CCRN Flashcards
ADH release
in reponse to increased serum osmolality; made in hypothalamus, stored in PP
ADH function
makes kidneys retain water
s/s SIADH
decreased Na, decreased serum Osmo, dec UOP
cardinal sign of SIADH
dilutional hyponatremia
Complication of SIADH
seizures
3 etiologies of SIADH
Oat Cell Ca
Viral PNA
Head Problems
Tx SIADH
Fluid Restriction
Treat Cause
Hypertonic Solutions
Contraindicated for use in SIADH
hypotonic solutions, D5W
s/s DI
increased Na level; Increased UOP; Increased serum Osmo; urine sg 1.001-1.005
etiology DI
Head problems/trauma
Dilantin
Complication of DI
hypovolemic shock
Tx DI and two things to monitor
Give ADH ; IVF
Monitor EKG for ischemia r/t vasopressin therapy and monitor urine sg
CV s/s of hypoglycemia and what causes them
tachycardia, palpitations, diaphoresis, irritability, restlessness; adrenal medulla releases adrenalin to get liver to release glucose
can mask CV s/s of hypoglycemia
beta blockers
CNS s/s of hypoglycemia
confusion, lethargy, slurred speech, seizures, coma
s/s DKA
bg 400-900; dehydration, acidosis, Kussmaul’s respirations
Tx DKA
Primarily-insulin gtt; also IVF (NS to hydrate IV, then 1/2NS to hydrate tissues, then D51/2NS to avoid hypoglycemia r/t insulin gtt)
HHNK
hyperglycemia hyperosmolar non-ketotic coma
risk factors of HHNK
elderly (pancreas ages) TPN (pancreatic fatigue) diet-controlled DM pancreatitis thiazide use (makes body retain glucose) steroid use (induces insulin resistance)
s/s HHNK
BG 1000-2000; severe dehydration; no acidosis; LTBB; make small amt insulin but doesn’t dec bg, just prevents fat b-d/ketosis
Tx HHNK
IVF; small amt insulin
In acidosis, potassium ions move
out of cell, as H+ ions move into cell; change in pH 0.1 should increase K level by 0.6
HA + nuchal rigidity + pos Kernig’s sign
SAH
TIA
reversible, s/s last
RIND
reversible ischemia neurological deficit; s/s last
CI
cerebral infarct-stroke
basilar vertebral artery cerebral infarct stroke
supplies brainstem, problem will be there
loss (opposite side of infarct)of 1/2 of both visual fields in CI
homonymous hemianopsia
eyes deviate toward here in CI
toward side of infarct
most important indicator of neurological status
LOC
goal of stroke TX
decrease cerebral edema
first sign of uncal herniation
pupil change
turn head side to side, eyes return to midline
Oculocephalic Reflex/Doll’s Eyes Reflex–indicates brainstem integrity.
2 holes in head
tentorial notch and foramen magnum
arms up and to center
decorticate posturing–problem with cortex
arms down and point out
decerebrate posturing–problem with brainstem
brain tracts that go from brain, cross at medulla, and go down opposite sides of SC
pyrimidal tracts–control movement
Pupil in ennervated by (3)
3rd CN (Optic) SNS (dilates) Pns (constricts)
uncal herniation
lateral shift (midline shift) of brain tissue
epidural bleed would cause this type of herniation
uncal herniation
ipsalateral dilated pupil is first sign of
uncal herniation; often happens with no change in LOC yet
CI in epidural bleed/uncal herniation
mannitol–only works on good tissue; would shrink brain and allow more room for bleed
respiratory patter in upper brainstem (midbrain) lesion is
hyperventilation
Pontine infarct s/s (2)
apneustic breathing (long pause b/t inspiration and expiration); bilateral pinpoint pupils
pressure on a pyrimidal tract will cause
positive Babinski on foot of opposite side
herniation through foramen magnum
supratentorial herniation
1st, 2nd, and 3rd and 4th signs of supratentorial herniation
- change in LOC (lethargy, stupor); measure with GCS
- pupils dilate bilaterally
- hyperventilation (body tries to induce alkalosis to dec ICP)
- Cushing’s Triad (inc SBP, widening pulse pressure, dec HR and dec RR)
Avoid with Increased ICP (5)
Acidosis; hypotonic IVF; hyperextension/flexion of neck; wrist restraints; decreased PRO intake
Normal CPP
70-95 mmHg
CPP formula
MAP-ICP= CPP
MAP formula
DBP + 1/3(pulse pressure)
Normal Ventricular Fluid pressure (most sensitive indicator of increased ICP)
0-10 mmHg
Basilar Skull Fx, presenting s/s (4)
Raccoon Eyes
Battle’s Sign (bruising over mastoid bone)
CSF leak (otorrhea and rhinorrhea)
Anosmia (Lose CN #1)
CSF leak: how to test otorrhea and rhinorrhea
otorrhea is bloody, look for Halo sign with clot in the middle.
rhinorrhea is clear–check for glucose (CSF is 60% glucose)
s/s bacterial meningitis
usually Staph
CSF has elevated PRO and decreased glucose, is purulent with positive leukocytes.
s/s viral meningitis
enterovirus and herpes virus usually;
CSF has elevated PRO (not as much as bacterial), normal glucose, and positive lymphocytes
bacterial vs. viral meningitis
bacterial: Low glucose, leukocytes
viral: normal glucose, lymphocytesauto
in a seizure this can point to the problem
eye deviation
autoimmune destruction of ACh receptors at NMJ; post-synaptic defect; chronic d/o with abnormal fatiguability brought on by activity.
myasthenia gravis
hallmark of MG
symptoms improve with rest
initial findings in MG
ocular muscle weakness, diplopia dysphagia hoarseness limb weakness ...........respiratory difficulty/failure
precipitating factor of MG crisis
inadequate meds
flu/menses/pregnancy
stress/ surgery
Tx MG
Mestinon (pyridostigmine), Steroids, Respiratory management
Dx Mg
Symptomatic improvement with Tensilon 2 mg IV
medications that interact with Mestinon
aminoglycosides, procainamide, quinidine
*careful use with narcs and barbiturates
acute d/o in which antibodies attack peripheral nerves causing demyelination and loss of nerve conduction
Guillian-Barre Syndrome
Hallmark of Guillian-Barre
bilateral and symmetrical ascending paralysis
improvement is descending
Causes of GB
Viral infections- URI, Epstein-Barr, HIV, Hep A,B,C
Campylobacter jejuni infection
Vaccines
Tx GB
High PRO levels in CSF
Kernig’s Sign
Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees; indicates meningeal irritation
Brudzinski’s sign
Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed.
trousseau’s sign
sign of latent tetany that occurs in hypocalcemia; spasm of hand after arm compressed by bp cuff for several minutes
etiology of pancreatitis
obstruction of pancreatic ducts secondary to gallstones or infection, causes autodigestion of fatty pancreas (less common causes- EtOH, trauma, drug toxicity from cyclosporine, steroids, thiazides, or tetracyclines.)
These problems develop with pancreatitis (4)
- hypocalcemia (Ca used to digest fats)
- HHNK
- Left pleural effusion and Left sided atelectasis (pancrease swells and lifts diaphragm
- Bilateral rales (right are sympathetic rales)
how pancreatitis can lead to ARDS
phospholipase A released during pancreatic autodigestion, which kills Type II alveolar cells that make surfactant
s/s pancreatitis (3)
+ Cullen’s sing-bruising around belly button d/t pancreatic bv b-d
+ Turner’s sign-bruising in flank/groin
Elevated Amylase
order of abdominal assessment
IAPP; inspect, Auscultat, Percuss, Palpate
Assessment of bowel infarction
Hypoactive bowel sounds
Leukocytosis
Hyperresonance and abd tenderness
Tympanic note/absence of dullness in liver area (last two d/t air)
LBO vs. SBO
LBO: large distention, no v/d
SO: small distention, n/v/d
LIver disease causes problems with: (3)
Coagulopathy, blood glucose control, and excretion of ammonia
Avoid these with liver disease (4) because they increase NH3
- Hypokalemia (kidney will retain NH3 with K)
- dehydration (inc BUN)
- increased protein intake (can happen with GIB)
- Acidosis, hypotension; LR
(Lactate converted to bicarb by liver; dec liver function with LR can lead to Lactic Acidosis)
LR used in OR to
counteract hypotension induced acidosis
Neomycin treatment in liver disease-use and complication
reduces gut bacteria that make NH3; complication is vitamin deficiency since gut bacteria also produce riboflavin, folate, and vitamin K
jaundice + increased indirect bilirubin indicates problem in
liver. Indirect is unconjugated, liver conjugates bilirubin (attaches to an albumin)
jaundice + increased direct bilirubin indicates problem in
gallbladder, which stores direct (conjugated) bilirubin
+Kehr’s sign (left shoulder pain) indicates
Ruptured Spleen
Acute renal failure is characterized by decreased UOP of
prerenal RF cause and treatment
decreased UOP d/t renal hypoperfusion (CHF, HoTN); Tx IVF, inotropes
renal RF cause and Tx
decreased UOP d/t kidney damage (tissue or tubules) caused by ischemia or nephrotoxicity
damage to kidney tubules
acute tubular necrosis; caused by ischemia or nephrotoxicity; 50% MR, 25% recover 1 year, 25% need lifetime HD
causes of ischemic ATN
prolonged HoTN (hemmorrhage, burns, sepsis, HF), transfusion reactions
causes of nephrotoxic ATN
heavy metals, medications, street drugs, rhabdomyolysis, radiocontrast (esp to dehydrated pt)
do not treat nephrotoxic ATN with
Lasix; will worsen toxicity
oliguric stage of ATN recovery
10-17d; increased BUn/cr, hyperkalemia, FVO, CHF, dialysis Tx
Polyuric stage of ATN recovery
proximal tubule is necrotic, fluid and lytes are leaking out, cannot concentrate urine; 2 wks-3 mos; increased BUN,cr, hypokalemia, pt is fluid depleted
recovery stage of ATN recovery
3 mos to 1 yr; pray
wt gain of 1 Kg in 24 h is fluid retention of
1000 mL
ischemia to kidneys begins when MAP is
Best measurement of GFR is
creatinine clearance
prerenal vs renal (oliguric) ATN: Urine sodium
prerenal:
normal urine sodium
20-200
prerenal vs. renal ATN: BUN/creatinine ratio
prerenal: 20:1
renal: 10:1
prerenal vs. renal ATN: Lasix/fluid challenge
prerenal: +urine
renal: - urine
4 stages of chronic renal failure
Diminished renal reserve (50% nephron loss) Renal Insufficiency (75% loss) ESRD (90%) Uremic syndrome (100%) (creatinine increases as you progress)
EKG change not caused by hyperkalemia
ventricular irritability
progression of EKG changes in hyperkalemia (5)
- peaked T wave
- prolonged pri, flattened p wave
- lose p wave
- qrs widens
- qrs biphasic–sine wave
s/s hyperkalemia
muscle weakness and ekg changes
CaCl treatment for hyperkalemia
doesn’t decrease K level; cardioprotective to allow normal conduction at higher K level; effective in one minute
hyperkalemia treatment (4)
CaCl, insulin/D50, NaHCO3 (pushes K into cell), kayexelate (removes K from cell and puts in bowel)
ekg changes with hypokalemia (3)
u wave, ST depressions, ventricular irritability
s/s hypercalcemia
muscle weakness, apathy
s/s hypocalcemia
+Chvostek’s, +Trousseau’s, twitching, seizures
renal pts tend to have low Ca and high Phos because
kidneys activate Vitamin D, less kidney function, less Vitamin D, less Ca absorbed from gut
vented pts can have decreased Phos because
only source is leafy greens; need TPN or phos infusion
cryoprecipitate
contains Factors 8,13, and fibrinogen; used to treat hemophilia and DIC
DIC patho
overstimulation of clotting cascade–>bleeding once clotting factors used up—>clots breakdown into anticoagulant split productis—>further bleeding
DIC most often caused by
OB emergency (placenta high in tissue thromboplastin)
labs in DIC
**decreased fibrinogen level
increased PT/PTT, FSPs, D-Dimer
decreased plts
intrinsic clotting cascade is stimulated by
endothelial injury
seen in ARDS, septic shock
extrinsic clotting cascade is stimulated by
tissue injury, which releases tissue thromboplastin
DIC treatment
(in OB emergency, just deliver baby) Heparin FFP cryoprecipitate remove trigger
Functions of heparin
neutralizes thrombin which inhibits fibrin formation
HIT patho
if pt doesn’t have antithrombin III heparin will cause clotting instead, plts get used up
HIT treatment
Argatroban (ACOVA)–direct thrombin inhibitor, doesn’t use antithrombin III
TPN causes decreased
Phos, because builds muscles
antibodies form and destroy platelets (
Idiopathic (Immune) Thrombocytopenic Purpura
ITP vs. DIC (present similarly)
ITP–no increase in FSPs
plt transfusion for ITP
usually unneeded since problem is not with production of plts
massive blood transfusion cause decreased
calcium
medication to decrease Phos
amphogel-phosphate binder
Accelerated HTN
DBP>120, associated with retinal hemmorrhages
Malignant HTN
DBP>140, associated with retinal hemmorhages and papilledema (optic disc swelling)
Tx hypertensive crisis
vasodilators and sympathetic blockers
Dilated CM responds to
digoxin
Hypertrophic CM, AKA and definition
Hypertrophic Obstructive CM (HOCM)
Idiopathic Hypertrophic Subaortic Stenosis (IHSS)
“Fat Septum” Thickening of heart muscle at expense of LV chamber. Decreased filling, SV and CO, pools blood in periphery
HCM treatment
Beta Blockers and CCBs (negative inotropes) Decreased contractility and HR to increase filling
Contraindicated in treatment of HCM
positive inotropes, dig, dopa
nitrates, morphine
S1
Tricuspid and Mitral valves close
S2
Aortic and Pulmonic valves close
systolic murmur
S1 lub (murmur) S2 dub AS and MI
diastolic murmur
S1 lub S2 dub (murmur)
MS and AI
aortic area
right 2nd ICS
pulmonic area
left 2nd ICS
mitral area
5th ICS MCL
tricuspid area
4th ICS left sternal border
holosystolic (heard through entire systole), rough radiating murmur, “washing machine,” increases with holding breath
aortic stenosis
blowing murmur, causes giant V waves on PA waveform
mitral insufficiency
pt teaching re: stents
ASA and plavix after
nursing post op cath
manual pressure 20-30 minutes after until bleeding controlled; VS, distal pulses, CSTM, assess site for bleeding/hematoma
most common complication of heart cath
local vascular problem at insertion site: hematoma, RP bleed, thrombosis, distal embolism
complications of heart cath (4)
death, MI, CVA, renal dysfunction r/t contrast
prevent contrast-induced nephropathy by
lowest dose possible; IVF; acetylcysteine day before and day of cath (antioxidant and vasodilating effects)
hold these nephrotoxic meds 24 hours before a heart cath (4)
some antibiotics, cyclosporine, NSAIDS, metformin
IABP assessments
HOB 15-no higher
pulses
monitor bleeding
s/s cardiogenic shock
confusion/restlessness, increased RR, rales, rapid thready pulse, JVD, narrow pulse pressure, S3S4, Hypotension, dec UOP, dec CO, increased CVP, SVR, and PAWP d/t vasoconstriction
functions of IABP
perfuse coronary arteries during diastole, decreased afterload, increased suction out of LV, increased CO
contraindication to IABP
aortic insufficiency (balloon would put blood back into LV), PVD
IAPB used in treatment of
cardiogenic shock post MI, post CABG and heart caths
complications of IABP
limb ischemia, aortic dissection, infection
causes increased PAP but normal PAWP
Pulmonary HTN
oxygen deprivation to heart begins to cause irreversible injury after
20 minutes
RCA supplies
Inferior wall; half SA node, most of AV node, RA and RV, mitral valve
complications of RCA occlusion
SB, CHB/AV dissociation, RV infarct, mitral insufficiency
LAD supplies
Anterior and Septal Walls; Bundle of His; Bundle Branches; ventricular septum
Complications of LAD occlusion
Mobitz II HB, RBBB( if these develop post-MI, 94% mortality rate, need PPM); VSD
EKG sign of myocardial contusion
STE in injured leads
EKG sign in pericarditis
STE in all leads
1 COD in surgical/trauma patients
MSOF/MODS
Assess with trauma: AMPLE
A=Allergies M=Meds P=Past Illness L=Last meal E=Events preceding injury
Tx Tylenol poisoning
acetylcysteine: 140 mg/Kg loading dose, 70 mg/Kg q4h for 17 doses; activated charcoal if
3 grades of Tylenol poisoning
Grade 1: n/v
Grade 2: RUQ pain
Grade 3: increase in LFTs
danger of ASA poisoning
ASA-induced renal tubular acidosis, kidney damage
Tx ASA poisoning
lavage/induced emesis; activated charcoal; urinary alkalinization with NA HCO3 to increase speed of excretion and counteract renal tubular acidosis; HD
watch for this lyte imbalance with ASA poisoning
hypokalemia
s/s compensatory stage of shock
anxiety, irritability, cool & pale (vasoconsriction), inc HR, dec UOP
s/s progressive stage of shock
lactic acidosis–>vasodilation–>hypotension
dec CO, CVP, PAWP
inc SVR
septic shock causative organisms
Gm - bacteria: E. coli, Klebsiella, Enterobacter, Pseudomonas, Serratia
1 COD in ICU
septic shock, 40-60% mortality rate
normal HCO3`
23-27
Causes of Metabolic Alkalosis
Multiple blood transfusion (sodium citrate in banked blood to dec clotting is converted by liver into bicarb); hypokalemia, vomiting, contraction alkalosis
causes of respiratory alkalosis
hypoxemia (body tries to blow off CO2); CNS d/o (body tries to dec ICP by inducing alkalosis); ASA OD; sepsis
causes of respiratory acidosis
OD, cardiac/respiratory arrest, COPD, d/o’s that cause dec ventilation (MG, ALS, GB)
causes of metabolic acidosis
DKA, starvation ketoacidosis, diarrhea, renal failure
breath sounds are louder than normal in
pneumonia; bronchial bs on expiration and not over trachea d/t inc noise conduction in semisolid tissue
breath sounds are quieter than normal in
atelectic tissue
bronchial bs
over trachea, harsh, heard on expiration
bronchvesicular bs
over mainstem bronchi; heard equally insp and expir
vesicular bs
heard over lung lobes on inspiration
pulmonary consolidation/lobar PNA causes these signs
dull percussion note, dec tactile fremitus, bronchial bs
hallmark of ARDS
refractory hypoxemia
ARDS treatment
PEEP to distend alveoli and inc gas exchange and preven hyaline membrane from absorbing fluid
danger of high O2 over 24 h
destruction of Type II alveolar cells which make surfactant
initial vent setting for adult in respiratory failure
10 ml/Kg (2x normal volume)
massive PE can cause
right sided HF; JVD, inc CVP, liver engorgement
elevates within 3 h of AMI; high sensitivity
myoglobin
blown pupil indicates
increased pressure on CNIII
bilateral pinpoint pupils can indicate
pons infarct
opioids cause bilateral pupil
constriction
these murmurs are low pitched and best heard with bell
AV valve stenosis
nursing care post pneumonectomy
no CT, just regular drain; position on operative side to facilitate drainage and prevent mediastinal shift; TCDB; avoid unneeded suction and fluids
anxiety vs. fear
anxiety-can’t identify cause
fear-can identify cause
IMV
intermittent manditory ventilation (vent mode)
ARDS + this lab increase is poor prognosis, multisystem involvement
lactate dehydrogenase
synthesis of best evidence r/t a clinical question
systematic review
derived from systematic reviews to use clinically
clinical practice guidelines
hypovolemic shock-PA readings
dec PAWP, inc CO and SVR
PAWP is an indicator of
preload
cardiogenic shock-PA readings
dec CO, inc PAWP and SVR
distributive shock-PA readings
Dec SVR, and PAWP
inc CO
this invalidates PAWP readings
PEEP
inferior wall MI 12 lead changes
STE in leads II, III, aVF
anterior wall MI 12 lead changes
STE in v1-v6
posterior wall MI 12 lead changes
STE in lead I and aVL and ST dep in v1-v3
lateral wall MI 12 lead changes
STE in I, aVL, v5-v6
PAD correlates with
PAWP and LVEDP
PAWP vs. PAD
PAWP should be less than PAD by 1-4 mm Hg (blood flows hi to low pressure)
if PAWP > PAD
overwedged cath or cath in wrong zone or PEEP>10
take wedge reading when
end of exhalation-fluctuates with breathing
a wave of PA waveform
atrial contraction; falls just after QRS
c wave of PA waveform
mitral valve closing (can be inside a wave)
v wave of PA waveform
atrial filling (falls just after t wave)
normal PAWP
4-12 mmHg
PAWP elevated in
MV d/o, tamponade, pericarditis, LV failure, FVO
PAWP decreased in
IV depletion/shock
to find PAWP
take mean of a wave
normal PAS
20-30 mm Hg; when RV is pushing blood into PA
PAS is elevated in
lung d/o, pulmonary vascular resistance and pulmonary vasoconstriction
PAD reflects
LVEDP-pulmonic valve is closed during diastole
normal PAD
6-12 mmHg
