REFRESHER: RENAL FABS

LECTURER: PROFESSOR KEITH KAINNE D. GARINO

FLUIDS AND ELECTROLYTES ● 0.25 NaCL

● 0.45 Nacl (half normal saline)

BODY FLUID COMPARTMENTS

FLUID IMBALANCES
① EXTRACELLULAR
- It is composed of intravascular and interstitial.
FLUID VOLUME DEFICIT
②INTRACELLULAR ① ISOTONIC (HYPOVOLEMIA)
- Water loss is equal to electrolyte loss
BODY FLUID TRANSPORT - Give isotonic IV fluids
① OSMOSIS

LO
- Movement of fluids from low to high concentration of ② HYPERTONIC
solute - Water loss is greater than electrolyte loss
- Example: cellular dehydration - Condition is cellular dehydration
- Give HYPOTONIC IV fluids
② DIFFUSION
- Movement of solute from high to low concentration ③HYPOTONIC
- Example: gas exchange - Water loss is less than electrolyte loss
- Condition is cellular edema
IV FLUIDS - Give HYPERTONIC IV fluids.

IL
① ISOTONIC
-
-
-
-
Equal concentration, osmolality or osmolarity to blood.
Stays in the intravascular space.
Usually used when refilling intravascular space
Always RAPID infusion
FLUID VOLUME EXCESS
① ISOTONIC (HYPERVOLEMIA)
-
-
Excess fluid in intravascular
Do not give IV fluids

② HYPERTONIC
R
Examples
- Increase concentration in sodium ⇒ hypernatremia
● 0.9 NaCl
- Give HYPOTONIC IV fluids
● Lactated Ringers – usually given to burn patients
● D5W (in the bag)
③ HYPOTONIC
- Decrease concentration of blood due to water
② HYPERTONIC (>.9 NaCL, D5W, D5W with other solution)
AR

intoxication, decreasing the concentration of sodium.

- High concentration, osmolality or osmolarity to blood
- Give HYPERTONIC IV fluids
- Attracts water outside the cell, making the cell shrink,
causing cellular dehydration.
- Fluids from the cell will shift to blood. ASSESSMENT FVE FVD
- Always SLOW infusion
Body weight High Low
Examples (1kg = 1L; best
● 3% saline indicator of fluid
status)
● 5% saline
● 10% dextrose in water (D10W) Skin Cool, edema Dry, poor
C

● 5% dextrose in 0.9 saline turgor/tenting

● 5% dextrose in 0.45 saline (best site for
● 5% dextrose in LR turgor: sternum)

③ HYPOTONIC (<.9 NaCl, D5W) Eyes N/A Sunken

- Low concentration, osmolality or osmolarity to blood
Neck vein Distended Flat
- Attracts water inside the cell, making the cell swell
causing cellular edema. Lung sound Crackles or rales N/A
- Fluids from blood will shift to cell
- Always SLOW infusion GIT Diarrhea Constipation

Examples Muscle Weak

● D5W (in the body)
● 2.5% Dextrose
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

ELECTROLYTES IMBALANCES
LOC Altered

Vital signs High BP, HR, and Low BP, High HR POTASSIUM
RR and RR
HyperTachyTachy HypoTachyTachy - Always PRIORITY; POTA ARTE
- Any increase or decrease in K:
Serum ○ Damages the heart, thereby decreasing its
osmolality function.
(275-300 ○ Decreases BP or HR
mOsm/kg; ○ May lead to cardiac arrhythmias or
concentration of
dysrhythmias
solute)

LO
- Normal value: 3.5-5 mEq/L (same with serum
Hematocrit albumin)
(M:42-52%; F: - Major intracellular cation
35-45%) Low High - Increases musculoskeletal contraction
○ Hyperkalemia ⇒ diarrhea
BUN (10-20 ○ Hypokalemia ⇒ constipation
mg/dlL) - Abnormality can cause cardiovascular irregularity
(decreased).
Creatinine
(0.6-1.2 mg/dL)
Cause Hypokalemia Hyperkalemia

IL
Serum sodium
(135-145 mEq/L)

Urinary output

Urine specific
gravity
High

Low
Low

High
Loop diuretics (K,
Na, Mg wasting)

Addison’s disease
(decrease K
excretion)
✓

✓
R
(1.010-1.025;
retention) Diarrhea ✓
(increase K
Central venous High Low excretion)
pressure (8-12
mmHg)
AR

Chronic Renal ✓
Failure (increase
Urine output is inversely proportional to urine specific K retention)
gravity.
Metabolic ✓
Central venous pressure is directly proportional to water. acidosis
(decrease ph →
Intravascular
Intervention FVE FVD shift)

Body weight Monitor daily (done in the morning; Fasting (low ✓

same clothes, time and weighing scale) potassium intake)
C

Intake and I > O → Retention Burn injury (K ✓

output (should be I < O → Loss [cell] → blood)
approximately Monitor per shift
equal) Steroids (increase ✓
K excretion)
Fluid intake Restrict Replace,
(800-1000 increase, or force Insulin ✓
mL/day) fluids (intracellular shift)

Diet Low sodium (salt) N/A

Assessment Hypokalemia Hyperkalemia
Medication Diuretics IV fluids
GIT Constipation Diarrhea
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

Heart rate Diarrhea (Na ✓

LOW excretion)
Blood pressure
Chronic renal ✓
ECG Changes HypUkalemia Wide PRolonged failure (Na
ShuT Down FlaT Tall but Plat retention
● ST ● Flat P wave
depression ● Wide QRS Cushing’s ✓
● Flat T wave ● Prolonged syndrome (Na
● U wave PR interval retention)
● Tall T wave
Fasting (Na ✓

LO
intake)

Fluid loss (water ✓

Intervention Hypokalemia Hyperkalemia 1st)

Diet Increase K Decrease K SIADH (water 1st) ✓

Priority V/S Monitor HR (any irregularities) → Salty foods ✓

REPORT
Heart failure ✓
Medication ● Oral K Do It SO Cardiac (water 1st)

IL ●

●
IV
NEVER
KCl =

BOLUS AND
RAPID
Potassium
sparing
diuretics
Problem Subside
● Diuretics →
Loop
(furosemide)
● Insulin with
dextrose
● Salbutamol
Assessment

CNS
Hyponatremia

Cerebral edema,
decreased LOC,
Hypernatremia

Cerebral shrink,
decreased LOC,
R
increase ICP, seizure,
(spironolacto (adrenergic seizure polydipsia (thirst)
ne) agonist)
● Calcium Renal Polyuria Oliguria
gluconate for
cardiac
Skin FVD FVD → dry
arrhythmia
AR

FVE → edema
● Sodium
Polystyrene
Sulfonate
(Kayexalate) Intervention Hyponatremia Hypernatremia

Fluid intake FVE → RESTRICT

SODIUM FVD → REPLACE
- Normal value: 135-145 mEq/L
- Major intravascular cation Medications FVE FVE
● Osmotic ● Loop
- Major determinant for concentration of blood
○ High Na = High concentration = Hypertonic FVD FVD
C

○ Low Na = Low concentration = Hypotonic ● Hypertonic ● Hypotonic

- Regulates neuromuscular activity fluids fluids
- Sodium and water are not mutual
○ If sodium increases/decreases first, water Sodium Diet High Low
also increases/decreases.
○ If water increases/decreases first, sodium CALCIUM
decreases/increases.
- Normal value: 9-10 mg/dL
- Major components of the bones
Cause Hyponatremia Hypernatremia - Decrease musculoskeletal contraction
○ Inversely proportional
Loop diuretics (K, ✓ ■ High Ca = hypoactive
Na, Mg wasting) ■ Low Ca = Hyperactive
- Increases cardiac muscle contraction
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

○ Directly proportional
spasm)
■ High Ca = High BP, HR ● Chvostek’s
■ Low Ca = Low BP, HR (cheeks)
- Abnormality can cause dysrhythmia ● Spasm
- Excess in the kidneys can cause supersaturation (larynx and
(solid) and osmotic diuresis (attracts water) bronchus)
○ High Ca in the kidneys ● Seizure
■ Renal calculi
GIT Diarrhea Constipation
■ Polyuria → FVD → thirst
Renal Renal calculi
Cause Hypocalcemia Hypercalcemia Polyuria → FVD

LO
→ Thirst
Lactose ✓
intolerance (low ECG changes Hypolonged ST ShorT
Ca absorption) QT ● Short ST
● Prolonged ST ● Wide T
Diarrhea ✓ ● Prolonged
(increase Ca QT
excretion)

Thiazide diuretics ✓ Intervention Hypocalcemia Hypercalcemia

(increase Ca

IL
reabsorption)

Vitamin D
deficiency (low Ca
absorption)

Hyperparathyroidi
✓
Diet

Medication ●

●
High Ca (milk,
dairy)
Vitamin D

Calcium
gluconate
Calcium
●
Low Ca

Calcitonin
(Ca
blood
from
—>
R
✓
sm (high PTH = carbonate bones)
Ca [bones) → ● IV
blood phosphorus
(calcium
Immobility (Ca ✓ binder ––
[bones] → blood) Always
AR

PABABA)
Chronic renal ✓
failure (low MAGNESIUM (MAG-ISA; MAGNUM)
Calcitriol → low
Ca absorption) - Normal value: 1.5-2.5 mEq/L
- Vasodilator
Dehydration (low ✓ ○ Increased blood flow → warm, flushed
fluids → increase appearance
Ca concentration) ○ Decreased BP, HR
- Neuromuscular effects are similar to those of calcium
Acute pancreatitis ✓
C

(Ca [blood] →
pancreas) Cause Hypo Hyper
magnesemia magnesemia

Assessment Hypocalcemia Hypercalcemia Antacids (Mg OH) ✓

Heart rate Low High Fasting (low Mg ✓

intake)
BP Low High
Loop diuretics ✓
Neuromuscular TwiTChing Hypoactive
SpaSm ● Weaknees Laxatives (milk of ✓
● Tetany ● Reflex → low magnesia)
● Trousseau’s
(carpopedal
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

Alcoholism ✓ m (low PTH = low

(decreases Ca)
electrolytes,
vitamins and Chronic renal ✓
minerals) failure (low Ca)

Magnesium ✓ Respiratory ✓
sulfate alkalosis (High pH
→ Intracellular
Chronic renal ✓ shift)
failure (Mg
retention) Tumor lysis ✓

LO
syndrome (P
Insulin (Mg ✓ inside tumor →
intracellular shift) blood)

Assessment Hypo Hyper Assessment Hypo Hyper

magnesemia magnesemia phosphatemia phosphatemia

Heart rate Refer to Hypercalcemia Hypocalcemia

High Low
BP

IL
Neuromuscular

ECG Changes
Hypocalcemia

Tall but depreST

● Tall T wave
● Depressed
ST
Hypercalcemia

HyPRolong and
wide QRS
● Prolonged
PR
Intervention

Diet

Medication
Hypo
phosphatemia

High P (protein)

IV phosphorus
Hyper
phosphatemia

Low P

Al OH (Amphogel)
R
● Wide QRS
ABG ANALYSIS

Intervention Hypo Hyper - To assess ventilation and acid-base balance

- Blood withdrawal at the radial artery
AR

magnesemia magnesemia

Diet High (fiber) Low CONSIDERATIONS

● Before assessing ABG, perform ALLEN’S TEST.
Medication ● Magnesium ● Calcium ○ Done by testing the patency of ulnar artery
sulfate gluconate or collateral circulation
● Loop
● Use heparinized syringe
diuretics
● Send to laboratory immediately with ice after
withdrawal
PHOSPHORUS
- Normal value: 2.5-4.5 mg/dL ABG INTERPRETATION
C

- Inversely proportional to calcium 1. Label if acidosis or alkaline

○ High Ca = Low P 2. Identify
○ Low Ca = High P a. Respiratory: if pH and PCO2 have the same
label
b. Metabolic: if pH and HCO3 have the same
Cause Hypo Hyper
label
phosphatemia phosphatemia
c. Mixed (respiratory and metabolic): all have
Antacids (Al OH) ✓ the same label
3. Compensation
Fasting (low P ✓ a. Fully compensated: PCO2 and HCO3 are
intake) opposite (abnormal); pH is normal
b. Partially compensated: PCO2 and HCO3
Hypoparathyroidis ✓ opposite; pH is abnormal (all are abnormal)
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

c. Uncompensated: if PCO2 or HCO3 is within PHASES

normal range; pH is abnormal ① Onset / Initiation
- Start of injury with no clinical manifestations

② Oliguric Phase
- 8-15 days
- Urine output:
○ < 30 ml/hr
○ < 400 ml/day

- Decreased GFR (Normal: 120 ml/min) → :

LO
○ Decreased removal of waste products (
increased BUN and creatinine) → uremia
and azotemia → renal encephalopathy
○ Decreased removal of water → decreased
urine → oliguria and FVE
○ Decreased removal electrolytes → increased
potassium
- Decreased production of calcitriol → decreased
calcium absorption → decreased Ca = increased P
- Decreased reabsorption of HCO3 → decreased

💡
IL PRACTICE HERE 💡
-
HCO3 → metabolic acidosis

③ Diuretic Phase
- 4-5 L/day
Increased GFR → increased removal:
○ Waste products → Decreased BUN and
R
creatinine (ABN)
https://survivenursing.com/abg/ ○ Water → Decreased H20 → increased urine
→ polyuria and FVD
○ Electrolytes → Decreased electrolytes →
RENAL DISORDERS decreased Na and K
AR

ACUTE KIDNEY INJURY / ACUTE RENAL FAILURE ④ Recovery / Convalescent Phase

- 1-2 years
- Sudden loss of kidney functions
- Normal value
- Reversible
CHRONIC KIDNEY INJURY
CAUSES
① Prerenal –– decreased blood flow going to the kidneys - Progressive loss of function of the kidneys
● Dehydration - Irreversible
● Liver cirrhosis - GFR: < 30ml/min
● Hemorrhage - Duration: 3 months or more
C

● Heart failure
● Burns STAGES ESTIMATED GFR (mL/min)

② Intrarenal or intrinsic –– there is damage in renal Risk > 90

parenchyma or any part of the kidneys.
● Antineoplastic medication Mild CKD 60-90
● Glomerulonephritis
● Nephritis Moderate CKD 30-60
● Rhabdomyolysis
Severe CKD 15-30

③ Postrenal –– obstruction of urine. ESRD < 15

● Renal calculi
● Bladder cancer
● BPH
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

CLINICAL MANIFESTATIONS ○ Diuretics (loop)

🟨
Early CKD

🟩
If one of the kidneys is not functional, the other Hyperphosphatemia

🟩
kidney will compensate → increased GFR → Diet: low P (protein)
Polyuria Medication: Al OH

🟨 🟩
Oliguric Hypocalcemia

🟩
Decreased GFR Diet: high Ca
○ Increased BUN and creatinine Supplement: Vitamin D
○ Oliguria and FVE

🟨 🟩
○ Increased K, Na, and Mg Metabolic Acidosis

LO
Decreased calcitriol Medication: sodium bicarbonate
○ Decreased Ca = increased P → bone

🟨 🟩
disorders Anemia

🟨 🟩
Metabolic acidosis Laboratory: low Hct and Hgb

🟩
Low erythropoietin → decreased stimulation of bone Medication: epoetin alfa

🟩
marrow → decreased RBC → anemia; decreased Supplement: iron and folic acid
O2 and nutrients delivery → both leads to weakness Procedure: blood transfusion if the level of Hgb is 7
and fatigue ○ Hgb 7 will go to heaven

🟩
MANAGEMENT Uremia and Azotemia
FVE

IL
🟩
🟩
🟩
🟩
🟩
🟩
Body weight: monitor daily
I & O: monitor every shift
V/S: monitor every 4 hours
Lung sounds: crackles
Fluid intake: limit or restrict to 800-1L/day
🟩
🟩
🟩
Monitor: BUN and creatinine; LOC
Avoid sedatives
Diet: low protein, high carbs
Activity: bed rest

TREATMENT
R
🟩
Diet: low Na
Medications: diuretics
HEMODIALYSIS
- Functions:
🟩
FVD
○ Removal of excess fluid and wats products
🟩
Body weight: monitor daily
○ Correction of electrolyte and acid-base
AR

🟩
I & O: monitor every shift
balance.
🟩
V/S: monitor every 4 hours
- Dialyzer –– an artificial kidney that has a filter and is
🟩
Lung sounds: crackles
semi permeable (cellophane).
🟩
Skin: dry and poor turgor
Fluid intake: increase ○ Warms the blood
- Dialysate –– nonsterile
○ Content: water, electrolytes, bicarbonate
🟩
Hyperkalemia
(depends on what the clients need)
🟩
V/S: monitor HR

🟩
Diet: low K

🟩
Medication MANAGEMENT
○ Diuretics (loop) Body temperature:
C

○ Insulin with dextrose a. Normal: Warm

🟩
○ Salbutamol b. Fever → Infection → REPORT

🟩
○ Calcium gluconate Laboratory: BUN, creatinine, CBC
○ Sodium polystyrene sulfonate (Kayexalate) Body weight:
for Na and K exchange in GIT a. Before: FVE

🟩
b. During and after: FVD

🟩
Monitor signs of bleeding
🟩
Hypermagnesemia

🟩
Meals are ALLOWED during dialysis
🟩
V/S: monitor HR and BP
Withhold water soluble supplements ––
🟩
Monitor neuromuscular

🟩
antihypertensive medications
🟩
Diet: low Mg (fiber)
Medications: Complications: STOP, SLOW, REPORT!
○ Calcium gluconate
○ Avoid magnesium based meds
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

VASCULAR ACCESS 🟩 Warm dialysate

① External ○ Dry heating –– uses heating pad,
- Subclavian, jugular and femoral –– short term. ■ Causing vasodilation → increased
- Has portal of entry blood → increased urea excretion
- AV shunt –– can be used immediately. ■ Decreasing abdominal pain/cramps
- WOF: → CONTINUE (normal) as it will

🟩
○ Infection disappear after few exchanges
○ Bleeding Drainage appearance:
○ Clotting ○ Pink/clear/yellow – normal
○ Skin erosion ○ Cloudy – peritonitis
○ Red – bleeding

LO
② Internal ○ Brown – perforated bowel

🟩
- Gold standard; very fragile ○ Urine/amber – perforated bladder
- Takes several weeks to mature Position: semi-fowler to relieve pressure in the

🟩
- Patients are encouraged to perform arm exercises diaphragm.
through the use of a stress ball. If the drainage stops, there is an obstruction:
- Long term use ○ Check patency

🟩
- AV fistula –– most common ○ Turn side to side → increases drainage
- AV graft Post monitoring:
- WOF: ○ Check glucose in the urine and blood.
○ Arterial steal syndrome

IL ■ Decreased arterial flow → pallor

hand → report
■ Increased venous flow
○ Hematoma
○ Aneurysm
KIDNEY TRANSPLANT
Graft Rejection –– inflammatory reaction/response
● Fever, malaise, increased WBC → REPORT
● Pain (incision) → REPORT
● Renal failure → REPORT
R
🟩
NURSING RESPONSIBILITIES Medications
Assess for patency ● Immunosuppressant → LIFETIME!
○ Palpate for thrill ○ WOF: infection
○ Auscultate for bruit
■ If both are absent, there is an
🟩
Health Teaching
AR

🟩
obstruction → REPORT Avoid prolonged contact to ill person

🟩
Avoid pressure and puncture ○ Sitting
Cannula clamp for external AV shunt to prevent risk ○ Contact sports

🟩
for bleeding ○ Infection
Occlusive dressing for external access

PERITONEAL DIALYSIS
- Semipermeable membrane → peritoneum
- Dialysate
○ Content: water and sugar (hypertonic)
C

○ Sterile
- Insertion site: below the umbilicus (avascular––
pinkish)
- Dwell time: 30 minutes
- Complications:
○ Peritonitis –– board-like rigid abdomen;
blumberg (rebound) tenderness
○ Hyperglycemia –– due to over dwell time;
reverse absorption happens.
○ Hypertriglyceridemia

🟩
MANAGEMENT
Pre-insertion instruction:
○ Empty bladder and bowel
 REFRESHER: RENAL FABS
LECTURER: PROFESSOR KEITH KAINNE D. GARINO

ANAPHY
TFN
HA
FNP
HE ❓ RANDOM QUESTION ❓
MCN
NUTRI
CHN
PHARMA
BIOETHICS
NI

LO
MEDSURG
GERON
NURSING RESEARCH
PSYCH
NLM
DWET
DISASTER NURSING
INP
ACPS
SPAT

IL
①②③④⑤⑥⑦⑧⑨⑩ ❶❷❸❹❺❻❼❽❾ →←↑↓ ≤ ≥
💡
✅
🟩
Remember / Important notes
Purpose
R
🔏
Nursing action | Intervention

🖋
Must to know

🚨
Nice to know

🟨
Emergency

🟥
Signs and symptoms
AR

📝
Contraindication

🌟
Diagnosis

💊
Rationale
Medications

💡 WALA PA ME MAISIP HERE 💡

❗ ❗
C

WALA PA ME MAISIP HERE

❗❕ WALA PA ME MAISIP HERE ❗❕

❓❔ BOARD EXAM QUESTION ❓❔