Q

upper vs lower GIB

A

upper: proximal to upper ligament of trites (which connects to lower parts of duodenum)

266
Q

what labs for GI hemorrhage

A

ABG-check for met acidosis
CBC
T/S
coags
lytes
LFTs
pancreatic enzymes

267
Q

what access for GI hemorrhage

A

2 large bore IVs

268
Q

GI hemorrhage management

A

support ABCs
fluids, blood
NGT room temp saline lavage
vaso
octreotide
endoscopic management

269
Q

s/s of liver failure

A

hepatosplenomegaly
varices, ascites
malnutrition
pruritus
telangiectasis (spider veins)
jaundice
hepatic encephalopathy
renal failure
cogaulopathy

270
Q

liver failure tx

A

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 )

271
Q

postop liver transplant care

A

pulm toilet
treat HTN
monitor drain output
correct coagulopathies

272
Q

what is intusussception preceded by

A

gastroenteritis

273
Q

why is intusussception bad

A

intestinal segments fold over and telescope on themselves.
venous then arterial obstruction > perf, infarct, shock

274
Q

s/s of intusussception

A

paroxysmal severe abd pain
bloody currant jelly stools
sausage mass in RUQ
bilious emesis
abd distention

275
Q

intussusception tx

A

NPO, IVF
barium enema
then surgery

276
Q

NEC s/s

A

temp instability, feeding intolerance, abd distention, guaiac pos stools, apnea, brady

late: met acidosis, thrombocytopenia, coagulopathy, shock

277
Q

NEC diagnostics

A

abd xray: pneumatosis intestinalis, dilated bowel loops, pneumoperitoneum

abd us: intraabd free fluid

278
Q

NEC tx

A

NPO, IVF (monitor lytes)
gastric decompression
ABX
surgery for perf, peritonitis, or deterioration
30-45% mortality

279
Q

where does filtration occur in kidney

A

functional unit of kidney: glomerulus

280
Q

normal UOPs by age

A

infant: 2ml/kg/hr
child: 1ml/kg/hr
adolescent: 0.5ml/kg/hr

281
Q

prerenal AKI causes

A

decreased preload: altered heart fx/heart failure, vasodilation, altered vascular volume

282
Q

manifestations of prerenal AKI

A

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
Q

prerenal AKI tx

A

dc K in fluids
bolus for dehydration
diuretics to differentiate btwn prerenal and renal failure
avoid nephrotoxics

284
Q

renal AKI causes

A

immune (glomerulonephritis, lupus)
vascular (HUS, DIC, TTP)
interstitial nephritis
trauma
nephrotoxins (ABX, contrast)

285
Q

renal AKI s/s

A

aka intrarenal/intrinsic/ATN

oliguric phase
diuretic phase
recovery phase

286
Q

postrenal aki s/s

A

abd / flank pain
palpable mass obstruction
failure to thrive

287
Q

overall for AKI, want to avoid and prevent what?

A

infections!

288
Q

common electrolyte imbalances of AKI

A

hyperkalemia
hyperphosphatemia
hyponatremia
hypocalcemia
hypo or hyper magnesemia

289
Q

hyperkalemia s/s

A

muscle weakness
confusion
ascending paralysis
nausea
diarrhea
tall peaked T waves > wide QRS long PRI > ventricular dysrhythmias, cardiac arrest

290
Q

most immediate hyperkalemia tx? what other tx are there?

A

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

291
Q

hyponatremia s/s

A

muscle twitching
tremors
weakness
abd cramps
n/v
lethargy
disorientation
seizures
coma

292
Q

hyponatremia tx

A

underlying cause
3% saline if Na<120 or if symptomatic
frequent neuro assessments and Na monitoring

293
Q

hypocalcemia caused by what

A

increased phosphate
decreased production of vitamin D
hypoalbuminemia

294
Q

s/s hypocalcemia

A

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

295
Q

hypocalcemia tx

A

cause
tx hyperphosphatemia
EKG
iv calcium
monitor serum Mag since hypomagnesemia can also affect correction of hypocalcemia

296
Q

CKD tx

A

anemia tx
prevent bone loss (meds)
meds for growth
diuretics
diet restrictions
dialysis
transplant (ESRD)

297
Q

HUS s/s

A

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

298
Q

HUS causes

A

e coli, salmonella, shigella, strep pneumoniae, or atypical hereditary HUS

299
Q

HUS Patho

A

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
Q

HUS tx

A

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
Q

ADH is aka

A

vasopressin (which is why its used in resus events-also has vasoconstrictor effects)

302
Q

where is ADH from

A

made in hypothalamus, released by posterior pituitary (problem in either of these areas can cause ADH imbalances)

303
Q

how does ADH affect water balance

A

increases renal collecting ducts’ permeability to water –> decreased UOP, body holds onto water –> increased intravascular volume

304
Q

what stimulates production/release of ADH

A

serum osmo, extracellular fluid volume, changes in arterial BP

305
Q

adh is secreted in SIADH despite

A

despite serum hypo-osmolality, hyponatremia, euvolemia

306
Q

SIADH causes

A

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
Q

siadh s/s other than low UOP

A

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
Q

SIADH labs

A

Na<135
serum osmo<227
BUN<10
urine osmo>200
urine SG>1.020

309
Q

normal serum osmo

A

270-290

310
Q

SIADH primary tx, goal

A

MIVF restriction/fluid restriction to 75% maintenance

main goal to normalize serum sodium, osmo, and prevent or correct neuro sequelae

311
Q

siadh tx other than fluid stuff

A

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
Q

DI causes

A

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
Q

DI s/s

A

AMS, seizures, coma, weakness,
twitching,
THIRST,
UOP>4ml/kg/hr, dilute urine, hypovolemia s/s (hypovolemic shock posisble if not tx)

314
Q

DI labs

A

serum osmo>300
Na>145
urine osmo<200
urine spec grav <1.005
imaging studies

315
Q

DI tx/goal

A

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
Q

5 hormones for energy production/glucose homeostasis

A

insulin
glucagon
epi
cortisol
growth hormone

317
Q

insulin is what kind of hormone

A

anabolic hormone

318
Q

insulin secreted where and why

A

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
Q

glucagon secreted where and why

A

by pancreas in response to low serum glucose to stimulate glycogenolysis and gluconeogenesis

320
Q

what can neonatal sepsis present as in terms of glucose

A

hypoglycemia, hyperglycemia, and glucosuria

321
Q

hypoglycemia threshold, s/s, causes

A

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
Q

hypoglycemia tx

A

0.5-1g/kg of D25

323
Q

how to decrease PaCo2

A

increase rate or TV
increase PIP
decrease PEEP

324
Q

patho of DKA

A

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
Q

DKA s/s and labs

A

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
Q

DKA tx

A

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
Q

DKA cerebral edema

A

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
Q

PKU

A

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
Q

galactosemia

A

no milk even breast milk.
may heave jaundice, diarrhea, hepatosplenomegaly, lethargy, hypotonia, cataracts
lactose free soy formula

330
Q

croup sounds

A

upper airway sounds: dyspnea, stridor, hoarse, barky cough. no crackles/rales tho (thatd be distal lung disease)

331
Q

normal serum aminophyllin

A

10-20mcg/ml

332
Q

aerosol asthma meds

A

epi, albuterol, terb, isoproterenol, atropine, isoetharine, metaproterenol

333
Q

bronchiolitis also has air trapping t/f

A

true: with low fever, WOB, nonproductive cough, etc

334
Q

BPD pts have increased risk for?

A

bronchiolitis with air trapping

335
Q

normal mixed venous po2

A

35-40

336
Q

normal mixed venous sat svo2

A

60-80

337
Q

DI priority tx

A

restore fluid. THEN ddavp

338
Q

half life IV insulin

A

3-5min

339
Q

transplant rejection PPX meds

A

tacro, azathioprine, cyclosporin (dont use too soon postop-can cause htn and hUS), methylpred, FK506

340
Q

what is calcium inverse with

A

po4 (maybe also mag)

341
Q

normal Ca
K
mag
phos
Cl
bicarb

A

Ca:8.5-11
K: 3-5
mag: 1.5-2.5
phos: 3-5.5
cl: 102-112
bicarb: 18-29

342
Q

normal WBC, hgb, hct

A

WBC: 4.5-17
hgb: 11.5-14.5
hct: 33-43%

343
Q

how to increase paco2

A

decrease PIP
increase PEEP
decrease rate

344
Q

how to decrease pao2

A

decrease PIP
decrease PEEP
decrease I/E ratio

345
Q

how to increase pao2

A

increase PIP
increase PEEP
no change to rate, does not affect
increase I/E ratio

346
Q

normal LAP

A

2-15

347
Q

normal RAP

A

2-8

348
Q

normal pulmonary artery pressure

A

<2/3 SBP

349
Q

RDS is from?

A

decreased surfactant

350
Q

BPD is?

A

need for o2 longer than 28days after birth
from overinflation and etelectasis
has increased pulm vascular resistance, PHTN, cor pulmonale
key: hypercarbia, hypoxemia

351
Q

when might cervical SCI result in chronic ventilation

A

3rd-5th vertebrae

352
Q

meningococcemia

A

this is sepsis cause by n meningitidis. classically comes with purpura fulminans: petechial purpuric rash from coagulation of microvasculature

353
Q

stroke to imaging time

A

30 mins from door to CT
noncontrast CT, CT angio, and MRI

354
Q

goal aPTT on heparin infusion (only for stroke goal?)

A

60-85seconds

355
Q

early septic shock presentation

A

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
Q

where do u zero art line to

A

right atrium using mid axillary, 4th intercostal space (nipple line)

357
Q

heliox

A

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
Q

what do a waves on icp monitoring mean

A

plateau waves that usually appear when already high ICP becomes critically high from hypercapnia, hypoxia, cerebral edema. call MD

359
Q

hypokalemia EKG findings

A

flat/inverted T, increased P wave amplitude, prolonged PRI, U waves, PVCs

360
Q

tricyclic antidepressant OD

A

depressed LOC, sz, vent arrhythmias, acidosis, dry mouth (anticholinergics), dilated pupils, blurry vision
-amitriptyline, noritriptyline, doxepin, clomipramine (fluoxetine is SSRI)

361
Q

metoclopramide

A

treats GERD (normally treats gerd by stimulating gut motility aka prokinetic), gastroparesis, n/v

362
Q

carbamazepine OD

A

dizzy, diplopia, drowsy, blurred vision, headache, ataxia, n/v, hyponatremia, resp depression, prolonged PT/PTT

363
Q

PHB OD

A

CNS depression, sedation, rash, paradoxical excitement, hyperactivity

364
Q

clonidine OD

A

sedation, dry mouth, drowsiness, headache, bradycardia

365
Q

theophylline OD

A

GIB, sz, palpitations

366
Q

class 1 drugs

A

sodium channel blockers: procainamide, lidocaine, quinidine.
decrease automaticity and conduction velocity.

367
Q

class 2 drugs

A

beta blockers

368
Q

class 3 drugs

A

potassium channel blockers: sotalol

delays repolarization and increases refractory time

369
Q

class 4 drugs

A

calcium channel blockers: amlodipine, nicardipine, diltiazem, verapamil
treat SVT but not ventricular arrhtyhmias.
contraindicated in WolffParkinson White.

370
Q

status epilepticus

A

1st line benzos like rectal diazepam.
if continue, then fospheny/pheny

371
Q

what does ventricular preexcitation show as on EKG

A

initial portion of QRS is prolonged with initial slurring. appears as delta waves

372
Q

acute esophageal bleeding varices tx

A

octreotide, vasopressin

373
Q

what to check before giving digoxin and why

A

potassium and PRI.
hypokalemia aggravates digoxin cardiac toxicity. digoxin can cause arrhythmias and heart block. (indicated by long PRI)

374
Q

autonomic dysreflexia s/s

A

happens below level of injury, something uncomfortable
HTN, bradycardia, flushing, sweating, headache, nasal congestion

375
Q

halperidol side effects

A

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
Q

What does sudden increase in ETCO2 indicate?

A

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
Q

Dopamine vs dobutamine

A

Dopamine for perfusion and can help renal perfusion. Dobutamine for better cardiac output and heart perfusion

378
Q

Phenylephrine used for?

A

Hypercyanotic spells in: tet, SVT, severe hypotension

379
Q

Digoxin can worsen what

A

Outflow tract obstructions so use with caution for things like tet

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