Fluids and Electrolytes

Fluids
60% of an adults body weight is water
Factors affecting body fluid composition:
1. Age
2. Gender
3. Body fat
Fluid Compartments in the body:
1. Intracellular space
-fluid in the cells
-approximately 2/3 of the total body water
-primarily located in the skeletal muscle mass
2. Extracellular Space
-body fluid outside the cells
-divided into:
a. intravascular
>contains plasma
>approximately 3L out of 6L blood volume
b. interstitial
>fluid that surrounds the cells
>approximately 11-12L in an average adult
c. transcellular
>smallest division of the ECF
>approximately 1L of fluid
>CSF, synovial, pericardial, pleural, intraocular

Regulation of Body Fluid Compartments

1. Osmosis and Osmolality
2. Diffusion
3. Filtration
4. Sodium-Potassium Pump

Routes of Gains and Losses

1. Kidneys
> Approximately 1L in an average adult
> 1mg/kg/hour
2. Skin
> may vary from 0 1000ml or more
3. Lungs
> Approximately at 400ml a day
4. GI tract
> At 100 200ml a day

Laboratory Tests for Evaluating Fluid Status

1. Osmolality
Serum Na x 2= glu/18 +BUN/3= Approx value of serum osmolality
Osmolality
2. BUN
10 20mg/dl or 3.5 7 mmol/L
3. Creatinine
0.7 1.5 mg/dl or 60 130mmol/L
4. Hematocrit
males: 0.44 - 0.52
females: 0.39 - 0.47
5. Urine Sodium
50 220mEq/24 hours
Homeostatic Mechanisms
1. Kidneys
-filters 170L of blood a day
-excretes only 1.5L of urine/24 hours
2. Heart and Blood Vessel Functions
3. Lungs
4. Pituitary Function
5. Adrenal Functions
6. Parathyroid Functions
7. Baroreceptors
a. high pressure baroreceptors
-in the aortic arc and carotid sinus
-in the juxtaglomerular cells of the nephron
b. low pressure baroreceptors
-in the cardiac atria (left atrium)
8. Renin - Angiotensin - Aldosterone System
Liver > Angiotensinogen > Angiotensin (kidneys)
renin
Angiotensin 2 (lungs) > Aldosterone (adrenals)
ACE
9. ADH and Thirst
10. Osmoreceptors
11. Atrial Natriuretic Peptide
-at 20 77pg/ml (20 -77ng/L)

Third Space Fluid Shift

Fluid Volume Deficit

Dehydration
Causes:
a. inadequate intake
b. abnormal fluid losses
c. other causes
-diabetes insipidus
-osmotic diuresis
-hemorrhage

-coma
Signs and Symptoms:
weight loss, poor skin turgor, oliguria, concentrated urine, postural
hypotension, rapid heart rate, decreased CVP, cool clammy skin,
increase temperature

Assessment:
BUN and Crea
Hematocrit
Serum elecrolytes
Urine specific gravity
Fluid Challenge Test

Management:
a. oral route of fluid replacement
-preferred method
b. IV route
-isotonic then hypotonic
c. monitoring
-weight, intake and output, V/S, CVP level of consciousness,
breath sounds and skin color

Nursing management:
a. prevent fluid volume deficit
B. correct fluid volume deficit

Fluid Volume Excess

-isotonic expansion of body water
Cause:
a. abnormal retention of water and sodium

Signs and Symptoms:

a. edema
c. crackles
d. tachycardia h. increased weight
e. increased BP
f. increased PP
Assessment:
BUN
Hematocrit
Serum Osmolality
Serum Electrolytes

b. distended neck veins

g. increased CVP
i. increased urine output
j. shortness of breath

CXR

Management:
a. withholding excessive administration of IVF
b. diuretics
c. restriction of oral fluids (sodium)
1. Pharmacologic Therapy
2. Hemodialysis
3. Nutritional Therapy

Nursing management:
a. preventing fluid volume excess
b. detecting and controlling fluid volume excess
c. teaching patients about edema

Sodium Deficit
-refers to serum sodium level below 135mEq/L

Causes:
a. vomiting
b. diarrhea
c. diuretics

d. fistulas
e. sweating
f. dilutional hyponatremia

S/sx:
Similar to dehydration

Assessment:
serum sodium of less than 135mEq/L
urine sodium
SIADH - >20mEq/L
Sodium loss - <20mEq/L

Management:
a. sodium replacement
-by mouth, NGT or through parenteral route
-parenterally, must not exceed
12mEq/L in 24 hours > osmotic demyelination
b. SIADH
-give Demeclocycline or Lithium
c. water restriction
-safer than sodium replacement

Sodium Excess
-sodium level higher than 145mEq/L
-can occur in patients with normal fluid volume or in those with FVE or FVD

Causes:
a.
b.

gain of sodium in excess of water

(administration of hypertonic saline)
loss of water in excess of sodium
(unconscious, cognitively impaired individuals, diarrhea,
hyperventilation, burns, diabetes insipidus, heat stroke and sea
water drowning)

Signs and symptoms:

Predominantly neurologic (cellular dehydration)

Management:
> Serum sodium should be reduced at a rate of 0.5-1mEq/L
1. IVF Therapy
-hypotonic solution or isotonic non saline solution
2. Diuretics
3. Desmopressin Acetate

Nursing Management:
1. Look for the hidden sources of sodium
2. Monitor for: body temperature, thirst and level of consciousness
3. Prevent hypernatremia
4. Correct hypernatremia

Potassium Deficit
-potassium serum level <3.5mEq/L
Causes:
>alkalosis, GI losses, hyperaldosteronism, potassium losing diuretics, other
drugs (corticosteroids, amphotericin B, carbenicillin and sodium penicillin),
insulin hyper secretion, inability or unwillingness to eat a normal diet,
magnesium depletion, Cushings syndrome

Signs and symptoms:

>fatigue, anorexia, nausea, vomiting, muscle weakness, leg cramps, decreased
bowel motility, paresthesias, dysrhythmias and increased sensitivity to
digitalis, glucose intolerance

Confirmatory tests:
1. Decreased serum potassium
2. ECG changes
-flat or inverted T waves and depression of the ST segments
-elevation of the U waves
3. Metabolic Alkalosis
4. Urine potassium concentration of >20mEq/24 hours

Medical Management:
1. Potassium replacement therapy
-if without abnormal potassium loss, 40-80mEqs/day
-oral (Kalium Durule) or IV (K chloride, K phosphate or K acetate)

Nursing Management:
1. Monitoring for s/sx or progression of hypokalemia
2. Preventing hypokalemia
3. Correcting hypokalemia
4. Administering IV potassium
-after adequate urine flow
-20mEqs/hour or less
-30-40mEqs/L and below unless severe

Potassium Excess
-less common but more severe than hypokalemia

Causes:
> renal failure, excessive intake of potassium, infection, hyporaldosteronism
and Addisons disease, medications (KCl, heparin, ACE inhibitors, NSAIDS
and K sparing diuretics) and acidosis

Clinical manifestations:
> dysrhythmias, skeletal muscle weakness and paralysis
> CNS and PNS involvement
> Flaccid quadriplegia, respiratory and speech muscle paralysis

Confirmatory tests:
1. ECG
-peaked, narrow T waves, ST segment depression and a shortened QT interval
-prolonged PR interval then absence of P wave
2. ABG
3. Serum potassium level increase
Medical Management:
1. Monitoring of serum potassium with ECG findings
2. Emergency pharmacologic therapy
>calcium gluconate or calcium chloride
>sodium bicarbonate
>insulin and glucose
>beta 2 agonist
3. Dialysis
Nursing Management:
1. Monitoring
2. Preventing hyperkalemia
3. Correcting hyperkalemia
Pseudohyperkalemia
> Use of tourniquet in an exercising muscle
> marked leukocytosis and thrombocytosis
> Familial pseudohyperkalemia

Calcium Deficit
-less than 8.5mg/dl of calcium in the serum
Causes:
>hypoparathyroidism
>those who received citrated blood
>pancreatitis, renal failure
>vitamin D deficiency, magnesium deficiency
>medullary thyroid carcinoma
>low albumin levels, alkalosis and alcohol abuse

Signs and symptoms:

> tetany, seizures and mental changes
Confirmatory test:
> ECG- prolonged QT interval

Management:
1. Administer calcium salts
-calcium carbonate, calcium chloride, calcium gluceptate
Risks:
a. Sloughing of tissues
b. Bradycardia then cardiac arrest
c. Digitalis toxicity
2. IVF but not normal saline or solutions containing phosphates and
bicarbonate
3. Vitamin D therapy
4. Aluminum hydroxide, calcium acetate, calcium carbonate
5. Nutritional therapy
6. Screen for and treat hypomagnesemia

Nursing Management:
1. Monitor hypocalcemia for patients at risk
2. Airway management
3. Seizure precaution
4. Patient education
-caffeine and alcohol decreases absorption
-nicotine increases excretion
-medications to decrease bone loss
(alendronate, raloxifene and calcitonin)

Calcium Excess
-with high mortality rate
Causes:
>malignancies and hyperparathyroidism
>immobilization
>use of Thiazide diuretics
>milk-alkali syndrome
>Vitamin A and D intoxication

Signs and symptoms:

*proportional to the elevation of serum calcium
>muscle weakness, incoordination, anorexia and constipation
>cardiac arrest
>dehydration
>abdominal and/or bone pain
>abdominal distention and paralytic ileus
>excessive urination then polyuria
>s/sx of PUD
>changes in the LOC and mental status
*hypercalcemic crisis

 Laboratory tests:
1. Serum calcium determination
2. ECG
- shortening of the QT interval and ST segment
- prolongation of the PR interval
- dysrhythmias
3. Double antibody PTH test
4. X-Ray - osteoporosis
5. Sulkowitch test

Management:
1. Pharmacologic therapy
-dilute the serum calcium and promote its exc.
(normal saline, administer phosphates, diuretics, calcitonin)
-Cancer treatment
-Corticosteroid therapy
> to decrease bone turnover and tubular reabsorption
-Biphosphonates (pamidronate)
>causes myalgia, pyrexia and decreased WBC
-Mithramycin
>causes thrombocytopenia and nephrotoxicity and
hepatotoxicity
-IV phosphates should be used with caution
>Phospho-Soda, Neutra-Phos

Nursing Management:
1. Monitor the s/sx
2. Increase mobility
3. Increase oral fluid intake

Chloride Deficit
-serum chloride level below 96mEq/L
Causes:
>chloride deficient formulas, salt restricted diets
>GI tube drainage, severe vomiting and diarrhea

Signs And Symptoms:

>hypokalemia, hyponatremia and metabolic alkalosis
(hyperexcitability of muscles, tetany, hyperactivity of deep tendon reflexes,
weakness, twitching, muscle cramps, cardiac dysrhythmias, seizures and
coma)

Lab Tests:
>serum chloride determination
>serum potassium and sodium determination
>ABG
>urine chloride level decrease (normal value- 110-250mEq/L)

Medical Management:
>chloride replacement
normal saline and half strength saline
>reevaluate the use of diuretics
>nutritional therapy
tomato juice, salty broth, canned vegetables, processed meats and
fruits
>restriction of free water intake
>ammonium chloride

Nursing management
>monitoring of intake and output, ABG determination values, serum electrolyte
levels, LOC, muscle strength and movement
>vital signs and respiratory assessments
>patient education as regards to replacement therapy

Chloride Excess
-serum chloride level higher than 106mEq/L
-associated with hypernatremia, bicarbonate loss and metabolic acidosis
Causes:
>loss of bicarbonate (GI and/or renal)

Signs And Symptoms:

>metabolic acidosis, hypervolemia and hypernatremia
(tachypnea, weakness, lethargy, deep rapid respirations, diminished cognitive
ability and hypertension)
>decrease in CO, dysrhythmias and coma

Lab Tests:
>serum sodium and chloride determination
>ABG- Bicarbonate less than 22mEq/L
-normal anion gap (8-12mEq/L)
>urine chloride concentration greater than 250mEq/L
Medical Management:
>IVF therapy
-Lactated Ringers Solution
>IV sodium bicarbonate
>Diuretics
>Fluids, sodium and chloride restriction
Nursing Management:
>monitoring V/S, ABG, I&O
>assessment of neurologic, respiratory and cardiac functions
>patient education as regards to nutrition

Acid-Base Balance
Normal blood pH
-7.35 to 7.45
Blood pH compatible with life
-6.80 to 7.80
Buffer Systems
-maintains the blood pH by removing or releasing H+ ions
1. Bicarbonate-Carbonic Acid Buffer System
-the major extracellular buffer system
-Bicarbonate to Carbonic Acid Ratio is 20:1
2. Phosphate Buffer System
3. Plasma proteins, RBC and Hemoglobin
Organs involved in HCO3-H2CO3 System:
1. Kidneys
-activation is slower (hours to days) but more efficient
-has the ability to regenerate and reabsorb or excrete bicarbonates
-has the ability to retain or excrete H+
-in acidosis: excrete H+ and conserve bicarbonate
-in alkalosis: retain H+ and excrete bicarbonate
-cannot compensate in renal failure
2. Lungs
-adjust ventilation in response to CO2 content of the blood
-activation is faster but less efficient
Acute and Chronic Metabolic Acidosis(Base Bicarbonate Deficit)
-low pH; low plasma bicarbonate

Causes:
>gain of hydrogen ions or loss of bicarbonate
2 forms:
A. High Anion Gap Acidosis
-due to the accumulation of the unmeasured anions
(phosphates,sulfates and proteins)
B. Normal Anion Gap Acidosis (hyperchloremic acidosis)
-due to the direct loss of bicarbonates
>diarrhea
>diuretics
>lower intestinal fistulas
>renal ins.
>excessive administration of chloride
>excessive administration of parenteral solution without bicarbonate

Signs And Symptoms:

>headache, confusion, drowsiness
>increased respiratory rate and depth
>nausea and vomiting
>peripheral vasodilatation and decreased CO
>decreased BP, cold and clammy skin, dysrhythmias and shock

Lab Tests:
>ABG - low bicarbonate level and a low pH
>Serum potassium determination
>Anion Gap Calculation
>ECG

Medical Management:
>Eliminate excessive sources of chloride
>Sodium bicarbonate
-if pH is less than 7.1
-if bicarbonate is less than 10mEq/L
>Serum potassium monitoring and reversal of potential hypokalemia
>Reversal of potential hypocalcemia
>Sodium Bicarbonate
>Dialysis

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess)

-high pH; high plasma bicarbonate concentration
Causes:
(due to gain of bicarbonates or loss of hydrogen ions)
>vomiting or gastric suction- most common
>diuretics- loop and thiazides
>hyperaldosteronism and Cushings syndrome
>excessive alkali ingestion or administration
>villous adenoma and cystic fibrosis

Signs And Symptoms:

>decreased calcium ionization (tingling of the fingers, toes, dizziness and
hypertonic muscles)
>depressed respirations
>atrial arrhythmias then ventricular arrhythmias
>decreased motility then paralytic ileus

Lab Tests:
>ABG - pH greater than 7.45
- bicarbonate greater than 26mEq/L
>Serum potassium determination
>Urinary chloride levels

Medical Management:
>Chloride replacement (KCl)
>IVF containing sufficient sodium and chloride
>H2R antagonists- in GI suctioning
>Carbonic Anhydrase Inhibitors
>I&O monitoring

Acute and Chronic Respiratory Acidosis(Carbonic Acid Excess)

-pH is less than 7.35; paCO2 is higher than 42mmHg
Causes:
(Due to inadequate excretion of CO2 > elevated plasma CO2 > elevated plasma

H2CO3)
>acute pulmonary edema
>aspiration of foreign body
>atelectasis
>pneumothorax

>sedative overdose
>severe pneumonia
>RDS
>MG, GBS

Signs And Symptoms:

>increased HR, RR, BP, mental cloudiness and feeling of fullness in the head
>ventricular fibrillation
>increased intracranial pressure, papilledema, dilated conjunctival bloodvessels
>hyperkalemia

Lab Tests:
>ABG
>Serum electrolyte determination
>Chest X-Ray
>ECG
>Drug screen for overdose

Medical Management:
>Pharmacologic
*bronchodilators
*thrombolytics
*antibiotics
*anticoagulants
>Pulmonary hygiene
>Adequate hydration
>Supplemental O2 with caution
>Mechanical ventilation

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit)

-arterial pH of greater than 7.45; PaCO2 of less than 38mmHg

Causes:
(due to hyperventilation > blowing off of CO2 > decreased plasma carbonic acid
concentration)
>extreme anxiety, hypoxemia, early phase of Aspirin intoxication, gram
negative bacteremia and inappropriate ventilator settings
>chronic hepatic insufficiency, cerebral tumors

Signs And Symptoms:

>lightheadedness, inability to concentrate
>numbness and tingling from reduced ionized calcium
>tinnitus, loss of consciousness
>tachycardia, atrial and ventricular arrhythmias

Lab Tests:
>ABG
>Serum electrolyte determination

Management:
>breath slowly or into a closed system
>sedatives

Acid Base Disturbances and Compensation

Disorder

Initial Event

Compensation

Respiratory Acidosis

PaCO2;or N HCO3; pH

Kidneys eliminate H+ & retain HCO3

Respiratory Alkalosis

PaCO2;or N HCO3;pH

Kidneys conserve H+ & excrete HCO

Metabolic Acidosis

or N PaCO2; HCO3; pH

Lungs eliminate CO2 & conserve HCO

Metabolic Alkalosis

or N PaCO2; HCO3; pH

Lungs to PaCO2, kidneys conserve

BURNS
Autograft
Heterograft
Homograft
Carboxyhemoglobin

Escharotomy
Fasciotomy
Rule of Nines

4 Major Goals Relating to Burns

1. Prevention
2. Institution of lifesaving measures for the severely burned person.
3. Prevention of disability and disfigurement through early, specialized, individual treatment.
4. Rehabilitation through reconstructive surgery and rehabilitation programs.
Burn Categories
1. Thermal
2. Chemical
3. Radiation

Burns are sustained through

1. Conduction
2. Electromagnetic radiation

Skin destruction can lead to;

1. Increased fluid loss 4. Scarring, change in body image
2. Infection
5. Compromised immunity
3. Hypothermia
6. Changes in function
Classification of burns:
A. According to burn depth:
1. Superficial Partial Thickness (Similar to First Degree Burn)

Causes:

*sunburn
*low intensity flash
-involves the epidermis and possibly a portion of
the dermis

Signs And Symptoms:

*tingling
*pain that is soothed by
*hyperesthesia
cooling
*reddened
*possibly blisters
*minimal or no edema
-complete recovery within a week; no scarring

-peel off
2. Deep Partial thickness (Similar to Second Degree Burn)
Causes:
*scalds
*flash flame
-involves the epidermis, upper dermis, portion of the deeper dermis

S/sx:
*pain
*sensitive to cold air
*hyperesthesia
*blistered, weeping surface
*broken epidermis
*edema
-recovery in 2-4 weeks
-some scarring and depigmentation contractures
-infection may convert it to full thickness

3. Full Thickness (Similar to Third Degree)

Causes:
*flame
*prolonged exposure to hot liquids
*electric current
*chemical
-involves the epidermis, entire dermis and sometimes subcutaneous tissue, may
involve connective tissue, muscle and bone

S/Sx:

*pain free
*hemolysis
*shock
*entrance and exit wounds
*hematuria
*broken skin with exposed
*edema
fats
-eschar sloughs
-grafting necessary
-scarring and loss of contour and function; contractures
-loss of digits or extremity possible
Physiologic Responses to Burns
Local Pathophysiologic Response
-if only less than 25% of the TBSA is involved
Local and Systemic Pathophysiologic Response
-if more than 25% of the TBSA is involved
-maximal if burns cover 60% or more of the TBSA
1. Cardiovascular Response
Fluid loss > hypovolemia > decreased cardiac output > decreased BP > decreased
perfusion and oxygen delivery
> onset of burn shock > sympathetic response > peripheral vasoconstriction > further
decrease in the CO

-the greatest volume of fluid leak occurs in 24 36 hours after the burn, peaking at 6 8 hours

-basically caused by increased capillary permeability

-diuresis occurs for several days to 2 weeks
2. Burn Edema
-swelling maximal after 24 hours
-begins to resolve 1-2 days post burn
-Completely resolved after 7-10 days post injury
Edema > pressure on the small blood vessels and nerves of distal extremity >
Ischemia > compartment syndrome
3. Effects on Fluids and Electrolytes and Blood Volume
-evaporative loss through the burn wound (3-5 L)
-hyponatremia (dilutional due to fluid shift from interstitial to intravascular space)
-hyperkalemia due to massive cell destruction
*later results in hypokalemia due to dilution caused by fluid shift
-anemia due to blood loss and hemolysis
(though may be seen as polycythemia due to excessive plasma loss)
4. Pulmonary Response
-inhalation injury > release of histamine, serotonin and thromboxane > catecholamine
release > hypoxia
-atelectasis may be present due to decreased surfactant
-types of pulmonary injury:
*upper airway injury
-results from direct heat and edema
*inhalation injury below the glottis
-usually results from carbon monoxide poisoning
-respiratory acidosis may occur over the first 5 days after the burn
-indicators of a possible pulmonary damage;
*hx indicating that burn occurred in an enclosed space
*burns of the face and neck
*singed nasal hair
*hoarseness, voice change, dry cough, stridor
*bloody sputum
*Labored breathing or tachypnea
*Erythema or blistering of the oral or pharyngeal
mucosa
-possible consequences will be respiratory failure and acute respiratory distress
syndrome
5. Other Systemic Responses
-hemolysis and muscle damage > release of hemoglobin and myoglobin > acute tubular
necrosis and renal failure
-decreased immune response > sepsis
-loss of skin tissue > altered thermoregulation > hypothermia > later hyperthermia due to
hypermetabolism
-sympathetic hyperactivity > paralytic ileus and Curlings ulcer

Management:

1. Emergent/ Resuscitative Phase of Burn Care

A. On the scene Care
-airway, breathing and circulation
-disability, exposure and fluid resuscitation
-duration (from onset of injury to completion of fluid resuscitation
-priorities:
*first aid
*prevention of shock
*prevention of respiratory distress
*detection and treatment of concomitant injuries
*wound assessment and initial care
-emergency procedures at the burn scene:
*extinguish the flames
*cool the burn
*remove restrictive objects
*cover the wound
*irrigate chemical burns
B. Emergency Medical Management:
-transport to the nearest hospital > life-saving measures
-ABC
-humidification, bronchodilation, mucolytic agents, coughing
-ET tube insertion and assisted ventilation
-continuous positive airway pressure
-assessment for head and neck injuries
-burn wound management
-IV access, CVP insertion
-indwelling urinary catheter insertion
-baseline data
-tetanus prophylaxis
-adequate pain relief
C. Transfer to Burn Center
D. Management of Fluid Loss and Shock
-fluid replacement therapy
-fluid requirements
Problems Associated:
>Acute Resp and Renal Failure
>Distributive Shock
> Compartment Syndrome
2. Acute or Intermediate Phase of Burn Care
-begins 48 to 72 hours after the burn injury
-goals:
A. Infection Prevention
-Staphylococcus, Pseudomonas, Proteus, E. coli, and Klebsiella
-Candida is also being implicated
-3 characteristics of burn wound sepsis:

*100,000 bacteria/gram of tissue

*inflammation
*sludging and thrombosis of dermal blood vessels
-early enteral feeding can be used for prevention
B. Wound Cleaning
-hydrotherapy
>use of tap water
>temperature of water should be maintained at 37.8C
>room temperature should be maintained at 26.6-29.4C
>should be limited to a 20-30 minute period
C. Topical Antibacterial therapy
-criteria for choosing antibiotics:
*effective against gram negative organisms
*clinically effective
*penetrates the eschar but without systemic toxicity
*does not lose its effectiveness
*cost effective, available and acceptable
*easy to apply
-examples:
1. Silver sulfadiazine
2. Silver Nitrate
3. Mafenide Acetate
D. Wound Dressing
E. Dressing Changes
F. Wound Debridement
2 goals:
*to remove tissue contaminated by bacteria
*to remove devitalized tissue or burn eschar in preparation for grafting
and wound healing
G. Pain Management
H. Nutritional Support

Shock
Types:
1. Hypovolemic Shock
2. Cardiogenic Shock
3. Circulatory Shock (Distributive Shock)
> Septic Shock
> Neurogenic Shock
> Anaphylactic Shock
*Obstructive Shock
-Effect of shock to normal cellular functions
-Vascular Responses
1. Central Regulatory Mechanisms
2. Local Regulatory Mechanisms
-Blood Pressure Regulation
BP= CO x TPR
CO= SV x HR
>Maintained by:
a. nervous system
b. endocrine system
c. chemicals
>Maintain tissue/organ perfusion:
a. MAP= systolic BP + 2 (diastolic BP)
3
*should exceed 70-80 mmHg
Stages of Shock
1. Compensatory Stage
>BP is maintained within normal limits due to the effect of normally functioning
regulatory mechanisms
S/Sx:
*metabolic acidosis
*mental status change
*tachypnea

Medical Management:
a. identify the cause of shock
b. correction of shock
c. support of the regulatory mechanisms

Nursing Management:
a. monitoring tissue perfusion
*LOC
*urine output
*V/S
*skin
*laboratory values
b. reducing anxiety
c. promoting safety

2. Progressive Stage
-exhaustion of the compensatory mechanisms
*myocardial depression
*increased capillary permeability

Assessment and Diagnostic Findings:

a. respiratory effects
hypoxemia and hypercarbia
intense inflammatory response
decreased surfactant production
acute respiratory distress syndrome
(acute lung injury, shock lung, non cardiogenic pulmonary edema)
b. cardiovascular effects
dysrhythmias
myocardial infarction
cardiac depression
c. neurologic effects
decreased cerebral perfusion
*mental status change
*behavioral change
*pupillary dilation
d. renal effects
MAP<80mmHg
acute renal failure
e. hepatic effects
decreased blood flow
Less ability to perform hepatic functions
f. gastrointestinal effects
decreased blood flow
*PUD
*bloody diarrhea
*sepsis
g. hematologic
DIC
Shock

Medical Management:
a. depends on the type of shock
b. depends on the decompensation of the organ systems

Management Common To All Types Of Shock

a. optimize intravascular volume
b. supporting the pumping action of the heart
c. improving the competence of the vascular system
Nursing Management:
a. preventing complications
b. promoting rest and comfort
c. supporting family members

3. Irreversible Stage
-severe organ damage
-can no longer respond to treatment
-survival is less likely
Medical Management:
a. same with the progressive stage

Nursing Management:
a. same with progressive shock
b. moral support to the family
c. ethical issues (living will)

Finding

Compensatory

Progressive

Irreversible

BP

normal

Systolic <80 -90mmHg

HR

>100bpm

>150bpm

Mechanical or
support
erratic, asystole

Respiration

>20 breaths/ min

Rapid, shallow crackles

Intubation

Skin
Urine Output

cold, clammy
decreased

Mottled, petechiae
0.5ml/kg/hr

Jaundice
anuria, needs dialysis

Mentation

confusion

Lethargy

Coma

A/B Balance

Resp Alkalosis

Met Acidosis

Profound Acidosis

HYPOVOLEMIC SHOCK
-most common type of shock
-characterized by decreased intravascular volume of 15-25%
-predisposing factors:
External: Fluid Losses
Internal: Fluid Shifts
a. trauma
a. hemorrhage
b. surgery
b. burns
c. vomiting
c. ascites
d. diarrhea
d. peritonitis
e. diuresis
e. dehydration
f. diabetes insipidus
-medical management:
>goals:
a. restore intravascular volume
b. redistribute fluid volume
c. correct the underlying cause
*pharmacologic therapy
desmopressin anti-emetic
insulin
anti-diarrhea
-nursing management:
a. administering blood and fluids safely

pharma

CARDIOGENIC SHOCK
-due to cardiac failure
-either coronary and non coronary
Coronary Factors
Non Coronary Factors
a. myocardial infarction
a. cardiomyopathies
b. valvular damage
c. cardiac tamponade
d. dysrhythmias
-signs and symptoms:
a. anginal pain
b. hemodynamic instability
c. dysrhythmias
-medical management:
a. correction of underlying cause
b. initiation of first line treatment
*supplemental oxygen
*controlling chest pain*controlling HR
*selected fluid support
c. pharmacologic therapy
*dobutamine
*dopamine
*anti-arrhythmic meds
d. fluid therapy

*vasoactive medications
*mechanical cardiac support
*nitroglycerine
*vasoactive meds

-nursing management:
a. preventing cardiogenic shock
b. administering meds and IV fluids
c. maintaining mechanical devices
d. enhancing safety and comfort

CIRCULATORY SHOCK
Vasodilation
Maldistribution of blood volume
decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased tissue perfusion
A. Septic Shock
-risk factors:
a. immunosuppression
b. extremes of age
c. malnutrition
-medical management:
a. pharmacologic therapy
b. nutritional therapy

d. chronic illness
e. invasive procedures

-nursing management:
a. supportive to the medical management
B. Neurogenic Shock
-occurs due to the loss of sympathetic tone
-predisposing factors:
a. spinal cord injury
c. depressant meds
b. spinal anesthesia
d. hypoglycemia
-medical management:
a. restoring sympathetic tone
-nursing management:
a. elevate the head of the bed 30 degrees
(In spinal/epidural anesthesia)
b. immobilize the patient
(In spinal cord injury)
c. elastic compression stockings
d. feet elevation
e. heparin/low molecular weight heparin
f. pneumatic compression of the legs
g. passive ROM
C. Anaphylactic Shock
Antigen-antibody reaction brought about by severe allergic reaction
provokes mast cells to release chemical mediators like histamine and bradykinin
widespread vasodilatation and capillary permeability
-predisposing factors:
a. drug sensitivity
b. transfusion reaction

c. bee sting allergy

d. latex sensitivity

-medical management:
a. removal of the causative agent
b. restore vascular tone (epinephrine)
c. antihistamines and bronchodilators
-nursing management:
a. assess for previous hypersensitivity reactions
b. prevention of future exposure to antigens
c. identification of new antigens
d. patient education

RENAL DISEASES
Terms:
1. aldosterone
2. antidiuretic hormone
3. anuria
4. bacteriuria
5. clearance
6. dysuria
7. frequency
8. GFR

9. hematuria
10. nocturia
11. oliguria
12. proteinuria
13. pyuria
14. Valsalva Leak Point
Maneuver
15. vesicoureteral reflux

Test of Urine Specific Gravity:

1. Osmolality
2. Specific gravity
Kidneys
-retroperitoneal organs
-120 170g
-12cm long, 6cm wide and 2.5cm thick
-with 8 18 pyramids
-with 4 -13 minor calyces
-with 2 3 major calyces
-with protective structures:
a. Pararenal fat
b. Gerotas fascia
c. Perirenal fat
d. Renal capsule
Kidneys
-retroperitoneal organs
-120 170g
-12cm long, 6cm wide and 2.5cm thick
-with 8 18 pyramids
-with 4 -13 minor calyces
-with 2 3 major calyces
-with protective structures:
a. Pararenal fat
b. Gerotas fascia
c. Perirenal fat
d. Renal capsule
Nephron
-basic structural and functional unit of the kidney

3 Processes of Urine Formation

1. Glomerular Filtration
2. Tubular Reabsorption
3. Tubular Secretion
Renal function begins to decrease at a rate of 1% each year at 30.

A. Acute Pyelonephritis
-bacterial infection of the renal pelvis, tubules and interstitial tissue
-an ascending infection
-predisposing factors:
a. vesico-ureteral reflux
b. urinary tract obstruction
-enlarged kidney
-with abscess on the renal capsule and at the cortico-medullary junction
-s/sx:
>fever and chills
>leucocytosis
>bacteriuria and
pyuria dysuria

>costo-vertebral angle
tenderness
>flank pain
>inc. urinary frequency

-dx:
>UTZ
>Nuclear scan
>CT scan
>IVP
>Urine Culture & Sensitivity Test
-Medical Management:
a. uncomplicated
-no dehydration, no nausea and vomiting, no
>2 weeks of oral antibiotics
Trimethoprim-Sulfamethoxazole
Ciprofloxacin
Gentamicin with or without Ampicillin
Third Generation Cephalosporins
>6 weeks of oral antibiotics if with relapse
*urine culture 2 weeks after antibiotic therapy
b. complicated
-pregnant patients
>hospitalization (antibiotics from IV to oral)

B. Chronic Pyelonephritis
-repeated acute pyelonephritis >> chronic pyelonephritis
-no s/sx unless theres an acute exacerbation
-kidneys scarred, contracted and non functional
-signs and symptoms:
fatigue
headache
anorexia

polyuria
excessive thirst
weight loss

-diagnosis:
creatinine and BUN clearance
creatinine levels
intravenous pyelography

sepsis

-complications:
a. ESRD
b. hypertension
c. formation of renal stones
-may be due to the presence of urea splitting microorganisms
-medical management:
a. urine culture and sensitivity guided antibiotic therapy
Nitrofurantoin
TMP-SMZ
-nursing management:
a. monitoring
-I&O
b. oral fluids (3-4L/day)
c. symptomatic
-antipyretics
d. education
-advise bed rest
-prevention of UTI

C. Acute Glomerulonephritis
-primarily a disease of children older than 2 years old
-may affect any age
-causes:
>autoimmune
SLE
>streptococcal
Acute Post Streptococcal Glomerulonephritis
Acute Post Streptococcal Glomerulonephritis
-2 to 3 weeks after
>impetigo
>sorethroat
-signs and symptoms:
hematuria
hypertension
tea colored urine
headache, malaise, flank pain
proteinuria
(+) kidney punch
inc serum BUN and crea
congestion
anemia
confusion, somnolence
edema
and seizures
Group A Beta-Hemolytic Streptococcal Infection
Antigen-Antibody Reaction
Deposition in the Glomerulus
Increased Production of Epithelial Cells in the Glomerulus
WBC Infiltration
Thickening
Scarring

Decreased GFR
-diagnosis:
a. kidney biopsy
b. electron microscopy
c. immunoflourescence analysis
d. Anti-Streptolysin O Titer
Anti-DNAse B Titer
e. Serum Complement Determination
-decreased
-will normalize in 2 8 weeks
IgA Nephropathy
-most common type of primary glomerulonephritis
-Inc IgA; with normal serum complement
-complications:
a. Hypertensive Encephalopathy
b. Heart Failure
c. Pulmonary Edema
Rapidly Progressive Glomerulonephritis
-patient deteriorates in weeks to months
-course is more severe and more rapid
Management to Glomerulonephritis
Goals:
1. Treat symptoms
2. Preserve renal function
3. Treat complications
a. antibiotics
b. steroids
c. cytotoxic agents

d. protein restriction
e. sodium restriction
f. diuretics
g. dialysis

D. Chronic Glomerulonephritis
-components:
repeated acute glomerulonephritis
Hypertensive nephrosclerosis
Hyperlipidemia
Chronic tubulo-interstitial injury
Hemodynamically mediated glomerular sclerosis
-contraction of the kidneys to 1/5 of its original size
-deformed kidneys
-may result to ESRD
-signs and symptoms:
may be asymptomatic
Inc BUN and Crea
retinal hemorrhages
papilledema
weight loss
weakness and irritability

hypertension
bipedal edema

nocturia
GIT disturbances
anemia
heart failure
peripheral neuropathy, decreased DTR
pulsus paradosus
-diagnosis:
1. Urinalysis - fixed sp. Gravity at 1.010
proteinuria; urinary casts
2. Serum chemistry
-hyperkalemia
-hypoalbuminemia
-hyperphosphatemia -hypocalcemia
-hypermagnesemia
3. CBC
-anemia
4. Chest X-Ray
-cardiomegaly
-pulmonary edema
5. ECG
-left ventricular hypertrophy
-management:
1. treatment of hypertension
2. weight monitoring
3. give proteins of high biologic value
4. adequate calories
5. dialysis
-nursing management:
1. monitoring

E. Nephrotic Syndrome
-components:
proteinuria
hypoalbuminemia

hyperlipidemia

-causes:
a. chronic glomerulonephritis
b. diabetes mellitus
c. amyloidosis
d. SLE
e. multiple myeloma
f. renal vein thrombosis
-signs and symptoms:
edema (soft and pitting)
-eyes, dependent area and abdomen
malaise
irritability
headache
fatigue

-diagnosis:
1. Urinalysis
-proteinuria (3-3.5g/day)
-Inc WBC
2. Protein Electrophoresis
Immunoelectrophoresis
3. Biopsy
4. AntiC1q antibodies (SLE)
-complications:
a. infection
d. acute RF
b. thromboembolism e. pulmonary emboli
c. accelerated atherosclerosis
-management:
1. diuretics
2. ACE inhibitors
3. immunosuppressants
4. steroids
5. hypolipidemic agents
6. sodium restriction
7. CHON intake of 0.8g/kg/day
low saturated fats

Urolithiasis
-stones or calculi in the urinary tract
-supersaturation of substances such as calcium oxalate, calcium phosphate and uric
acid
-signs and symptoms:
>depends on:
*the site of obstruction
*edema
*infection
-assessment and diagnosis
>IVP, Intravenous Urography
>Retrograde Pyelography
>UTZ
>serum chemistries and 24 urine tests

-causes of hypercalcemia and hypercalciuria:

a. hyperparathyroidism
b. renal tubular acidosis
c. cancers
d. granulomatous disease
e. excessive intake of Vitamin D
f. excessive intake of milk and alkali
g. myeloproliferative disease
-substances other than calcium that may precipitate and form stones
a. uric acid
-5%-10% of renal stones
-gout, myeloproliferative disorders
b. struvite
-15% of renal stones
-in persistently alkaline and ammonia rich urine
(caused by urease-splitting bacteria)
-in neurogenic bladder, foreign bodies and recurrent UTI
c. cystine
-1%-2% of renal stones
-hereditary defect in the renal absorption
-medicines that increases the risk of urolithiasis
a. acetazolamide
d. laxatives
b. Vitamin D
e. high doses of aspirin
c. antacids
-management:
a. eradicate the stone
b. determine the stone type
c. prevent nephron destruction
d. control infection
e. relieve any obstruction
>Opioid Analgesics
NSAIDs
>Hot Baths and Moist Heat to the flank
>Advise to increase oral fluid intake
(urine output of >2L/day is advisable)

area

-specific management:
1. Calcium stones
-restrict proteins and sodium in the diet
-acidify the urine using Ammonium chloride or Acetohydroxamic Acid
-Cellulose sodium phosphate(binds calcium from food)
-thiazide diuretics (if caused by inc PTH)
2. Uric Acid Stones
-low purine diet (shellfish, mushrooms, asparagus, organ meats)
-Allopurinol
-alkalinize the urine

3. Cystine
-low protein diet
-penicillamine (to decrease excretion through the urine)
4. Oxalate
-dilute the urine
-limit oxalate containing foods
(spinach, strawberries, rhubarb, tea, peanuts and wheat bran)
-surgical management:
a. Ureteroscopy
b. Extracorporeal Shock Wave Lithotripsy
c. Percutaneous Nephrostomy or Nephrolithotomy

Acute Renal Failure

-sudden and almost complete loss of renal function
-signs and symptoms:
*oliguria
*normal urine output
*anuria
*rising serum creatinine and BUN
Categories of ARF
1. Prerenal
-shock
2. Intrarenal
-the result of actual parenchymal damage
-use of nephrotoxic drugs (NSAIDs and ACE inh)
3. Postrenal
-the result of an obstruction in the distal urinary tract
Four Clinical Phases of ARF
1. Initiation
-begins with the initial insult and ends when oliguria develops
2. Oliguria
-rise in the serum of waste products of metabolism
-rise in serum potassium and magnesium
3. Diuresis
-with gradually increasing urine output
-renal function may still be markedly abnormal
4. Recovery Period
-improvement of renal function
-may take 3-12 months
-with normal laboratory values
-with permanent 1-3% reduction in GFR

Characteristics

Prerenal

Intrarenal

Postrenal

Etiology

hypoperfusion

parenchymal
damage

obstruction

BUN value

increased

increased

Increased

Creatinine value

increased

increased

Increased

Urine output

decreased

varies, often
decreased

varies, may be
decreased or anuria

Urine sodium

Decreased,
<20mEq/L

Increased,
>40mEq/L

Varies, often
<20mEq/L

Urinary Sediment

Normal, few hyaline

casts

Abnormal casts

Usually normal

Urine osmolality

Increased to
500mOms

Abnormal casts
and debris

Usually normal

Urine specific gravity

Increased

Low normal, 1.010

Varies

-associated problems:
*metabolic acidosis
*hyperphophatemia and hypocalcemia
*anemia
-prevention:
*prevention of exposure to nephrotoxic drugs
-aminoglycosides, cyclosporine,
amphotericinB
*serum BUN and creatinine monitoring
-management:
a. restore chemical balance and prevent complications
b. identification and treatment of the underlying cause
c. maintain fluid balance
-BP, CVP, serum and urine elect., fluid loses
d. monitoring for over hydration
-dyspnea, crackles, distended neck veins
-Furosemide, Ethacrynic Acid
e. dialysis
-to prevent serious complications
*hyperkalemia
*severe metabolic acidosis
*pericarditis
*pulmonary edema
f. pharmacologic
-cation exchange resin
(sodium polystyrene sulfonate-kayexalate)
-retention enema
-diuretic therapy
-low dopamine dose (1-3g/kg)
-phosphate binding agents (AlOH)

g. nutritional therapy
-give additional proteins (1g/kg/day during the oliguric phase)
-high potassium and phosphate foods are restricted (banana, citrus and coffee)
-potassium restricted to 20-40mEq/day
-sodium restricted to 2g/day
-may require parenteral nutrition
-nursing management:
a. monitoring fluid and electrolyte balance
b. reducing metabolic rate
-bed rest, prevention of fever and infection
c. promoting pulmonary function
-assistance in changing positions
-advise to cough and deep breath
d. preventing infection
-asepsis
-avoid inserting an indwelling urinary catheter
e. providing skin care
f. providing support

Chronic Renal Failure

-is a progressive irreversible deterioration in renal function
-with uremia or azotemia (severity of buildup will be proportional to the severity of s/sx)
-prognosis will be determined by the presence or absence of hypertension and
proteinuria
-causes:
*diabetes mellitus- most common
*hypertension
*chronic glomerulonephritis
*obstruction of the urinary tract
*polycystic kidney disease
*infections
*nephrotoxic medications
- stages:
Stage 1
-Reduced Renal Reserve
-40%-75% loss of nephron function
-usually asymptomatic
Stage 2
-Renal Insufficiency
-75%-90% loss of nephron function
-increase in serum BUN and creatinine
-inability to concentrate urine
-anemia may develop
-with polyuria and nocturia

Stage 3
-End Stage Renal Disease
-<10% of nephron function remaining
-regulatory, excretory and hormonal functions are lost
-requires dialysis
-signs and symptoms:
Cardiovascular
*hypertension *pulmonary edema
*heart failure
*pericarditis
dermatologic
*pruritus
*uremic frost (deposit of urea crystals)
GI and Neurologic s&sx
-assessment and diagnosis
a. glomerular filtration rate
creatinine clearance
b. serum electrolytes
c. ABG
d. CBC
-complications
a. Hyperkalemia
b. Pericarditis, Pleural Effusion and Cardiac Tamponade
c. Hypertension
d. Anemia
e. Bone Disease
-medical management:
a. maintain kidney function and homeostasis
b. treat the underlying cause and contributory factors
>medications
>dialysis
>diet therapy
1. Pharmacologic Therapy
a. antihypertensives
> includes intravascular volume control
*fluid restriction
*sodium restriction
b. sodium bicarbonate
c. erythropoietin
>will achieve a Hct of 33%-38%
>IV or SC 3x a week
>takes 2-6 weeks to increase Hct
>A/R:
*hypertension
*increased clotting of vascular access sites
*seizures
*depletion of body iron stores
d. iron supplementation

e. antiseizure agents
>Diazepam
>Phenytoin
f. antacids
>aluminum based antacids
neurologic symptoms
osteomalacia
>calcium carbonate
2. Nutritional Therapy
-regulation of protein intake
-regulation of fluid intake
(500-600ml more than the previous days 24 hour UO)
-regulation of sodium intake
-regulation of potassium
-adequate calories and vitamins
3. Dialysis
-to prevent hyperkalemia
-nursing management:
a. avoid the complications of reduced renal function
b. assess fluid status
c. identify potential sources of the imbalance
d. implement a dietary program
e. encourage self-care and independence