FLUID VOLUME ASSESSMENT

Parameters Fluid volume deficit Fluid volume Excess

Weight Decrease Rapid increased

-most accurate measurement of fluid status

-measured at the same time, on the same scale, and the same
clothes on the client

Mild

-1-2 Liters of water/2% of the body weight

Moderate

- Loss of 3-5 liters of water/5% of the body weight

Severe

- 5-10L of water loss/8% of the body weight

Pulse Weak Full

-reflects the amount of blood ejected with each heart beat Thready- weak difficult to Bounding- full and spring
palpate, fairly rapid, like on palpation
-normal is 60-100beats/min difficult to count
Increase rate
-palpate one of the pts arterial pulse using the pads of your index Increase rate
and middle finger

-count the rate for 1 minute (normal or abnormal)

-Assess the rhythm (regular/irregular)

-Assess Pulse Amplitude using scale

0—Absent pulse

1—Weak/Thready- difficult to palpate

2—Normal pulse-easily felt

3—Bounding-full and spring like on palpation

Blood pressure Decrease Increase

-is related to the amount of blood the heart pumps

Indirect Measurement The pulmonary artery PCWP-is the pressure

pressure (PA pressure) measured by wedging a
a. BP apparatus- using appropriate size of the bladder cuff to avoid is a measure of the pulmonary catheter with
false readings blood pressure found in an inflated balloon into a
the pulmonary artery. small pulmonary arterial
b. Automated blood pressure- designed to take readings
This is measured by branch.
repeatedly, computes and digitally records the readings
inserting a catheter into
provides an indirect
the pulmonary artery.
c. Palpable pressure- estimates SBP estimate of left atrial
The mean pressure is
pressure (LAP).
-is used if there’s difficulty hearing the patient’s blood pressure typically 9 - 18 mmHg,
during hypotension and the wedge measured by inserting
pressure measured in the balloon-tipped, multi-
-place the cuff on the pts arm left atrium may be 6- lumen catheter (Swan-
12mmHg Ganz catheter) into a
-palpate the brachial or radial pulse, then inflate the cuff till the pulse peripheral vein (, jugular
is no longer felt or femoral vein), then
advancing the catheter
-Then, slowly deflate the cuff, note when the pulse is felt Normal pulmonary into the right atrium, right
artery pressure is 8-20 ventricle, pulmonary
-Record a palpable pulse as “90/P. mm Hg at rest. If artery, and then into a
the pressure in the
DIRECT Measurement branch of the pulmonary
pulmonary artery  artery. The catheter has a
- invasive to obtain BP readings, and measure fluid volume lumen (port) that opens at
is greater than 25 mm Hg
the tip of the catheter
at rest or 30 mmHg during
-use an arterial catheter if frequent BP measurements are required distal to the balloon. This
physical activity, it is
port is connected to a
1. ARTERIAL LINE abnormally high and is
pressure transducer.
called Pulmonary 
- continuously monitor BP and can be used to sample arterial blood
for ABG analysis Hypertension - Normal is 6-12
mmHG 
-it’s inserted into radial, brachial or femoral artery

2. Pulmonary Artery Catheter  

-it measure fluid volume status, PAP, pulmonary artery wedge

pressure, CO and CVP

- inserted into the subclavian vein/inter jugular vein-SVC-RA

and RV--PA

-the TIP of catheter rest in pulmonary artery

- Normal Systolic PAP is 15-25mmHg

-Systolic PAP reflects pressure from the contraction of RA

-Normal Diastolic PAP is 8-15mmHg

-Diastolic PAP reflects the lowest pressure in the pulmonary

vessels

-Mean PAP is 10-20mmHg

3. Central Venous Catheter

- can measure CVP another useful indication of patient’s fluid status

-it measures the pressure of the blood in the central circulation

- CVP is a measure of blood volume and venous return. It reflects

RIGHT-SIDED filling pressures. It is primarily used to monitor fluid
volume status.

- considered a direct measurement of the blood pressure in the right

atrium and vena cava. It is acquired by threading a central venous
catheter (subclavian double lumen central line shown) into any of
several large veins.

 - Normal range for CVP is 2-8 cm H20 or 2-6 mmHg.

Mucous membrane (mouth) Dry, crack lips Moist

SKIN Poor skin turgor Dependent edema

Color: No presence of bruising, cyanosis, pallor, erythema. Normal turgor- skin +1pitting edema- slight
Uniformity of color. Hypopigmented or hyperpigmented quickly return to original imprint of finger
shape.
Moisture: Relatively dry with minimal amount of perspiration, +4 pitting edema- a deep
Skinfolds is fairly dry. Abnormal-skin returns imprint, skin is slow to
slowly over 30 seconds return to its original
Turgor- gently squeezes the skin on the forearm or sternal area contour
using between thumb and forefinger.
Tenting

Urine Input Decreased/ oliguria Increased

Eyes Sunken Papillary edema

LOSSES CAN BE:

⮚ MILD- loss of 1to 2 liters/2% of the body weight
⮚ MODERATE- loss of 3-5liters/5% of the body weight
⮚ SEVERE-5-10 L of water/8-% of body weight

Clinical Manifestations Mild (1-2liters) Moderate (3-5 liters) Severe (5-10 liters)

LOC Alert Lethargic Obtunded

Capillary refill time 2 seconds 2-4 seconds Greater than 4 secs, cool limbs

Mucous membrane Normal Dry Cracked

HR Slight increased Increased Very increased

RR Normal Increased Increased/Hyperpnea

BP Normal Normal but orthostasis Decreased

 Pulse Normal Thready Impalpable

Skin turgor Normal Slow Tenting

Eyes Normal Sunken Very Sunken

Urine output Decrease Oliguria Anuria

FLUID IMBALANCES
▪ When the body can’t compensate for fluid deficit or excess, an imbalance occurs.
▪ These include DHN, Water intoxication, Hypervolemia, and Hypovolemia.

DEHYDRATION/ Extracellular Fluid Volume Deficit (ECFVD)

⮚ Most common fluid and electrolyte imbalances in US
⮚ More than 1M people are admitted in the hospital for DHN
⮚ Common among older people 60% and infants due to inability to obtain fluid without help, inability to express feelings
Main Problem
⮚ Loss of body fluids in the body. The water molecule shifts out of cells (from ICF to ECF) into more concentrated blood;
Cells shrinks as more fluid shift out of them
⮚ loss it from the vascular and interstitial fluids
⮚ Loss of body fluids from the body resulting to decrease blood volume will lead to HYPOVOLEMIA.
⮚ There is Sodium excess but Water deficit
⮚ Body loses fluid, Blood solute concentration increases (Normal Serum Osmolality280-295 mOsm/L blood), serum sodium
rises;
CAUSES OF DHN
⮚ Lack of fluid intake/Long term NPO- bedridden client, confused client, pts with dysphagia, pts with NGT, elderly,
impaired thirst mechanism.
⮚ Hemorrhage
⮚ Severe diarrhea, Severe vomiting, Severe draining wounds, Severe diaphoresis, Systemic infection
⮚ Diuretics, Draining fistulas
⮚ Fever- losing of fluid through perspiration, Frequent enemas
⮚ Diabetes Insipidus- Hyposecretion of ADH/Deficit of ADH. Inability of the kidneys to retain water/absence of ADH allows the
filtered water to excreted in the urine instead of being reabsorbed, and the patient excrete large quantities of urine
⮚ DKA- hyperglycemia
⮚ Hyperglycemia- cause osmotic diuresis creating shifting of electrolytes with losses in potassium, sodium, phosphate and
water.
⮚ Colostomy
LOSSES CAN BE:
⮚ MILD- loss of 1to 2 liters/2% of the body weight
⮚ MODERATE- loss of 3-5liters/5% of the body weight
⮚ SEVERE-6-10 L of water/8-% of body weight

Clinical Manifestations Mild (1-2liters) Moderate (3-5 liters) Severe (5-10 liters)

LOC Alert Lethargic Obtunded

Capillary refill time 2 seconds 2-4 seconds Greater than 4 secs, cool limbs

Mucous membrane Normal Dry Cracked

HR Slight increased Increased Very increased

RR Normal Increased Increased/Hyperpnea

BP Normal Normal but orthostasis Decreased

Pulse Normal Thready Impalpable

Skin turgor Normal Slow Tenting

Eyes Normal Sunken Very Sunken

Urine output Decrease Oliguria Anuria

TYPES OF DEHYDRATION

ISOTONIC DHN/ ECF VOL HYPERTONIC DHN HYPOTONIC DHN

DEFICIT

-Most common type of DHN
-H2O and electrolytes (Na) losses are
equal
-H2O loss is greater than Electrolytes
loss
- Fluids move from ICF to ECF
causing CELL shrinks
-More electrolytes loss than H2O loss
-Fluids moves from plasma and
interstitial space to Cells

CAUSES ❖ HYPERVENTILATION Causes

❖ Hypovolemia ❖ DKA ❖ Renal failure

❖ Excessive fluid replacement

- Decrease circulating blood volume ❖ Diarrhea (Hypotonic)

- Inadequate tissue perfusion ❖ DI ❖ Malnutrition

❖ Inadequate intake of fluids ❖ Fever

❖ Vomiting and diarrhea

❖ Profuse sweating

❖ Draining intestinal fistulas,

colostomies
Clinical Manifestations
⮚ THIRST: initial signs of DHN among Adult among conscious person. Thirst is diminished in older adult that’s
why is not an accurate indicator
⮚ Weight loss: The most objective indicator of dehydration. Mild(1-2 Liters of water/2% of the body weight )Moderate (3-5
liters of water/5% of the body weight) Severe (5-10L of water loss/8% of the body weight)
⮚ Weight is most accurate measure of fluid status
⮚ Next is Decreased urine output due to retention of water by the kidneys
⮚ The vital sign changes in dehydration are as follows:
⮚ Increased body temperature (Hyperthermia)
⮚ Increased pulse rate (tachycardia)
⮚ Increased respiratory rate (tachypnea)
⮚ Decreased blood pressure (hypotension); Narrow pulse pressure
⮚ Decrease CVP,PCWP
GI
❖ THIRST: initial signs of DHN among Adult in a conscious person.
❖ Decrease GI motility and bowel sounds
❖ Constipation-feces becomes hard due to compensatory reabsorption of water in colon
Integumentary
❖ Dry warm skin
❖ Poor skin turgor
❖ Dry mouth and throat
Cardiovascular
❖ Thready pulse Increase PR
❖ Decrease Systolic BP (orthostatic/postural hypotension)- most sensitive indicator of decrease fluid volume resulting to altered
tissue perfusion.
❖ Flat neck and hand veins in dependent positions
❖ Decrease peripheral pulse
Respiratory
❖ Increase RR and Depth- indicator of decrease fluid volume resulting to altered tissue perfusion.
Neuro muscular
❖ Skeletal Muscle weakness (hypotonic)-due to imbalance of Na and K
❖ Altered LOC due to CNS depression
Renal
❖ Decrease UO- because of the effects of ADH and aldosterone, due to conservation of water by the kidneys
❖ Increase specific gravity (1.010-1.025)

NURSING DIAGNOSIS
⮚ Deficient fluid volume r/t insufficient fluid intake, vomiting, lbm, bleeding or third space fluid loss
⮚ Impaired oral mucous membrane related to lack of oral fluid intake;
⮚ Risk for injury
LAB DATA
Increased hematocrit
- (male: (42-52%), Female: (35-45%)
- Greater than 55, due to hemo concentration
SERUM osmolality greater than 300mOsm/kg
- N- 280-295mOs/L blood
- Indicates hypernatremia and DHN
Increase Na level (n=135-145)
Increase Urine specific gravity (1.010-1.025) or less than 1.005 for pt. with DI.
- Urine is usually concentrated with specific gravity of 1.30.
- High specific gravity indicates DHN or increased ADH production
Increased BUN more than 25mg/dl (10-20mg/dl)
- May not be an accurate indicator in someone with protein deficit due to lack of intake, kidney disease
- Elevated from bleeding or excessive nitrogen breakdown

OUTCOMES
▪ Restoration of normal fluid volume, improvement in fluid volume or no further fluid loss
Management
⮚ GOAL of TX: restore fluid vol., replace elec., eliminate the cause
1. Fluid replacement/Restoration –to prevent further DHN
- Begin emergency tx pt. manifest impaired mental status, seizures or coma
- Encourage the pt. to drink salt free oral fluids if conscious tolerated. Provide 100 ml for the first 10kg, and 50 for the next 10
kg and add 15 for the remaining number of kg. Another formula is 1.5ml/kg of fluid intake
- Oral glucose replacement solutions- palatable, inexpensive and good source of fluids, glucose and electrolytes
- Pedialyte is good alternative
- Avoid caffeine/cola drinks they don’t contain adequate electrolyte replacement and the sugar content may lead to osmotic
diuresis, and Caffeine lead to diuresis
- IV fluids using hypotonic solutions; low sodium solutions such as .45 Saline Solution
2. IV replacement to severely dehydrated client
❖ Hypertonic DHN- Hypotonic IVF- low sodium solutions such as d5% water
❖ Hypotonic DHN- Hypertonic IVF
❖ ISO DHN- Isotonic IVF
3. Assess for signs and symptoms of cerebral edema resulting from rapid administration of IV solutions
❖ Ss & Sx of Cerebral edema (Headache, Confusion, Irritability, Lethargy, NV, Widening Pulse pressure, Decrease PR,
Seizure)
4. Identify and treat underlying cause
- Administer vasopressin- in case of DI to control fluid balance and prevent dehydration
- Administer anti emetic and anti-diarrheal drugs to correct problems with diarrhea and vomiting
- Antimicrobial, Anti pyretic
5. Oral care for dry mouth and throat- regular tooth or foam brush and lip moisturizer
6. Assess for diaphoresis- can be a major source of DHN
7. Safety measures for altered level of consciousness
8. Weight the patient at the same time, on the same scale, and with the same clothes of the client
9. Monitor sodium level, urine osmolality, urine specific gravity
10. Monitor VS every 2-4hrs
11. Monitor I and O
12. Monitor Na and K
Indicators of Adequate fluid Volume
▪ Increasing body weight of about 0.5 to 1 pound/day
▪ Urine output greater than 0.5ml/kg/hr.
▪ Moist tongue and mucous membrane
▪ Oral intake between 1500-2000 ml or more in 24 hrs.
▪ Stable blood pressure and pulse
▪ Mental status returned to baseline and Normal diagnostic test
HYPOVOLEMIA HYPERVOLEMIA

Problem ⮚ Refers to Isotonic Fluid loss and
Solutes from Extracellular space
⮚ If Hypovolemia is not detected early
and treated, it will progress to
HYPOVOLEMIC SHOCK.
⮚ Excess of isotonic fluid (water and
sodium) in the extracellular
(intravascular or interstitial)
compartment
⮚ this fluid imbalance does not affect
osmolality because fluids and solutes
are gained in equal concentrations.

⮚ Mild-Moderate Hypervolemia-
increase weight 5%-10%.

⮚ Severe Hypervolemia- more than

10%.

Pathophysiology What Happens in Hypovolemia with Third ⮚ Excess sodium or fluid is consumed
Spacing or retained

1. Capillary membrane permeability increases/ ⮚ Fluid move out the blood vessels into
Decrease Plasma colloid Osmotic Pressure the INTERSTITIAL space/Intravascular

2. Fluid moves out of the intravascular space ⮚ Extracellular fluid accumulates in the
interstitial or intravascular
3. Fluid shift into the abdominal cavity, pleural compartment
 cavity or pericardial cavity
4. Reduced fluid intake may exacerbate the
fluid shift
5. Patient displays weight loss, mental status
changes and orthostatic hypotension
⮚ EDEMA develops in the lungs or other
tissues/ PE there is an abnormal
accumulation of fluid in the air
sacs of your lungs that limits your
breathing capacity.

Causes Excessive fluid loss Excess sodium and water intake

- abdominal surgery, Diarrhea, Excessive -IV administration of normal saline/LR

diuretic therapy, Excessive laxative use,
Excessive sweating, Fever, Fistulas, -Blood or plasma replacement
Hemorrhage, Vomiting, NG tube drainage
-High dietary intake of sodium
Third space shifting
⮚ Fluid and sodium retention
⮚ accumulation of fluids in the interstitial
- Heart failure-fluids build ups in the
space (from vascular-interstitial
heart-the heart is not able to pump
⮚ Third space fluid is not the fluid in the
properly, the fluids backs up into the
lungs causing Pulmonary edema. Other
vessel or in the cells. Fluid around the
organs cannot receive adequate O2
cells and vessels.
leading to 0rgan failure and death
⮚ Third space fluid is useless because it
- Cirrhosis
does not circulate to provide nutrients
for cells. - Nephrotic syndrome

⮚ Common sites of third spacing are in - Hyperadosteronism

3P’s Pleural cavity, Peritoneal
cavity, pericardial sac - Low intake of dietary CHON

⮚ Burns, Hypoalbuminemia due to

decrease protein intake, Acute
peritonitis, Acute intestinal obstruction,
Pleural effusion, trauma, crush
injuries, surgery, acid base imbalance,
sepsis causes fluid shifting

⮚ Liver and kidney disease will lead

hypoalbuminemia/ Decreased
Colloidal osmotic pressure

CM ⮚ Altered mental status-confusion ⮚ Tachypnea and dyspnea-early sign

⮚ Tachycardia ⮚ HPN

⮚ Orthostatic hypotension ⮚ Wt gain

⮚ Decrease urine output/ Oliguria ⮚ Crackles-early sign

⮚ Weight loss ⮚ Rapid bounding pulse

⮚ Cool, pale skin over arms and legs ⮚ Increase CVP, PAP and PAWP

⮚ Distended jugular and hand veins

⮚ Delayed capillary refill
⮚ Peripheral edema/PITTING
⮚ Thirst
 ⮚ Flat jugular veins
⮚ Decrease CVP
⮚ blood can back up into the veins that
Nursing Fluid volume deficit
Diagnosis
Diagnostic Test ⮚ Decreased Hemoglobin level and hct
⮚ Elevated BUN
⮚ Increased urine specific gravity-
kidneys trying to conserve water
⮚ Normal or greater sodium level-
depending on the fluids and sodium
lost
Interventions ⮚ Replace fluids lost with isotonic
solutions (same concentration) in
large amount over a short period of
time. Use short large bore needles for
rapid infusion. To treat hypovolemic
shock
⮚ Administer oxygen. To avoid tissue
anoxia or tissue hypoxia.
⮚ Lower the head of the bed or elevate
the foot of the bed to increased
cerebral reperfusion
⮚ Administer vasopressor such as
dopamine to increase the
patient’s blood pressure
⮚ Administer blood transfusion if the
patient is hemorrhaging
⮚ Monitor hemodynamic values- to
assess the patient’s response to tx
⮚ Monitor signs of fluid overload such as
crackles
⮚ Monitor pts mental status and vital
signs
⮚ Pulmonary edema (Severe
Hypervolemia)-  is often caused by
congestive heart failure. When the
heart is not able to pump efficiently,
take blood through the lungs. As the
pressure in these blood vessels
increases, fluid is pushed into the air
spaces (alveoli) in the lungs
Fluid Volume Excess
- low Hct due to hemodilution
-NORMAL Na level- does not affect osmolality
because fluids and solutes are gained in equal
concentrations.
-Low K and BUN bec of hemodilution
-Low oxygen
-Pulmonary congestion X-ray
⮚ Restrict Na (1-2g) and fluid intake
(1L/day
⮚ Semi to high fowlers- ease in breathing
allows greater lung expansion
⮚ Oxygen therapy 1-2L to minimize DOB
⮚ Assess for edema.
⮚ Diuretics-Lasix- diuresis begin 30 min
⮚ Monitor K level typically decreases with
diuretic use.
⮚ Monitor I and O 1L/day
⮚ Monitor the weight. 1-2 pound indicates
Fluid retention
⮚ Digoxin in heart failure
⮚ Morphine and Nitroglycerine- for
pulmonary edema that dilates blood
vessels
⮚ Dialysis -if patients has renal failure, .
COMPLICATIONS
⮚ CHF-fluids build ups in the heart-
the heart is not able to pump
properly, the fluids backs up into
the lungs causing Pulmonary
edema. Other organs cannot
receive adequate O2 leading to
 0rgan failure and death

FLUID OVERLOAD
▪ Is over hydration or ECF volume excess (ECFVE)
Types of Fluid Overload
▪ HYPERVOLEMIA- fluids excess in the vascular system
▪ THIRD SPACING- fluids excess in the interstitial spaces
▪ Water intoxication
▪ ISOTONIC FLUID VOLUME EXCESS (ECF VOLUME EXCESS)- water and sodium retained in same proportion in ECF
CAUSES
Fluid overload can develop into two processes
● Administration of too much fluid, administering fluid to rapidly
● Failure to excrete fluids.
a. Compromised regulation of fluid movement and excretion
▪ Renal disorders- impair Glomerular filtration of sodium and water. As the fluid volume increases, the heart attempts to
compensate through tachycardia and hypertrophy. When compensation fails, Heart Failure results.
▪ Uncontrolled Heart failure-can lead to multiple organ failure and death from massive water retention/ANASARCA-
▪ Cirrhosis of the liver/Protein malnutrition- Decrease plasma protein/albumin will result in decrease oncotic pressure will result
decrease absorption of water in from the capillary which will lead to peripheral edema or ascites
▪ Lymphatic or venous obstruction-
b. Excessive ingestion of foods or fluids containing sodium
▪ Excessive amount of saline intravenous fluids
▪ High sodium food consumption
▪ Excessive use of medication with sodium
Increase ADH and Aldosterone
▪ Cushing syndrome
▪ Glucocorticoid and narcotic (morphine) use
▪ Hyperaldosteronism
▪ Syndrome of Inappropriate Antidiuretic Hormone
PATHOPHYSIOLOGY
▪ Fluid overload, the hydrostatic pressure is higher at the arterial end of the capillary, Pushing the excess fluid into the
Interstitial spaces.
▪ Excess fluid is not reabsorbed at the venous end of the capillary because the Oncotic pressure is low to pull back the
fluids across the capillary membrane
▪ The residual fluid is usually removed by the lymphatics, but in case of EDEMA, the fluid volume overloads the lymphatic
system and stays in the interstitial space leading Peripheral edema.
▪ Edema can be progressive. As the fluid pressure increases in the Interstitial area and tissues, it creates a resistance
to forward blood flow and increases resistance throughout the Circulatory System. This is called, Increase Peripheral
Vascular Resistance, eventually it creates a gradient that resist Left Ventricular Output.
▪ Blood is unable to be propelled forward and it return backs up the alveolocapillary membrane of the lungs resulting to
Pulmonary Edema or fluid Overload. PE edema may develop quickly in those people with impair left ventricle
Clinical Manifestations
▪ Cough, dyspnea, crackles- excessive fluids in the lungs through auscultation. Alveolar fluid accumulation impairs O2
and CO2 transport between the capillaries and alveoli resulting to
▪ Jugular vein distension -delayed emptying and filling of RV
▪ Pallor, cyanosis due to decrease O2 levels, anxiety, and Increase CO2
▪ Bounding pulse
▪ Elevated Bp- due to increase peripheral resistance as a compensatory mechanism of the heart
▪ Pitting Edema on feet and sacrum- fluids accumulates in the interstitial compartments as influence by gravity
dependent tissues.
▪ Weight gain- classical sign of fluid overload, best indicator of edema
▪ Early changes in cerebral function- confusion and head ache- ICF shifting.
▪ As the fluid excess increases in the cerebral cells lethargy occurs, followed by seizures and COMA
NURSING DIAGNOSIS
▪ Fluid Volume Excess
▪ Impaired Gas Exchange
 ▪ Altered LOC
▪ Disturbed Body Image
Lab data
▪ Plasma osmolality less than 280 mOsm/Kg
▪ Low sodium level less than 135mEq/L
▪ Hematocrit less than 45%
▪ Specific gravity less than 1.010
▪ BUN level less than 8mg/dl
MANAGEMENT
▪ Restriction of Sodium and Fluids
- Sodium retains water, sodium intake is commonly restricted to those clients with renal or heart disease
- Mild Restricted Na diet contains 4-5g of sodium
- Moderately restricted contains 2g of sodium
- Severely restricted Na contains 0.5g of sodium
- High Sodium Foods (250mg/Serving)- Breads, Cereals (instant Hot and Cold), Chips, Cheeze (all types), Meats
(Sausage, Luncheon, Bacon, Ham), Convenience foods (Pizza,) Most fast items have 1-5times of this amount
- Low sodium Foods(50 mg/serving)-Fruits (fresh and frozen), Vegetables (fresh and frozen, canned), Oatmeal,
cooked, Low salt bread, unsalted popcorn, Shredded Wheat, Fresh meat, chicken and fish
▪ Diuretics- DOC for fluid excess. Used to promote fluid loss (K sparing and Wasting)
▪ ACE inhibitors, Angiotensin II receptor blockers Aldactone antagonist to improve overall cardiac function.
▪ Monitor K because of K sparring effects of these drugs

WATER INTOXICATON/ HYPOOSMOLAR IMBALANCE/ Intracellular Fluid Volume Excess

❖ Over hydration
❖ Occurs when excess fluid moves from the Extra cellular space to the Intra Cellular space
❖ Shifting of fluids from ECF to ICF
❖ The cells swell.
❖ There is sodium deficit or water excess. In Sodium deficit, the amount of water is NORMAL, but there are too few
particles per liter of water. In water excess, the number of solutes in NORMAL, but diluted by excessive water.
❖ The most dangerous effect of water intoxication is INCREASED ICP. Cerebral cells absorb hypo osmolar fluid more quickly.
❖ Normal ICP- <15mmHg
Signs of ICP
❖ Changes in mental status- earliest sign
❖ Changes in VS begin when the pressure is at the level of Hypothalamus and Brain stem (Late Signs)
❖ Increase BP (widening pulse pressure) N pulse pressure 30-40mmHg
❖ Decrease CR PR
❖ Decrease RR
CAUSES
⮚ Rapid infusion of hypotonic solution- 0.45 (half strength) saline solution or D5W- most common cause
⮚ SIADH- Inappropriate continued release of ADH in the absence of stimuli resulting water intoxication/excessive water
retention by the kidney tubules. More water will be reabsorbed by the kidneys leading to decrease urine output and fluid
overload. As the fluids build up in the blood stream, Osmolality decreases and the blood becomes diluted
❖ Excessive use of tap water as an NG tube irrigation or enema
❖ Psychogenic polydipsia- Schizophrenia- drink water compulsively
Clinical manifestations:
⮚ ICP - Bradycardia and Widened Pulse Pressure-common sign
⮚ Weight gain-
⮚ Oliguria
⮚ Tachypnea/Dyspnea on exertion
⮚ Changes in personality, behavior LOC
⮚ Muscle cramps and weakness
Lab data
Serum Osmolality below 280 mOsm/L
⮚ water excess
⮚ Amount of particles or solute is too small in proportion to the amount of water.
⮚ Too much water for the amount of solute
Serum sodium level - <125 mEq/L

Goal of Treatment
 ❖ Restore fluid balance
❖ Correct electrolytes imbalances
❖ Control or eliminate the Cause
Collaborative management for Water Intoxication:
⮚ Identify and treat underlying cause; excess intake of electrolyte-free fluid, repeated tap water enema, SIADH, sodium deficit
⮚ Administration of diuretics and steroids as prescribed. To reduce ICP
⮚ Fluid restriction- 500ml-1000ml/day
⮚ Replace hypertonic solutions IV - bec. Solute concentration is higher than the serum it draws fluid into the intravascular
space. Slow or temporary DC hypotonic solution- it shifts out of the intravascular compartment after administration
⮚ Promote safety by instituting seizure precaution- protecting the head of the pt. Keep suction equipment at the bedside.
Protect the head from injury and maintain the patent airway by turning into side.
⮚ Assess neurologic status (LOC, VS, reflexes,), staying alert for deterioration.
⮚ Monitor the serum sodium level
⮚ Monitor I and O and weight daily- Polyuria is a good sign that indicates fluid shifted to the vascular space to the renal
tubules where it can be excreted
⮚ Administer anti emetic to decrease the risk of vomiting which worsen ICP
ISOTONIC VOLUME EXCESS (ECF VOLUME EXCESS)
⮚ It is also known OVERHYDRATION.
⮚ Edema is the accumulation of fluids in the intestinal spaces (it surrounds the cells).
Edema occurs due to the following:
• Increased capillary hydrostatic pressure; administration of large volumes of IV fluids.
• Decreased colloidal osmotic pressure (COP) or oncotic pressure (OP); hypoalbuminemia
• Increased capillary permeability due damage to blood vessels in burns, vasodilation due to inflammation and release of
histamine.
• Lymphatic obstruction; removal of lymph nodes in mastectomy, malignant metastasis
• Sodium and water excess; congestive heart failure, renal failure, hypersecretion of aldosterone
Manifestations of EDEMA
• Weight gain- the best indicator of edema
• Dependent edema- sacral area, ankles and feet
• Tight, smooth, shiny skin.
• Cool, pale skin. This is due to poor circulation in the area.
• Neck vein engorgement.
• Weeping edema- fluid leaks out of the pores when skin is pressed
• Clothing and shoes feel tight
• Pleural effusion, pericardial effusion, ascites.
EVALUATE EDEMA
⮚ Using a scale of +1 to +4
⮚ Press your fingertip into the skin over a bony surface for a few seconds
⮚ +1 Pitting Edema- a slight imprint is observed
⮚ +4 Edema- a deep imprint with the skin slow to return to its original contour
⮚ Brawny Edema- the skin swells so much that fluid cannot be displace. The Skin resist the pressure but appears distended.
Collaborative management:
• Sodium and fluid restriction.
• High protein diet (except in renal failure and liver cirrhosis) . The diet in renal failure is low protein to reduce formation
of urea and nitrogenous waste products. The diet in the liver cirrhosis is low protein to reduce ammonia formation)
• Elevate edematous body parts. To promote venous return (except in CHF. In CHF, the legs are not elevated even if they are
edematous to prevent increase preload)
• Protect edematous body parts from prolonged pressure, injury, extremes of heat and cold. The area is susceptible to pressure
sore, trauma, and infection.
• Keep skin dry and well- lubricated. To maintain skin integrity.
• Regulate IV accurately. To prevent fluid overload
• Administer diuretics as ordered. To promote excretion of sodium and water.

ELECTROLYTES

❖ Are chemicals that conduct electricity when dissolve in water

❖ Works with fluids to maintain health and well being

❖ Are substances that when in a solution separates into electrically charges particles called IONS
 ❖ ANIONS-Are electrolytes that produce negative (-) charge.
- Bicarbonate, Chloride and Phosphorus
❖ CATIONS- Are electrolytes that generate positive (+) charge.
❖ K, Na, Mg and Ca
MAJOR ELECTROLYTES
1. EXTRACELLULAR electrolytes- exert their effects
OUTSIDE the cell
SODIUM (Na)
❖ Main ECF cation
❖ Affects serum osmolality and extracellular fluid
volume/ control water movement and retention
❖ Helps nerves and muscles cells interact
❖ Helps in maintain acid base balance-it acts with
CHLORIDE to maintain body osmolality.
❖ 135-145 mEq/L
❖ Decreased Na- hyponatremia cause by SIAD
(Snydrome of Inappropriate Antidieretic Hormone
❖ Increased Na-Hypernatremia cause by Diabetes
Insipidus
CALCIUM (Ca)
⮚ Major cation involved in density of bones and hardness
of teeth
⮚ Stabilizes cell membrane, reducing its permeability
⮚ Found in Fairly equal concentrations in ICF and ECF
⮚ Transmit nerve impulses
⮚ Contracts muscles
⮚ Coagulates blood
⮚ 8.5-10.1mg/dl (Total serum Calcium)
⮚ <9.8- Hypocalcemia- Acute pancreatitis/
Osteoporosis
⮚ >10.1- Hypercalcemia- Hyperparathyroidism
CHLORIDE
⮚ Main ECF anion
⮚ Maintains osmotic pressure and helps gastric mucosal cells
2. INTRACELLULAR Electrolytes- exert their efforts INSIDE
THE CELL
POTASSIUM (K)
⮚ Main ICF Cation
⮚ Regulates cell excitability, nerve impulse conduction ,muscle
contraction and myocardial membrane responsiveness,
⮚ Promotes contraction of cardiac, skeletal and smooth muscles
⮚ Helps control ICF osmolality and ICF osmotic pressure
⮚ Essential for conducting electrical impulses from cell to cell
because it Causes ions to shift in and out of the cell .
⮚ Needed for cellular activity and cardiac function
⮚ 3.5-5mEq/L
⮚ <3.5- HYPOKALEMIA- Diarrhea (metabolic Acidosis) ,
Vomiting (Metabollic Alkalosis) , Diuretic Therapy, bulimia,
Cushing syndrome
⮚ >5- Hyperkalemia- Burns, Acute Renal Failure, kidney
Transplant, Acidosis
PHOSPHORUS
⮚ main ICF anion
⮚ Promotes energy storage (CHO, CHON, and Fats) or
responsible for energy metabolism
⮚ Acts as hydrogen buffer
⮚ 2.5mg/dl -4.5 md/dl or 1.8-2.6mEq/L
⮚ <-Hypophosphatemia-DKA, Alcoholism, hyperpathyroidism
⮚ >-Hyperphosphatemia-renal insufficiency/Kidney failure,
hypoparathyroidism, accidental removal of parathyroid gland
Magnesium (Mg)
⮚ A leading ICF Cation
⮚ Influences enzyme reactions and metabolic processes
 to produce Hcl. ⮚ Regulates neuromuscular contraction and transmission

⮚ Acts with sodium to maintain body osmolality ⮚ Modifies nerve impulse transmission and skeletal muscle
response.
⮚ Plays vital role in in maintaining acid based balance
⮚ Responsible for normal functioning of nervous and
⮚ 98-108 mEq/L cardiovascular system, protein synthesis and transportation of
sodium and K ion
⮚ <98- Hypochloremia- caused by Severe vomiting
⮚ 1.5-2.5mEq/L
⮚ >108- Hyperchoremia- Hypernatremia

BICARBONATE (HCO3)

⮚ Regulates acid base balance

⮚ BICARBONATE (HCO3)

⮚ Regulates acid base balance

⮚ Buffers acidity of body fluids

⮚ 22-26 mEq/L

ELECTROLYTES IMBALANCES

SODIUM

⮚ 135-145mEq/L

⮚ Create much of the osmotic pressure of ECF

⮚ Most abundant/Major CATION in ECF (in the Vascular fluids)

⮚ PLAYS A VITAL PART IN DEPOLARIZATION of the MYOCARDIUM

⮚ Affects serum osmolality and extracellular fluid volume/ control water movement and retention

⮚ Helps nerves and muscles cells interact, Helps in maintain acid base balance-it acts with CHLORIDE to maintain
body osmolality.

HYPONATREMIA HYPERNATREMIA

MP - low serum sodium levels less than ⮚ Serum Na level greater than 145mEq/L
135mEq/L, Sodium loss or water
excess ⮚ Sodium and water excess results to EDEMA

- Decrease ECF volume, Increase ⮚ Due to Increase ECF vol. and Decrease
ICF volume- Cell SWELL ICF vol) “CELLS SHRINK”

- Body fluids are DILUTED and cell ⮚ Severe Hypernatremia can lead to coma
swells from decrease extracellular
⮚ Infants and children are greater risk because
fluid osmolality to increased ICF.
they tend to lose more water as a result of
diarrhea, vomiting, inadequate fluid intake
- When the blood vessels contain
and fever.
more water and less sodium,
fluids moves from extracellular
⮚ Elderly patients bec. They have impaired
area into intracellular area.
thirst response/ limited access to water bec
of confusion and immobility.
- When more fluid in the cells and
less in blood vessels, CEREBRAL
EDEMA and HYPOVOLEMIA
 occurs

- Severe Hyponatremia (Less than

110mEq/L) can lead to SEIΖURE,
COMA, and Permanent
Neurologic Damage

- Common among older adults

due to lower percentage of TBW

Types of Hyponatremia

Hypovolemic Hyponatremia

- both Na and water decrease

extracellular area.
Types of Hypernatremia
- Na loss is greater than H2O loss.
Hypovolemic hypernatremia
Hypervolemic hyponatremia
- TBW is greatly decreased relative to sodium
- Greater increased in TBW than total
body sodium

- Both Na & water are increased

extracellular fluid volume but
water gain is more impressive. Hypervolemic hypernatremia

ISOVOLEMIC HYPONATREMIA - Sodium gain exceed the water gain

⮚ Sodium levels may appear Low - Least common type of hyponatremia.

while too much fluid in the
body,

⮚ Extracellular fluid volume is

equal to intracellular fluid
volume

ISOVOLEMIC HYPERNATREMIA

⮚ Sodium is increase, while fluid is decreased in

the body

Patho ⮚ Patient has inadequate intake of ⮚ The body accumulates too much sodium or
sodium/excessive sodium loss from unable to excrete sodium
the body. As the sodium decreases
in the ECF, Water is pulled by ⮚ Na intake increases/water loss
excessive
osmotic pressure into the cells. In
relative decrease, the sodium is not
⮚ Osmolality Increases
lost from the body but leaves the
intravascular space and moves into ⮚ Fluids moves from ICF to ECF
the interstitial tissues.
⮚ Cells shrink/ Cellular DHN (inside the
⮚ As the Sodium decreases in the ECF, cell)
the fluid becomes hypoosmolar.
Water moves into the cell to the ⮚ ECF vol. Increases leading to
area of greater concentration to Hypervolemia
rebalance the water concentration.
⮚ When sodium level increases, through
 This osmotic shift lead to OSMOSIS, shifting of water from the
Intracellular Edema/ Cerebral cells to ECF in attempt to dilute the
Edema hyperosmolar state/Cellular DHN.

Causes ⮚ Most common of hyponatremia -Hyperventilation-increase h20 loss and Increase

that lead to fluid overload Na
Cardiac, renal and liver disease.
-High NA intake- sodium tablets, over consumption
⮚ Na loss of dietary sodium,

⮚ Diuretics, Diseases

⮚ Low sodium diet ⮚ Cushing syndrome and Hyperaldosteronism-

retention of sodium
⮚ edema, ascites,
⮚ Uncontrolled DM or DI- polyuria leading to
⮚ burns and diaphoresis, DHN and secondary HYPERNATREMIA

⮚ diarrhea, vomiting(DDDALEBV) ⮚ Renal failure- patients unable to

excrete sodium

Drugs
1. HYPOVOLEMIC HYPONATREMIA
⮚ antacids with sodium Bicarbonate, Salt tables,
⮚ Caused by: osmotic diuretics, Na Bicarbonate injections, Na polysterene
diuretic use, vomiting, diarrhea, suffonate
Fistulas, Adrenal insufficiency,
excessive diaphoresis, Burns,
Wound drainage

2. HYPERVOLEMIC
HYPONATREMIA

⮚ Heart or liver failure, Nephrotic

syndrome, excessive use of
hypotonic fluids, Hyperaldosteronism

3. ISOVOLEMIC HYPONATREMIA

⮚ Glucocorticoid deficiency-
inadequate filtration of kidneys

⮚ SIAD- causes excessive release of

ADH disturbing F and E. ADH is
release when the body does not
need it resulting to water retention
and sodium excretion.

⮚ Renal Failure-inability of the

kidneys to regulate F and E.

⮚ Hypothyroidism- limit water

excretion

CM Neuro EARLY signs

⮚ Headache, Confusion, Personality ⮚ Extreme thirst- main body defense against

Changes, Seizure and coma, hypernatremia. If you eat salty foods, the
amount of sodium increases and you
 ⮚ Muscle weakness, fatigue, apathy
GI: Anorexia, NV, Abdominal cramps,
diarrhea- sodium is a critical component of
normal neuromuscular activity of smooth
muscle. A decrease in sodium causes
increased excitability of the neurons that
innervate the smooth muscle
CARDIO: Low BP, shock, Weak and
thready pulse due to decrease vascular
volume secondary to sodium and water loss
Ss and Sx of Hyponatremia Caused By
Hypervolemia
⮚ Edema
⮚ Hypertension
⮚ Rapid bounding pulses
⮚ Weight gain
SS and SX (Hyponatremia caused by
Hypovolemia)
⮚ Dry mucous membrane
⮚ Low BP
⮚ Poor skin turgor
⮚ Tachycardia
⮚ Weak pulse
Diagnosis FLUID VOLUME EXCESS
Lab Data ⮚ DECREASE SERUM SODIUM,
⮚ Decrease Serum osmolality,
⮚ Decrease urine specific gravity
1.010 (except for SIAD)
⮚ Decrease Chloride- depleted
become thirsty.
⮚ Dry sticky mucous membrane
⮚ Polyuria in hypervolemic state
⮚ Oliguria- hypovolemic state as a method
of renal compensation
⮚ Spontaneous muscle twitches- early
Sign
⮚ Skeletal muscle weakness and
GI
⮚ Anorexia, NV-related to fluid retention
in gastric cells
Neurologic
⮚ Agitation, Restlessness, irritability and
muscle weakness r/t sensitivity of brain cells
to fluid shifting
⮚ Lethargy, stupor, seizure and coma-
when sodium levels reach 155mEq/L more
cells in the brain shrink due to increased ECF
osmolality.
⮚ Low grade fever
⮚ Decrease DTR- Late sign
CARDIOVASCULAR related to type of
Hypernatremia
⮚ Hypovolemic hyponatremia- orthostatic
hypotension with tachycardia
⮚ Hypervolemic- hypertensive blood
pressure jugular vein distention,
generalized weight gain and edema
⮚ Dysrhythmia- results from competition
of sodium ions with calcium ions in the
heart
Pulmonary
⮚ Crackles, dyspnea and pleural effusion.
Fluid Volume Deficit
⮚ increase serum sodium greater than 145
⮚ Increase Serum osmolality greater than 300
⮚ Increase urine Specific gravity greater than
1.030 except for DI (decrease SG)
 when Na is decrease

Management ▪ Administer NaCl 0.9% per IV,
plasma expanders- to correct
sodium deficit and counteract
decreased blood volume
▪ Sodium-rich foods in diet (Bacon,
Butter, Canned Goods, Cheese,
Ketchup, Process foods, Milk, Soy
Sauce, Snack food, Table salts,
tomato sauce)
▪ Restrict fluids if patient has
fluid excess
▪ Diuretics that rid the body fluids
but do not cause sodium loss
▪ STEROIDS as ordered to reduce
cerebral edema.
▪ Safety precautions; use of side
rails, supervision of ambulation
Hyponatremia with Hypovolemia
⮚ Replace oral fluids gradually over 48
hrs- to avoid shifting of water into brain
cells. If too much water is replace quickly,
water move into brain cells and they swell
causing cerebral edema
⮚ Restrict Na in the diet. Avoid the ff:
(Bacon, Butter, Canned Goods, Cheese,
Ketchup, Process foods, Milk, Soy Sauce,
Snack food, Table salts)
⮚ Replace fluids with a salt free IV
solution( D5 Water/0.45Na Chloride . To
decrease gradually excess sodium. Administer
SLOWLY. Use infusion pump to prevent
cerebral edema.
⮚ Monitor I and O and daily weight
measurements, sodium level, specific
gravity, and osmolality levels
⮚ Administer diuretics as prescribed with
oral or IV fluids. To excrete sodium

⮚ Administer Isotonic Fluids

(NSS)-to restore volume

⮚ Provide high sodium food.

Hyponatremia with Hypervolemia/

Isovolumia

⮚ Restrict fluid intake

⮚ Provide oral sodium supplement

POTASSIUM

⮚ Normal value: 3.5-5mEq/L

 ⮚ The most abundant cation in ICF

⮚ Creates much of the osmotic pressure in ICF

⮚ Major function in cardiac depolarization and repolarization

⮚ Main ICF Cation

⮚ Regulates cell excitability, nerve impulse conduction ,muscle contraction and myocardial membrane
responsiveness,

⮚ Promotes contraction of cardiac, skeletal and smooth muscles

⮚ Helps control ICF osmolality and ICF osmotic pressure

⮚ Essential for conducting electrical impulses from cell to cell because it Causes ions to shift in and out
of the cell .

⮚ Needed for cellular activity and cardiac function

⮚ <3.5- HYPOKALEMIA- Diarrhea (metabolic Acidosis) , Vomiting (Metabolic Alkalosis) , Diuretic Therapy, bulimia,
Cushing syndrome

⮚ >5- Hyperkalemia- Burns, Acute Renal Failure, kidney Transplant, Acidosis

HYPOKALEMIA (Potassium Deficit) HYPERKALEMIA (Potassium Excess)

MP ⮚ Potassium level below 3.5 meq/L
⮚ It occurs because the body can’t
effectively conserve K
⮚ Characterized by a serum K level greater than
5 mEq/L
⮚ The most dangerous electrolytes disorder.
Increase K level can affect neuromuscular
and cardiovascular system

Causes: ⮚ Inadequate potassium intake - Retention of K by the body due to

- Use of K deficient I.V. fluids
- Low consumption of K rich foods.
⮚ hyper secretion of Aldosterone-
Increased loss of K
- Aldosterone and hydrogen ions regulate
K levels.
decreased/inadequate urine output
- Excess dietary intake of K rich foods/
Excessive use of K supplement/Excess
parenteral administration of K
- Excess released of K from the cells
during the first 24 to 72 hours after
traumati injury/Shifting of K out of the
cells

- Aldosterone is Pro-Na; and Anti K. - Burns, extensive trauma, crush injury

- Increase Aldosterone- Hypokalemia - Decrease excretion of K due to

- Decrease Aldosterone-
Hyperkalemia
⮚ Gastrointestinal losses/ excessive K
output
- prolonged vomiting and diarrhea,
- GI suction and lavage
⮚ Severe diaphoresis
decreased aldosterone (renal failure,
adrenal insufficiency, ADDISONS DISEASE,
Hypoaldosteronism)
- Use of certain drugs- NSAIDS,
Spironolactone, chemo drugs, antibiotics,
ACE- K sparring diuretics/ retention of K
- Metabolic acidosis- shifting of K out of the cell
in exchange of hydrogen

⮚ Potassium wasting drugs/

Depleting drugs
 - Diuretics- furosemide and thiasides

- Laxatives- diarrhea

- Insulin- may shift K into the cells

- Corticosteroids

- Adrenergics- albuterol

- Antibiotics- gentamicin, amphotericin B

⮚ Newly transplanted kidney- diuresis

occurs leading to hypokalemia

⮚ Hyperglycemia- high urine glucose

levels cause OSMOTIC diuresis and K is
loss through urine

⮚ Metabolic alkalosis- Hypokalemia- K

ions moves into the cells as hydrogen
ions out.

⮚ Diseases

- Cushing syndrome

- Hepatic disease

- Alcoholism

- Heart failure

- Nephritis

CM HIGH IMPACT CONCEPT HIGH IMPACT CONCEPT

⮚ HYPOKALEMIA is characterized by ⮚ Due to INCREASED NEURO MUSCULAR

decrease neuromuscular irritability IRRITABILITY

⮚ Everything is Low and Slow ⮚ Everything is High and Fast

MUSCLES-slowed skeletal muscles due to Muscles:

decrease conduction of nerve impulse
⮚ Irritability (early), Weakness (late),
⮚ Skeletal muscles weakness-
⮚ Flaccid paralysis- without muscle tone
especially in the legs- INITIAL sign
⮚ Respiratory paralysis
⮚ Paresthesia and leg cramps as
weakness progresses - decrease
conduction of nerve impulse

⮚ Flaccid paralysis- without muscle tone

Kidneys: Oliguria, anuria- precursor to hyperK rather
⮚ Weakness of respiratory muscles than consequence of the imbalance
become tachypneic and tachycardeic
---arrest-deterioration of muscle
contraction

GI

⮚ N/V, Anorexia, Decrease bowel

 sound, abdominal distension, and
Paralytic ileus and constipation
CNS
⮚ Lethargy
⮚ Decrease DTR
⮚ Confusion
⮚ Mental depression
Cardiovascular- low K leads to decrease
decreased myocardial contraction.
⮚ Weak and irregular (dysrhythmias)
⮚ Hypotension
⮚ Myocardial damage and cardiac arrest
DANGER SIGNS OF HYPOKALEMIA
❖ Arrhythmias-due to increase excitability
❖ Cardiac arrest
❖ Digoxin toxicity-
❖ Muscle paralysis
❖ Paralytic ileus
❖ Respiratory arrest
SOME SIGNS OF HYPOKALEMIA
❖ S-Skeletal muscle weakness
❖ U-U wave (ECG changes)
❖ C-Constipation
❖ T-Toxic effects of digoxin
❖ I- Irregular weak pulse
❖ O-Orthostatic hypotension
❖ N-Numbness (paresthesia)
Common ss & sx of HypoK and HyperK
Muscle weakness
Paralysis
Dysrhythmias
Gastrointestinal tract
❖ Nausea, vomiting,
❖ diarrhea,
❖ colic pain
CNS:
⮚ numbness, tingling
Cardiovascular:
VENTRICULAR FIBRILLATION
⮚ Begin as a rapid heartbeat
called ventricular tachycardia (VT). This
fast, regular beating of the heart is caused by
abnormal electrical impulses that start in
the ventricles. Most VT occurs in people
with a heart-related problem, such as scars
or damage from a heart attack
⮚ The most  serious  cardiac rhythm
disturbance. The lower chambers quiver
and the heart can't pump any blood, causing
cardiac arrest. The heart's electrical activity
becomes disordered
⮚ Together, all four chambers pump blood to
and from the body. When the atria, the two
upper chambers, contract at an excessively
high rate, and in an irregular way, the patient
has atrial fibrillation, or AFib. When the
two lower chambers beat irregularly and
flutter, the patient has ventricular
fibrillation, or VFib
⮚ CARDIAC ARREST
Digitalis Toxicity:
⮚ Confusion. Irregular pulse. Loss of
appetite. Nausea, vomiting, diarrhea.
Fast heartbeat. Vision changes
(unusual), including blind spots,
blurred vision, changes in how colors
look, or seeing spots)
 Cardiac arrest- slowed neuronal excitability
Renal damage
Diagnosis Activity intolerance, Fluid and electrolyte
imbalance, Ineffective Breathing pattern
Altered Thought Process
LAB DATA ❖ Decreased serum potassium 3.5mEq/L
❖ ECG Changes
❖ Depresses T segment- ischemia
❖ Prolong and depressed ST- often a sign
of myocardial ischemia due to myocardia
hypoxia
❖ prominent U wave
❖ Elevated ph and Bicarbonate levels
❖ Slight increase of glucose levels
❖ Increase digoxin level
Managemen ❖ K rich foods- banana, dried fruits,
t orange, raw carrots, raw tomatoes,
baked potatoes, water melon, avocado,
strawberries, raisins, spinach
❖ Provide oral potassium supplements
- Kalium Durules (K chloride)
- With food- to prevent gastric irritation
- Don’t chew, crush or break- to prevent
quick load of K from entering the body
- Powder- dissolve powder in 120ml
- SE: bradycardia, confusion, NV, cramps
❖ In case of severe hypokalemia,
administer slow I.V drip KCl.
- NEVER give KCl per IV push or bolus
because rapid administration may cause
DYSRHYTHMIAS or CARDIAC ARREST.
Use infusion pump.
❖ Administer K sparing diuretics as
prescribed
❖ Monitor pts VS noting orthostatic HTN
❖ Assess respiratory status of Pt bec.
Hypokalemia can cause respiratory
paralysis. Keep a manual
resuscitation bag at the bedside.
Activity Intolerance
Fluid and Electrolyte imbalance
❖ Increase K level greater than 5mEq/L
❖ ECG changes-
Tall T waves- cardiac ischemia
Flat P waves- right atrial enlargement/ Fine AFib
Prolonged PR intervals- delay in electrical
conduction pathway/AV block
Widened QRS complexes – electrical impulse is in
ventricular in origin
Depressed ST segment- myocardial ischemia
ST elevation- Acute MI/injury
✔ Low K diet/ restrict K intake
✔ Closely monitor I and O
✔ Dextrose 10% in water with regular
insulin per IV as prescribed. Potassium
attaches to glucose. Then insulin transports
glucose with attached potassium into the
cells. This lowers serum potassium levels.
✔ Polysterene sulfonate (exchange resin
kayexalate) by mouth or per enema or
NGT as prescribed. Sodium ions exchange
with potassium ions in the GI tract. This
prevents absorption of potassium. The
exchange resin kayexalate with attached
potassium is excreted via the feces. Give this
drug with sorbitrol or another osmotic
substance to promote excretion
✔ Calcium gluconate per IV as prescribed.
Antidote for hyperkalemia. To decrease
the effect of K in Myocardium
❖ Administer sodium bicarbonate with acidosis
–it aids in shifting K to the cells
✔ Dialysis as prescribed if patient does not
respond to treatment
CALCIUM (Ca)

⮚ Major cation involved in density of bones and hardness of teeth

⮚ Stabilizes cell membrane, reducing its permeability

⮚ Found in Fairly equal concentrations in ICF and ECF

⮚ Transmit nerve impulses

⮚ Contracts muscles

⮚ Coagulates blood

⮚ 8.5-10.1mg/dl (Total serum Calcium)/4.5-5.5 mEq/L/9-11mg/dl

⮚ <8.5- Hypocalcemia- Acute pancreatitis/ Osteoporosis

⮚ >10.1- Hypercalcemia- Hyperparathyroidism

Calcium Regulation

a. Parathormone acts in Hypocalcemia

⮚ Produced and secreted by parathyroid glands located behind thyroid gland

⮚ Elevates serum calcium levels through withdrawal of calcium from the bones.

⮚ Increase PTH- Increase calcium

⮚ Decrease PTH- decrease Ca

b. Thyrocalcitonin acts in Hypercalcemia

⮚ produced by Thyroid Gland, acts as antagonist of PTH

⮚ Lowers serum calcium by depositing calcium into the bones. It keeps calcium in the bone

⮚ Increase Thyrocalcitonin- decrease serum calcium

⮚ Decrease Thyrocalcitonin- increase serum calcium

c. Vit D regulates calcium levels

⮚ Promotes calcium absorption in the intestines, resorption from bone, and kidney absorption of calcium

HYPOCALCEMIA HYPERCALCEMIA

MP ⮚ Decrease calcium in the blood less ⮚ Serum Calcium level above 10.1
than 8.5mg/dl mg/dl/increased ionized calcium level above
 Who are at RISK? 5.1mg/dl caused by increased in the
resorption of calcium from bone
a. Elderly
⮚ The rate of calcium entry into the ECF
⮚ Inadequate dietary intake of calcium exceeds the rate of calcium excretion by the
kidneys.
⮚ Poor calcium absorption
(postmenopausal women due to lack of
estrogen help prevent bone loss)

⮚ Reduce activity/inactivity- causing loss of

calcium from the bones and
osteoporosis.

Assessment

⮚ Assess if he had parathyroid or thyroid

surgery

⮚ Received massive BT

⮚ Breastfeeding mother- asses her for

adequate vitamin D intake and exposure
to sunlight.

CAUSES ⮚ Inadequate calcium intake ⮚ Excessive calcium intake

⮚ Chronic alcoholism ⮚ Cancer/Carcinoma with bone metastases.

Second cause of Hypercalcemia
⮚ Insufficient exposure to sun- may
lead to vit. D deficiency that lowers the ⮚ Immobility- can cause increase calcium
calcium. release from the bone

⮚ Hyperthyroidism- decrease serum ⮚ Hypothyroidism- increase calcium release

calcium as more than is resorbed from bone

⮚ Excess loss of calcium ⮚ Hypervitaminosis D- can lead to bone

⮚ Thyroid/parathyroid surgery- reduce
or prevent PTH secretion
⮚ Hyperparathyroidism- most common
⮚ Hypoparathyroidism- PTH secretion is
reduced that lower calcium level
⮚ Pancreatic insufficiency- cause
malabsorption of calcium and loss of
calcium in feces.
reabsorption of calcium resulting to
hypercalcemia.
cause where the body excrete more PTH than
normal that increase calcium resorption from
bone, reabsorption of calcium in the kidneys
and absorption of calcium in the intestines
increases,

⮚ Calcium malabsorption

⮚ Severe diarrhea-

⮚ Laxative use

⮚ Insufficient Vit D

Drugs- can interfere with Vit D metabolism

and calcium absorption

⮚ Anticonvulsant- phenytoin
phenobarbital, laxative

⮚ Loop diuretics- furosemide,

ethacrynic acid- increase excretion of
 calcium

⮚ Calcitonin/ Mitramycin- decrease

calcium resorption from bone

⮚ Hypomagnesemia- affects the

function of PTG and caused a decrease
in calcium in the GI tract and kidneys

⮚ Hypoalbuminemia- most common

cause of hypocalcaemia due to cirrhosis,
malnutrition, burns and sepsis

⮚ Hyperphospatemia- can cause

calcium level to fall. Excess phosphorous
combines with Cal to form salts.

⮚ Massive blood transfusions- are at ⮚ Hypophosphatemia- which increases

risk for hypocalcemia. ionization of calcium
⮚ Burns and infections- it traps calcium
ions from the ECF thereby reducing
serum calcium levels

CM Due to increase cell membrane permeability Due to decrease cell membrane permeability
resulting to increased neuromuscular that results to decreased neuromuscular
irritability irritability

CNS: CNS

⮚ T-Tingling sensations/paresthesia of ⮚ Depression

toes, fingers and face
⮚ Diminished DTR
⮚ A- Anxiety
⮚ Dec LOC
⮚ H-Hyperactive DTR
⮚ Lethargy
⮚ I- Irritability
⮚ Coma
⮚ C- Confusion

⮚ S- Seizure

GI:

⮚ Increase peristalsis,

⮚ diarrhea,
GIT
⮚ NV
⮚ Anorexia

⮚ Decrease peristalsis (constipation an -effects

of Ca in the smooth muscle that decrease GI
motility

⮚ Paralytic ileus
Muscles: ⮚ NV

⮚ Chvostek’s sign Muscles

- Abnormal spasm of the facial ⮚ Fatigue, muscle weakness, hyporeflexia

muscles I(upper lip) that is elicited hypotonia (decrease muscle tone)
by tapping the patient’s facial nerve
near his lower jaw

⮚ Trousseau’ s sign/ Carpopedal

spasm

- Early sign of hypocalcemia

- A sign of tetany

- Contraction of fingers and hand

(adducted thumb, flexed wrist and
metacarpal koints) elicited by applying of
blood pressure cuff on the upper arm for
1-5minutes

- Inflate 20mmHg above the systolic

pressure

⮚ muscle spasm/tremors

Cardiovascular

⮚ Low CO

⮚ Dysrhythmias

⮚ Decreased myocardial contractility—

angina, bradycardia, hypotension, heart
failure Cardiovascular- heart muscle and the cardiac
conductions system are affected
⮚ Cardiac arrest
⮚ Arrhythmias (such as bradycardia) can lead
⮚ Prolonged ST segment on ECG, widened to cardiac arrest.
QT interval
⮚ Depressed electrical activity
Others
⮚ ECG changes shortened QT interval and ST
⮚ BRITTLE Bones- fracture due to segment
decrease calcium in the bones
⮚ Look for digoxin toxicity if the patient is
receiving digoxin.

⮚ Cardiac arrest-

Kidneys- as the kidneys work overtime to remove

excess CA

⮚ Excessive thirst and Polyuria

⮚ DHN

⮚ Stones/calcification

⮚ Renal Damage

DANGER SIGNS OF HYPERCALCEMIA


NSG DX: Impaired physical mobility
Lab Data Decrease calcium level lower than
8.5mEq/L
Collaborativ - High Calcium diet
e
Managemen - Dietary sources of Calcium
t
- Canned sardines and salmon
- Diary products –milk, cheese and yogurt
- Green leafy vegetables
- Legumes
- Molasses
- Nuts
- Whole grains
- Calcium gluconate IV (not in cardiac
arrest) or IV Calcium chloride (cardiac
arrest)- Acute hypocalcaemia
- Mix IV calcium in dextrose solution only
- Mix IV Calcium gluconate in Dextrose 5%
in Water per IV as prescribed. Indicated
for severe hypocalcaemia
- Do not dilute in Normal saline (NaCL)
may cause calcium to be excreted
- Never dilute calcium in solution
containing BICARBONATE because
precipitation will occur.
- Administer IV calcium SLOWLY. Rapid
administration may cause SYNCOPE,
Hypotension, cardiac arrhythmias,
- Overcorrection may lead to Hyperkalemia
⮚ Arrhythmias (bradycardia)
⮚ Cardiac Arrest
⮚ Coma
⮚ Paralytic ileus
⮚ Stupor
Impaired physical mobility, fluid and electrolyte
imbalance. Altered LOC,
⮚ Increase serum calcium greater than
10.5mg/dl
⮚ X rays revealing pathologic fractures
⮚ ECG changes- shortened QT intervals,
shortened ST segments, Flattened T waves,
Prolong PR interval
- Low calcium Diet
- DC drugs that contain calcium
- Increase fluid intake. To prevent DHN and
stone formation
- Hydrate pt with normal saline. To
promote diuresis and calcium excretion
- Assess pt with arrhythmias
- Assess pt with renal calculi, strain urine
- Provide acid ash fruit juices. Cranberry
and prune juice
- Give furosemide/ethacrynic acid
(edecrin) as ordered. Promote calcium
secretion.
- Thiasides are NOT used because they
inhibit calcium excretion
- Administer corticosteroid therapy as
prescribed. It block bone reabsorption
and GI absorption of calcium
- Give Mithramycin to reduce calcium
levels.
- Hemodialysis- If with renal failure and
for pts with life threatening-to excrete
calcium
 - Observe IV site for signs of infiltration.
Calcium can cause tissue sloughing and
necrosis.

⮚ Oral calcium salts as prescribed

⮚ Vit D and parathormone

supplements as ordered.

⮚ Amphogel (Aluminum hydroxide) as

prescribed. calcium levels will
increase

⮚ Promote safety. Seizure may occur

⮚ Keep tracheostomy tray and

resuscitation bag at the bedside.
Laryngospasm may occur

⮚ Assess for Chovstek sign and

carpopedal spasm

⮚ Place pt in cardiac monitor to detect

changes in heart rate and rhythm.

Magnesium (Mg)
⮚ A leading ICF Cation
⮚ Influences enzyme reactions and metabolic processes
⮚ Regulates neuromuscular contraction and transmission
⮚ Modifies nerve impulse transmission and skeletal muscle response.
⮚ Responsible for normal functioning of nervous and cardiovascular system, protein synthesis and transportation of sodium and
K ion
⮚ 1.5-2.5mEq/L
⮚ Inhibits acethylcholine release

HYPOMAGNESEMIA HYPERMAGMESEMIA

❖ Serum magnesium less than 1.5 ❖ Increased serum magnesium greater

md/dl than 2.5mEq/L

❖ Can lead to:

❖ Respiratory muscle paralysis

❖ Complete heart block

❖ Coma

MP HYPOMAGNESEMIA-----increased HYPERMAGNESEMIA- There is decrease

acetylcholine release--------increased acetylcholine release---decreased
neuromuscular irritability neuromuscular irritability

Magnesium intake decreases/ Absorption Magnesium excretion decreases/magnesium

decreases/Magnesium loss increases----- intake increases----High Mg level suppresses
Magnesium moves out of cells to ACH release at myoneural junction----reduced
Acetylcholine neuromuscular transmission
compensate for low extracellular
and reduces cell excitability----CNS and
magnesium level----Cells become starved
Neuromuscular become depressed----LOC
for Mg----increased acetylcholine
decreases and respiratory distress occurs---
release-----Muscles become
hyperirritable/neuromuscular irritability
Causes ❖ Inadequate magnesium intake ❖ Excessive intake of magnesium

- Chronic alcoholism ❖ Use of drugs

- Prolonged IV therapy - antacids such magnesium aluminum hcl,

laxative that contain magnesium, supplements
- Use of TPN or enteral feeding formulas magnesium sulfate
without sufficient magnesium
- Use of magnesium rich dialysate for dialysis

❖ Impaired magnesium excretion

❖ Inadequate GI absorption of
Magnesium -renal failure

- Malabsorption syndrome -advance age

- Steatorrhea - Addison’s disease

- Ulcerative colitis

- Crohn’s disease

- Cancer

- Pancreatic insufficiency

- Excess calcium or phosphorous in GI

tract

❖ Excessive GI loss of Magnesium

-Prolonged diarrhea

-Fistula drainage

-Laxative abuse

-NG tube suctioning

❖ Excessive urinary loss of

Magnesium

- Primary aldosteronism

- DKA

- Use of drugs- aminoglycosides-

amikacin, gentamicin, streptomycin,
insulin, laxative, loop diuretics-
bumetanide and furosemide

- Renal disorders such as

glomerulonephritis, pyelonephritis

SS and Sx CNS ❖ Confusion

❖ Tremors ❖ Muscle weakness

❖ Paresthesia ❖ Arrhythmia

❖ Ataxia ❖ Hypotension
 ❖ Confusion ❖ Diminished deep tendon reflex (DTR)

❖ Convulsion ❖ Lethargy

❖ Hallucinations ❖ Drowsiness

❖ Seizure ❖ Nausea and vomiting

Muscles ❖ Bradycardia---cardiac arrest

❖ Leg and foot cramps ❖ Respiratory arrest

❖ Chvostek’s sign and Trousseau’s sign-

tetany

❖ Hyperactive DTR

❖ Tremors

Cardiovascular System

❖ Hypertension

❖ Arrhythmias- Ventricular
tachycardia, Atrial fibrillation, PVC,
Ventricular fibrillation.

Respiratory

❖ DOB

❖ Laryngeal stridor

Nsg Dx Electrolytes imbalance

Altered Nutrition Less Than Body

Requirement

Lab Data Decreased serum magnesium Increased serum magnesium greater than 2.5

ECG changes- Prolonged PR intervals and QT ECG changes- prolong PR intervals, widened QRS
intervals, widened QRS, depressed ST segment, complex and Tall T waves
prominent U waves, Flattened T waves

Management ❖ Provide food rich in magnesium/oral ❖ Calcium gluconate per IV. Calcium
supplement (MILD) antagonizes magnesium (emergency)

- Meat, milk, fruits, green vegetables, ❖ Administer oral or IV fluids to rid the
whole grain cereals, nuts, sea foods body of excessive magnesium

❖ Promote safety ❖ Administer loop diuretic such furosemide

to excrete magnesium
❖ Monitor client for laryngeal stridor-
indicates airway obstruction ❖ Provide mechanical ventilation if
compromises respiratory function
❖ Magnesium sulfate as ordered for
severe deficiency
❖ Avoid the use of drugs containing
❖ Assess the patients renal function (I magnesium
and O) before administering
❖ Restrict foods rich in Mg
magnesium sulfate

❖ Monitor neuromuscular status- to

detect hyperactive DTR, tremors
 and tetany

❖ Assess signs of tetany

❖ If pts receives digoxin, monitor signs of

toxicity bec. Hypomagnesemia
increase the risk of adverse
reaction

❖ Monitor electrolyte levels bec.

Hypocalcemia and hypokalemia
can cause hypomagnesemia

❖ Institute seizure precaution

ACID BASED BALANCE

The cells of the body function best when the body fluids and electrolytes are within a very narrow range. Hydrogen is another ion that
must stay within its normal limits. The amount of hydrogen determines whether a fluid is an acid or base.
ACIDS
⮚ A substance that releases hydrogen ion. The stronger the acid the more hydrogen ions released
⮚ Include solutions with a pH below 7.35 (ACIDOSIS)
⮚ Hydrochloric acid- a common acid in the body found in the stomach
⮚ Are formed as end products of glucose, fats and protein metabolism called Fixed Acid.
BASES
⮚ Molecules that can ACCEPT hydrogen molecules/ that binds hydrogen
⮚ ALKALI is another word for BASE
⮚ Include solutions with a pH ABOVE 7.35 (ALKALOSIS)
⮚ Bicarbonate

Acid Base Regulators

When pH rises or falls, three systems work to create acid base balance
1. Cellular/ Chemical Buffers
 ▪ First to attempt a return of pH to its normal range
▪ Instantly combined with the offending acids or base to neutralized the harmful effects
▪ examples are protein, hemoglobin, bicarbonate and phosphate
▪ They act as a type of sponge to “soak up” extra hydrogen ions if too acidic or release ion if too alkaline
2. Respiratory system
▪ uses hypoventilation and hyperventilation to regulate acid excretion or retention
▪ When the blood is too ACIDIC (pH is decreased), the lungs “blow off” additional CO2 through rapid, deep breathing. This
reduces the amount of CO2 available to make carbonic acid in the body.
▪ If the blood is ALKALINE, (decreased pH), the lungs try to conserve CO2 through shallow respiration.
3. KIDNEYS
▪ are the slowest to respond to changes in serum pH
▪ excrete or retain more acids or bases as needed
▪ If the serum pH DECREASE and becomes too acidic, the reabsorb additional bicarbonate rather than excreting it so that it
can neutralize the acid.
▪ If pH INCREASES and becomes too ALKALINE, the kidney excrete additional bicarbonate to get rid of the extra
base.

ABG ANALYSIS
⮚ Can help to assess ventilation and acid base balance
⮚ It helps to monitor patients response to therapy
⮚ Arterial blood is usually used to measure the pH. Radial Artery is the common site for withdrawal of specimen
⮚ Allen’s Test is done to assess for adequacy of collateral circulation of the hand
⮚ Use 10 ml heparinized syringed to draw the blood specimen. To prevent blood clotting.
⮚ Place the specimen in a container with ice. To prevent hemolysis. If hemolysis, OXYGEN and CO2 are release and cannot
be measure accurately.
AVOID INACCURATE ABG VALUES
❖ Be sure to use proper technique
❖ Avoid delays in getting the sample to the laboratory
❖ Don’t draw blood for ABG ANALYSIS within 15-20 minutes of a procedure such as suctioning or administering respiratory
treatment
❖ Remove air bubbles from the syringe because they could affect the oxygen level in the blood
❖ Don’t get venous blood in the syringe because it could affect the CO2 and O2 levels and pH

pH 7.35-7.45

paCO2 35-45

HCO3 22-26mEq/L

O2 95%-100%
Saturation

paO2 80-100mmHg

KEY FACTS
Understanding acids and bases requires to:
Understanding pH
⮚ To assess the pts Acid Base balance, you must know the pH level of the blood.
⮚ A pH within that range represents a balance between the percentage of Hydrogen ions and bicarbonate ions in the
blood.
⮚ Normally, pH ranges (7.35-7.45) which is slightly ALKALINE.
⮚ A solution that contains MORE ACID than Base has MORE Hydrogen ions, it has a lower pH. A pH less than 7.35 is
abnormally ACIDIC
⮚ A solution that contains more Base THAN Acid has fewer hydrogen ions. A pH level greater than 7.45 is abnormally
ALKALINE.
⮚ A ph below 6.8 or above 7.8 is FATAL
⮚ A lower pH than 7.35 is abnormally ACIDIC
⮚ A higher pH level than 7.45 is abnormally ALKALINE
⮚ Figure out if the cause is respiratory or metabolic.
 pH Low Below 7.35 Acidosis

High Above 7.45 Alkalosis

DETERMINE THE PaCO2

❖ paCO2 is the Respiratory Indicator
❖ 35-45 mmHg
❖ paCO2 provides information about the respiratory component of acid base balance
❖ CO2 acts as an acid. When combined with Plasma, Carbonic Acid is formed. (CO2 + H2O=H2CO3)
❖ If the paCO2 value is abnormal, determine if is LOW or HIGH.
❖ Increase CO2- Resp Acidosis, Decrease CO2- Resp Alkalosis

pH (7.35-7.45) CO2 (35-45)mmHg HCO3 (22-26)mEQ/L

Respiratory Acidosis Low High Normal

Respiratory Alkalosis High Low Normal

WATCH THE BICARBONATE

❖ Examine the HCO3 value, which provides an information about the metabolic aspect of acid base balance
❖ If the HCO3 is Abnormal, determine if is LOW or HIGH
❖ Normal value 22-26mEq/L
❖ Then determine whether the abnormal result corresponds with a change in pH
❖ If pH is HIGH, then HCO3 is HIGH- METABOLIC ALKALOSIS
❖ If pH is LOW, then HCO3 is LOW- METABOLIC ACIDOCIS

pH (7.35-7.45) HCO3 (22-26) CO2 (35-45)

Metabolic Acidosis Low Low Normal

Metabolic Alkalosis High High Normal

LOOK FOR COMPENSATION

❖ Check the relationship or change in the paCO2 and BCO3
❖ REMEMBER: the LUNGS and KIDNEYS normally attempt to help each other to maintain ACID BASE BALANCE
❖ If the LUNGS are unable to maintain acid base balance , the kidneys will attempt to adjust the level of HCO3
❖ If the KIDNEYS are unable to maintain acid base balance, the LUNGS will attempt to adjust the levels of CO2.
❖ If CO2 and HCO3 levels moves toward the SAME DIRECTION; ex: BOTH are HIGH or BOTH are LOW, then Acid
Base Imbalance is COMPENSATED

CO2 (35-45) HCO3 (22-26)

55- High (Acidosis) 34- High (Alkalosis)

24- Low ( Alkalosis) 20- Low (Acidosis)

❖ When is the Acid Base imbalance considered as Partial or Complete Compensation?

1. COMPLETE COMPENSATION occurs when pH fall into NORMAL.
pH CO2 HCO3

Resp. Acidosis with Normal High High

compensation
 Resp. Alkalosis with Normal Low Low
compensation

Metab. Acidosis with Normal Low Low

Compensation

Metab. Alkalosis with Normal High High

Compensation

2. When the Acid based is COMPENSATED, but the pH is still ABNORMAL: PARTIAL COMPENSATION

pH CO2 HCO3

Resp. Acidosis High High High

Resp. Alkalosis High Low Low

Metab. Acidosis Low Low Low

Metab. Alkalosis High High High

When is the acid base imbalance considered as UNCOMPENSATED?

1. When the CO2 and HCO3 levels move towards OPPOSITE DIRECTION
2. Ex: PaCO2 High (Acidosis) HCO3 Low (Alkalosis); PaCO2 LOW; HCO3 HIGH
3. When PaCO2 is ABNORMAL and HCO3 remains NORMAL and vice versa, still UNCOMPENSATED

Ex:
PaCO2 High- ACIDOSIS HCO3 Low-ACIDOSIS

PaCO2 LOW- Alkalosis HCO3 High- ALKALOSIS

Respiratory Acidosis
ABG Compensated Uncompensated

pH Normal Low pH

paCO2 High (>45) High (>45)

HCO3 High (>45) Normal

Respiratory Alkalosis
ABG Compensated Uncompensated

pH Normal High >7.45

paCO2 Low (<35) Low (<35)

HCO3 Low (<22) Normal

Metabolic Acidosis
ABG Compensated Uncompensated

pH Normal Low (<7.35)

paCO2 Low (<35) Normal

HCO3 Low (<22) Low (<22)

Metabolic Alkalosis
ABG Compensated Uncompensated

pH Normal High (>45)

PaCO2 High (>45) Normal

HCO3 High (>26) High (>26)

pH (7.35-7.45) PaCO2 (35-45) HCO3 (22-26)

Resp Alkalosis 7.5 H 31 L 26N

Uncompensated

Resp Alkalosis Complete 7.41 N 30 L 18L

Compensated

Resp Acidosis Partial 7.24 N 60 H 32 H

Compensation

Metabolic Acidosis 7.38 N 32 L 19 L

Complete compensation

RESPIRATORY ALKALOSIS and ACIDOSIS

Respiratory Alkalosis Respiratory Acidosis

Main Problem A condition characterized by loss of CO2 A condition characterized by retention of

due to CO2 due to:

-Hyperventilation->RR, Increase TV, causes -Hypoventilation- the vol.of air that enters
excessive and elimination of CO2 causing the alveoli is not adequate for the body
hyper oxygenation needs.

-Anxiety

-Fever

Causes Lung disorders (COPD)

-airway obstruction

-Drugs (sedative; Valium), MG

Step 2: As the pH drops, 2,3duphoglycerate

increases in RBC and causes a change in
Hgb that make the Hb release O2. Altered
Hb is strongly ALKALINE, picks up H+ and
and CO2 thus H+ and CO2 increases. (Look
for decrease arterial O2)

Step 3. As PaCO2 increases, CO2 builds up

in all tissues and fluids and in the
respiratory center in the medulla. Increased
CO2 and H+ stimulate the respiratory
center to increase the RR (rapid shallow RR)
to expel CO2 in the blood and other tissues

Step 4: Eventually, Carbon dioxide and

hydrogen ions cause vasodilation to dilate
 that increases the blood flow to the brain
that lead to cerebral edema and depressed
CNS activity (look for headache, confusion,
lethargy, nausea and vomiting)

Step 5: As respiratory mechanism fails, the

increasing PaCO2 stimulate the kidneys to
conserve HCO3 ions and Na+ and excrete
H+ in form of ammonium. The additional
Na and HCO3 combine to form NaHCO3 to
buffer more free H+. look for increased acid
content in the urine , increase pH and
HCO3, shallow depressed respiration.

Step 6. As the concentration of H+

overwhelms the body’s compensatory
mechanism, the H+ moves into the cells
and K+ moves out. Lack 0xygen causes in
the production of lactic acid that depresses
the neurologic and cardiac functions.

Manifestations -light headedness -Confusion, Dull Headache, Restlessness

-Numbness of hands and feet -Tachycardia, Dyspnea, Respiratory Failure

-Restlessness, Tachycardi, Syncope, Seizure

Lab Data ABG reveals: High pH Low PaCO2 ABG reveals: Low pH, High PaCO2

Chest xray- COPD, pneumonia

Electrolytes- High K

Nursing Dx Ineffective Breathing Pattern

Interventions Breathe into paper Bag Deep breathe and cough

Administer bronchodilator and oxygen as

prescribed

METABOLIC ALKALOSIS and ACIDOSIS

Metabolic ALKALOSIS METABOLIC ACIDOSIS

Main Problem A condition characterized by acid loss in A condition characterized by excessive

the body due to: blood acidity due to:

-Cushing disease -kidney disorders

- Hypokalemia -Diarrhea (GI Disturbance

- vomiting -DKA
Manifestations Headache Confusion

Lethargy Hypotension

Tetany Weakness

Arrhythmia Kussmaul’s breathing

Seizures

Lab Data ABG: High pH High HCO3 ABG: Low pH, Low HCO3

Nursing Dx Risk for Acid based Imbalance Risk for Acid based Imbalance

Interventions Administer 0.9% Saline solution Administer Sodium Bicarbonate as

prescribed
Administer acetazolamide to promote
excretion of excess HCO3