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intracellular fluid
fluid inside the cells
2/3 of body fluid
primarily in skeletal muscle
transports nutrients, electrolytes, and waste
assists with cell metabolism
extracellular fluid
fluid outside cells
intravascular, interstitial, transcellular
extracellular fluid - intravascular
in the vascular space (bloodstream)
extracellular fluid - interstitial
fluid in spaces between the cells, fluid reservoir
not in cells, not in bloodstream..
in the space between cells
extracellular fluid - transcellular
cerebral spinal fluid, pericardial fluid, synovial joints, intraocular space fluids
hydrostatic pressure
force within a fluid compartment that pushes fluid to follow diffusio/osmotic gradients
force that pushes into the capillaries
pulling force from capillary to tissue
oncotic pressure
force exerted by plasma proteins to keep fluid in the vasculature
holds fluids together in the vessels
pulling force from tissue to capillary
osmolality
measure of fluid concentration
reflects hydration status
normal serum value = 280-295 mOsm/kg
<240 or >320 mOsm/kg is critically abnormal
ways that fluid balance is regulated
renal
endocrine
cardiac
GI
renal regulation
ANG II is a potent vasoconstrictor
vasoconstriction
thirst
ADH release
aldosterone release
baroreceptors in the kidneys detect fluid volume imbalances
drop in BP → release ANG I → end result is ANG II to vasoconstrict and get more blood
endocrine regulation of H2O: ADH
the pituitary gland regulates fluid volume by controlling the release of ADH
increases reabsorption of H2O by real tubules
ADH is released when:
decr blood volume
incr plasma osmolality
incr serum Na+
pain/stress
incr catecholamines
cardiac regulation of H2O - ANP
released by the heart cells when atrial walls stretch
cardiac regulation of H2O - BNP
released by heart cells when ventricle walls stretch
use as a measure when there is too much volume in the heart
high BNP = too much volume in the blood stream
cause increased Na+ excretion to cause waterloss
GI regulation of H2O
involved in losses of fluids related to vomiting, diarrhea
can act to reabsorb normally secreted fluids and electrolytes when the patient is depleted
third spacing
fluid where it is not supposed to be and cannot be easily exchanged
1st spacing = intravascular
2nd spacing = interstitial and intracellular
third spacing assessment
fluid may be deep inside body structures
caused by cardiac, renal, liver damage, pancreatitis, decreased plasma proteins, increased capillary permeability
S/S:
renal: decreased urine output with adequate intake
cardiac: increased HR, decreased BP, decreased CVP
weight gain
pitting edema
ascites
third spacing - interventions/evaluations
interventions:
monitor edema
daily weights
intake and outputs
monitor VS
HOB > 30 degrees
monitor underlying cause
evaluations:
stabilized I&O
stabilized weight
VS normal
resolution of third-spacing/underlying cause
hypovolemia
not enough fluid in the vasculature
causes:
fluid loss:
increase insensible water loss (high fever, heatstroke, perspiration)
diabetes insipidus
diabetic ketoacidosis
osmotic diuresis (increased urination due to excess solutes in the kidney’s filtered fluids)
overuse of diuretics
third-space fluid shifts: burn, pancreatitis
inadequate fluid intake:
altered mental status
difficulty swallowing
decreased thirst (elderly)
inadequate access
hypovolemia assessment
thirst
acute weight loss
decreased skin turgor
oliguira/concentrated urine
weak, rapid pulse
longer capillary refill
decreased blood pressure (BP)
increased respiratory rate
increased HGB, HCT, osmolality
urine S.G. > 1.030
dry mouth, mucous membranes
weakness, dizziness, muscle cramps
confusion, restlessness, lethargy
older adults assessment
may be related to medications, so check med list
may be result of additional health problems
elderly have blunted thirst
vein filling better indicator than skin turgor → check cap refill..
if checking skin turgor, check on sternum instead of hand
normal HCT (hematocrit) range
41-50%
high HCT = fluid loss = more concentrated
low HCT = fluid gain = more dilute
normal BUN levels
8-24 mg/dL
kidney function
should be in proportion to Cr
10:1 - 20:1
>20:1 is bad
normal creatinine levels
0.3 - 1.2 mg/dL
serum osmolality normal levels
280-295 mOsm/kg
<240 or >320 is critically abnormal
urine osmolality normal levels
50-1400 mOsm/kG
urine specific gravity normal levels
1.005 - 1.030
urine volume normal levels
at least 0.5 ml/kg/hr
~ 30 mLs/hr
lab trends of hypovolemia
increased HCT
increased BUN
BUN out of proportion to Cr
increased creatinine
high serum osmolality
high urine osmolaltiy
increased urine specific gravity
decreased urine volume
hypovolemia interventions
goal: prevent/correct abnormal fluid volume status before acute renal failure (ARF occurs)
assess/monitor: daily weights, VS, mental status, skin turgor, I&O
interventions: encourage PO fluids, IV fluid replacement, monitor for fluid overload, fall precautions, oral care, moisturize skin
evaluation: normal skin turgor, increased urine output, normal SG, normal labs
isotonic fluid
keeps osmolality the same while increasing overall volume in the vasculature
we’re just adding volume.. no shifting of solutes
0.9% NS
lactated ringers
indications:
mild hyponatremia
maintenance fluid replacement
rehydration/resuscitation
caution:
can cause fluid volume overload in individuals with cardiac, renal, and even liver problems
hypertonic fluid
more concentrated than isotonic
fluid will shift out of cells → into the bloodstream to dilute → cells will shrink
3% or 5% saline
indications:
cerebral edema
hyponatremia (sometimes)
cautions:
fluid overload in the vasculature
pulmonary edema
hypotonic fluid
less concentrated than isotonic
fluid will shift into cells from the vasculature to dilute the cells → cells will swell
0.45% of 0.33% saline
DO NOT USE FOR PTS WITH BRAIN SWELLING/PEDIATRICS
indications:
dehydration from gastric losses
conditions in which cells are dehydrated
cautions:
can cause cell lysis
can worsen edema
may cause hyponatremia
depletes intravascular volume (can cause hypovolemia)
D5W
5% dextrose in water
isotonic in the bag, hypotonic in the body
dextrose gets metabolized in the body → left with just hypotonic water
hypotonic effects → NEVER USE IN BRAIN AND PEDIATRIC PATIENTS
bonus if use in hypoglycemic pt so they get some dextrose
D5NS
5% dextrose in 0.9% saline
hypertonic in the bag, isotonic in the body
dextrose is metabolized in the body, you’re left with NS..
bonus if use in hypoglycemic pt so they get some dextrose
plasma volume expanders (PVEs)
stay in the vascular space
“volume expander”
helps to increase volume in the bloodstream → provides oncotic pressure
go to for hemorrhage… we prefer blood products compared to IV bc IV fluids will just wash away clotting factors
3 types:
crystalloids: has glucose/electrolytes
colloids: has proteins/starches that exert oncotic pressure
whole blood/packed RBCs
patients at risk for fluid volume deficit
hemorrhage
vomiting
diarrhea
burns
diuretic therapy
fever
impaired thirst
causes of hypervolemia
cardiovascular: heart failure
renal: kidney failure
SIADH - too much ADH → too much retention of water
liver failure
excess IV fluids
high sodium intake
excess water ingestion
cancer, thrombus, drug therapy, hypertonic fluid infusion, too much aldosterone
assessment of hypervolemia
third spacing
pulmonary congestion
SOB, decreased O2 sat, increased HR, crackles in the lungs
peripheral edema
+3 or +4 pitting edema.. bounding bouncy sounding pulse
brisk cap refll
increased CVP
increased BP
JVD
confusion, altered mental status
peripheral vs pulmonary edema
peripheral edema = usually right sided HF
pulmonary edema = usually left sided HF → back into the lungs
pitting vs non-pitting edema
non-pitting: usually r/t thyroid or lymphatics
pitting: when someone has too much fluid
bilateral vs unilateral edema
bilateral: fluid everywhere.. fluid volume overload
unilateral: indicates a likely vessel blockage (DVT) instead of FVE
what are electrolytes?
essential ions found in the body
positively charged (+, cation)
negatively charged (-, anion)
cations
positive charge
ex)
Na+
K+
Ca+2
Mg+2
anions
negative charge
ex)
chloride:Cl-
bicarbonate: HCO3-
phosphate: PO4-3
sulfate: SO4-2
functions of electrolytes
nerve conduction
muscle function
fluid balance
acid-base balance
cellular function
normal Na+ lab values
135 - 145 mEq/L
normal Cl- lab values
98 - 106 mEq/L
normal K+ lab values
3.5 - 5.0 mEq/L
normal Ca+2 lab values
9.0 - 10.5 mEq/L
normal Mg+ lab values
1.3 - 2.1 mEq/L
normal PO4-3 lab values
3 - 4.5 mg/dL
Na+ functions
normal range: 135 - 145 mEq/L
influences fluid distribution
influences blood pressure
acid-base balance
muscle contraction
nerve impulse transmission
regulated by kidneys
nutrient transport
Cl- functions
normal range: 98 - 106 mEq/L
direct relationship with Na+
nerve conduction
acid-base balance
lost in sweat
part of stomach acid, pancreatic enzymes
nutrient transport
dietary intake - Na+
higher sodium
processed foods
preserved foods
cheese
dried meats
canned foods (not fruits)
lower sodium
fresh/frozen veggies and fruits
dried druits
canned fruit
rice, pasta
unsweetened oatmeal
fish, shellfish
fat-free/low-fat milk & yogurt
hypernatremia
serum sodium: >145 mEq/L
losing water → sodium is now more conc in the blood
or gaining more sodium than water → hypertonic fluid IV or eating crazy sodium
water shifting into the bloodstream and out of cells → sodium more concentrated in the blood → cells shrink
patients at risk for hypernatremia
Na+ retention
hyper-aldosteronism → aldosterone incr sodium/water retention
cushing’s
uncontrolled diabetes mellitus
Na+ intake
lots of dietary Na+
corticosteroids → incr sodium/water rentention
IV fluids
hypertonic tube feedings w/o free H2O
water loss
H2O deprivation
increased insensible water loss (fever)
diarrhea
diabetes insipidus (DI) → peeing out body’s volume
inadequate water intake
elderly
infants
comatose pts
pts with cognitive dysfunction
hypernatremia: assessment findings
extremely rapid shift/extremely high Na+
brain cell shrinkage
vascular rupture
cerebral bleeding
neurological damage
death
increased Na+ = thirst
CNS signs → confusion, restless, agitation, seizures, coma, death
hypovolemic hypernatremia
see this w dehydrated ppl → see neurosymptoms and hypovolemia symptoms
tachycardia
decreased BP
dry mucous membranes
hypervolemic hypernatremia
see neuro symptoms + hypervolemia symptoms
weight gain
peripheral/pulmonary edema
increased BP
increased JVD
hypernatremia: interventions
hypovolemic
NS or LR until hypovolemia improves
provider will calculate H2O deficit
if necessary, then admin hypotonic fluid (1/2 NS, D5W, or PO H2O) to replace fluid deficit
rehydrate them by giving fluids
euvolemic
provider will calculate H2O deficit
adminster hypotonic fluid (1/2 NS, D5W, or H2O) to replace water deficit
give hypotonic fluid bc that will balance sodium level faster without adding too much volume
hypervolemic
free water replacement (D5W) + loop diuretics
hemodialysis if renal failure
dietary
restrict Na+
meds
diuretics
no meds that contain sodium
monitor
physical assessment findings
Is & Os
daily weights
labs: HCT, glucose, electrolytes
comfort
mouth, lip care
alcohol-free mouthwash
skin care
education
teach abt sodium in foods (<2000 mg/day)
OTC meds that contain Na+ should be stopped
body positioning if FVE
hyponatremia
serum sodium <135 mEq/L
losing more sodium than water
higher concentration of sodium in the cells than in vasculature
water moves into cells → cells swell → BAD in brain cells
cerebral edema → serizures + confusion
patients at risk for hyponatremia
increased water
syndrome of inappropriate ADH secretion (SIADH)
increased ADH → body holds onto more water
CHF
psychogenic polydipsia
increased Na+ loss
renal loss
GI loss
NG suctioning
skin loss
wound damage
severe burns
hormonal
hypoaldosteronism → body doesn’t retain as much sodium anymore (uncommon)
decreased dietary Na+ intake
rare
extreme hyponatremia
serum sodium: <120 mEq/L
patient might be suddenly very confused when they were not before → check their sodium level
acute cases: brain swelling is big concern
signs of hyponatremic encephalopathy
lethargy
headache
restlessness
disorientation
seizures, coma, death
anorexia
nausea & vomiting
muscle cramps
weakness
weak/absent DTRs
hyponatremia assessment findings
neuro
cerebral edema → headache
confusion
headache
MS
decreased muscle tone
weakness
decreased DTRs
fatigue
CV
increased HR
increased JVD if hypovolemia
postural hypotension
GI
increased motility
cramping
nausea/vomiting
respiratory
severe muscle weakness can inhibit respiratory functions
labs
na+ , cl - will be decreased
increased serum osmolality
increased HCT
hyponatremia interventions
monitor
I & O
labs
daily weights
LOC
potential for seizures if severe
fluids
hypovolemia: IVF/PO - w Na+ replacement → 0.9% NaCl
euvolemia: treat cause, no additional fluids needed
hypervolemia: restrict fluids if delusional or too much intake
severe/rapid onset w lots of symptoms: 3% NS slowly
prevent major risks w correcting sodium too fast
brain cells are super sensitive to fluid shifts
other
prevent further decline in serum na+
reorient
safety interventions
educate pt and family
hypertonic NaCl safety
3% or 5% NaCl IV
restrict to CCU/ICU/ED
never override drug dispensing machine to obtain the med
use smart pump alerts for proper rate guidelines
central line recommended
monitor Na+ q6h
monitor for possible side effects
elevated intracranial pressure (ICP), renal impairment, subarachnoid hemorrhage (SAH), natriuresis, increased urine output (UOP)
program rate as prescribed
too-rapid rate can cause osmotic demyelination syndrome
permanent brain damage
be careful in bringing Na+ level down and up
can’t be too quick or too aggressive
strip myelin off of nervous cells → irreversible damage to the brain
potassium normal serum level
3.5 - 5.0 mEq/L
potassium functions
correlates frequently with Na+ (opposing), but not direct relationship
important in cardiac and muscle function
too much or too little causes arrythmias
maintaining electrolyte balance
nerve function
muscle function
cramping
heart function
arryhthmias
acid-base balance
kidney function
cellular metabolism
**K+ plays big role in depolarization of muscle
dietary intake - K+
higher K+
dried fruit
spinach
beef
chocolate
pork
tomatoes
potatoes
bananas
lower K+
eggs
bread
cherries
apples
peaches
cauliflower
celery
green beans
peppers
peas
hyperkalemia serum levels
serum potassium: >5 mEq/L
hyperkalemia patients at risk
decreased excretion → bc renal failure
decreased aldosterone → bc adrenal insufficiency/addison’s disease
potassium-sparing diuretic → spironolactone
K+ shift → excessive exercise, cell injury, catabolism, diabetes mellitus, medications
other→ salt substitutes, digoxin, beta-blockers
hyperkalemia: asssessment
GI
nausea/vomiting
abdominal cramping
diarrhea
cardiac
tall, peaked T-waves
widening QRS
deadly arrhythmias
mental
irritability (not confusion)
anxiety
fatigue
neuromuscular
paresthesia
weakness
muscle cramping
hyperkalemia: ECG changes
tachycardia → bradycardia
possible cardiac arrest
tall, tented T waves
hyperkalemia: interventions
eliminate K+ intake → no salt subtitutes
increased K+ elimination → loop diuretics, SODIUM POLYSTYRENE SULFONATE
promotes GI excretion of potassium in stool
force K+ out of ECF into ICF
insulin + glucose
insulin lowers blood sugar by moving sugar into cells
glucose goes into cells but K+ does too
K+ levels decrease because it moved inside the cells
give insulin IV to lower K+ levels → BUT ALSO GIVE GLUCOSE bc we made glucose also move inside the cells → prevent hypoglycemia
protect the heart
10% calcium gluconate IV
dialysis if renal failure
monitor: ECG, labs, bowel sounds, stool, muscle strength
educate: diuretic use, muscle weakness, avoid K+ rich foods, safety
hypokalemia serum level
serum K+: <3.5 mEq/L
hypokalemia: patients at risk
renal
hypoaldosteronism
skin
excessive diaphoresis
GI
vomiting, diarrhea, NG suctioning, poor PO intake
meds
K+ wasting meds → furosemide
corticosteroids → prednisone… in hyperaldosterone, high levels of steroids in body.. steroid hormones cause elevated blood sugar → increase insulin production. K+ goes into cell as a result along with glucose.
conditions/medications that cause elevated cortisol or blood sugar will result in hypokalemia → K+ moving inside cells
laxative overuse
excessive insulin
hypokalemia assessment
CV
prominent U waves
S-T depression
prolonged QRS
MS
weakness, parethesia
decreased smooth muscle function
neuro
decreased DTRs
depression
confusion
GI
decreased gastrointestinal motility
paralytic ileus
respiratory
shallow respirations
miscellaneous
hyperglycemia
fatigue
hypokalemia: ECG changes
prominent U wave
S-T depression
prolonged QRS → causes ventricular arrhythmias → deadly
hypokalemia: interventions
hydrate to maintain urine output of <0.5 mL/kg/hrHydrate
supplement oral: replace K+ in diet or supplements
supplement IV:
no more than 10-20 mEq/hr by IV pump
GIVE 10 MEQ/HR by IV PIGGYBACK → if give too quick, cause cardiac arrhythmias
NEVER GIVE K+ IV PUSH → WILL KILL PT
monitor: ECG, vitals, respiratory status, BS
other: treat constipation, hold K+ wasting diuretics, consider changing diuretic class change
education: S/S hypokalemia, laxative overuse, safety, S/S orthostatic hypotension
Ca+2 normal serum levels
serum level: 9 - 10.5 mEq/L
calcium functions
required for clotting
needed for muscle contractions
used in enzyme activity
assists with nerve impulses
important for strength and durability of bones/teeth
what is Ca+2 absorption influenced by
active vitamin D (calcitrol/sunlight) required for GI absorption
PTH → increased serum Ca+2
PTH releases Ca+2 and signals kidneys to activate vitamin D → GI tract will absorb more Ca+2
INCR PTH = INCR CA+2
INCR calcitonin = DECR Ca+2
Ca+2 and phosphate have an inverse relationship
when body detects high Ca+2 → stop producing PTH and instead secrete calcitonin
calcitonin tells bones to absorb calcium bc too much in blood and tells kidneys to not secerete vitamin D. also tells gut to not absorb calcium
CALCIUM CALMS
dietary intake Ca+2
higher in Ca+2
almonds
antacids
creamed soups
molasses
sardines
turnip greens
spinach
lower in Ca+2
fruits
beans
carrots
radishes
hypercalcemia serum concentration
serum calcium > 10.5 mEq/dL
patients at risk for hypercalcemia
RHINO
Renal Insufficiency
cannot decrease Ca+2 through kidneys
Hyperparathyroidism
parathyroid hormone is overactive
too much PTH = too much Ca+2 absorbtion
Immobilization
reduced mechanical loading on bones → calcium leaks out of bones
Neoplasms
cancer
bone metastasis → cancer eats away at bones and bone contents release
Other endocrineopathies
issues w thyroid → impact parathyroid
hypercalcemia assessment
neuro
LOC changes
confusion
depression
lethargy
GI
decreased peristalsis
constipation
abdominal discomfort
MS
weakness
fatigue, lethargy
decreased DTRs
bone pain
GU
kidney stones
polyuria
dehydration
CV
decreased HR
DVT risk
heart block
postural hypotension
ECG changes → shortened S-T
hypercalcemia interventions
hydration
3-4 L daily → decreases risk of calcium stones → flush it thru
promote excretion
IV NS → match rate up to UOP
loop diuretics
reduce serum Ca+2
calcitonin → inhibits bone breakdown
avoid Ca+2 containg meds
calcimimetics to regulate PTH
inhibit bone loss of Ca+2
weight-bearing activities
bisphosphonates → decrease calcium release from bones by inhibiting osteoclasts
safety/monitor
protect against fractures
ambulation
fall risk
telemetry
monitor VS, labs
other
strain urine (stones)
Tx constipation, nausea
decreased dietary intake of Ca+2
dialysis → if kidneys aren’t working at all
correct underlying cause
no thiazide diuretics
hypocalcemia serum level
serum Ca+2: <9 mg/dL
start seeing effects when less than 7 mg/dL
patients at risk for hypocalcemia
inadequate Ca+2 intake
inadequate absorption
ETOH → ethanol alcohol
vitamin D deficiency → not absorbing Ca+2
Ca+2 excretion
diuretics
anticonvulsants
calcitonin
laxatives
other
increased dietary phosphate
decreased PTH
calcium deposits in bone, tissue
blood transfusions
memory trick for patients at risk of hypocalcemia
DAILY PIC CAD
diuretics
alcohol
inadequate intake/absorption
laxatives
yielded photphate increase
pth decreased
iv blood transfusions
calcitonin
calcium depots in bone/tissue
anticonvulsants
vitamin D deficiency
hypocalcemia assessment → mild to moderate
NEURO SYMPTOMS: CATT (mild to moderate) HILLS (severe)
Confusion
Anxiety
Tremors & palpitations
Tingling & numbness in hands, toes, and lips
CV
palpitations
Miscellaneous
muscle cramping
fatigue
weakness
brittle nails, hair loss
hypocalcemia assessment → severe
NEURO SYMPTOMS: CATT (mild to moderate) HILLS (severe)
Hyperreflexia → big DTR reaction reflex
Irritability
LOC changes → delirium, non-responsiveness
Laryngospasm & stridor
not enough Ca+2 can cause muscle excitability
bad if have spasm in larynx bc can close airway and cause stridor
Seizures & tetany
overexcitability → missing calm component
CV
impaired clotting
hypotension
ECG changes
vtach, vfib
prolonged QT interval
*treat EKG changes with calcium gluconate..give calcium to lower threshold for cardiac arrhythmias
hypocalcemia assessment: mild to severe
chvostek’s sign
muscular contraction/twitching on the face
trousseau’s sign
arm curls in when BP cuff placed on
hypocalcemia: interventions
administer
Ca+2 supplements
PO: 1-1.5 hours after meals
IV: calcium gluconate
meds
vitamin D w/dietary Ca+2
phosphate binders: lower phosphate levels, increase Ca+2 due to inverse relationship
pain management
monitor
breathing
bone fx
chvostek and trousseau signs
labs
ECG
other
safety: seizure precautions, fall precuations, reorient if changes in LOC, lift/draw sheet
educate
decreased risk of osteoporosis: Ca+2, vitamin D, exercise (esp if weight bearing)
phosphate normal serum levels
serum phosphate: 3 - 4.5 mg/dL
phosphate functions
bone and teeth formation
essential to tissue oxygenation (RBCs)
cellular metabolism (ATP)
DNA and RNA synthesis
acid-base balance
Ca+2 regulation → inverse relationship
cell membrane structure
**influenced by PTH due to inverse relationship with Ca+2
phosphate is regulated by the kidneys → excreted by kidneys
phosphate dietary intake
most of the phosphate in our body comes from our diet
higher in phosphate
dairy products
meat and poultry
fish
lentils
split peas
chickpeas
almonds
sunflower seeds
whole wheat bread
brown rice
bran cereals
carbonated beverages (containing phosphoric acid)
lower in phosphate
fruits
vegetables
grains
starches
white bread
white rice
eggs
pasta
hyperphosphatemia serum level
serum level: > 4.5 mg/dL
hyperphosphatemia: patients at risk
increased intake
vitamin D intoxication
phosphate laxatives or enemas
production or release (cell damage)
hemolysis
rhabdomyolysis
tumor lysis syndrome
sickle cell, hemolytic anemia
hemolysis
reduced loss
renal insufficiency
hypoparathyroidism → less Ca+2 → more phosphate
thyrotoxicosis
hyperphosphatemia assessment
typically patients experience effects of hypocalcemia → bc inverse relationship w phosphate
neuro
tetany
faster nerve transmission
GI
abdominal cramping
diarrhea
nausea
CV
increased HR (prolonged QT interval)
other
decreased serum Ca+2
calcium deposits in skin, soft tissues, corneas, kidneys (longer-term consequence)
hyperphosphatemia interventions
prevention
identify and treat the cause (usually renal)
restrict phosphate-containing foods (stop diary)
IV fluids (to dilute) + diuretics to increase renal excretion
isotonic fluids → don’t wanna change serum osmolality → hydrate body and get rid of excess electrolytes
adminster phosphate-binding agents (sevelemer, Phos-Lo) → give with meals
bind to phosphate → less phosphate in the blood
hemodialysis may be necessary → if kidney’s aren’t functioning