Acute Biologic Crisis

Historical Theories
Claude Bernard:
19thcentury French
physiologist
There must be a
consistency or fixity of the
internal milieu

Walter Canon:
Used the term
homeostasis

Rene Jules Dubos (1965)

Homeostasis and adaptation
Acceptable ranges of
response to stimuli existed
and that this responses
varied for different individual
Stress and Adaptation
Stress is a state produced by a change in the
environment that is perceived as challenging,
threatening or damaging to the person s
dynamic balance or equilibrium.
Adaptation adjustment to the changes sothat
the person is again in equilibrium andhas that
energy and ability to meet newdemands.
 Coping a compensatory
process with physiologic
and psychological
components.
Stressors
Definition:
Internal or external event or situation that creates
the potential for physiologic, emotional, cognitive or
behavioural changes in an individual.

Types:
Physical stressors
Physiologic
Psychosocial
Classification:
Day to day frustrations or hassles:
Includes such common occurrences like traffic jam,
having an argument with a spouse.

Major complex occurrences involving large groups or

even entire nations:
Includes events in history and war.
 Stressors that occur less
frequently and involve
fewer people
Life events such as deaths,
birth, marriages, divorce
and retirement.
FACTORS INFLUENCING THE MANIFESTATIONS
OF STRESS:
Nature of the stressor
Perception of the stressor
Number of simultaneous
stressors
Duration of exposure to
the stressor

Experiences w/ a
comparable stressors
Age
Support people

F:\pics\is_ani_e0.gif
PERSONALITY TYPE:
Type A
Impatience, competitiveness, aggressiveness, insecurity, a sense
of urgency, inability to relax

Type B
More relaxed & unhurried approach to life, enables to enjoy
work & play

Type C
Coping personality challenge, commitment, control

baby
Physiologic Response to Stress:
The General Adaptation
Syndrome (Selye, 1963)
first described a syndrome
consisting of enlargement
of the adrenal cortex;
shrinking of the thymus,
spleen, lymph nodes and
other lymphatic structures.
And the appearance of
deep, bleeding ulcer in the
stomach and duodenum.
Phases:
Alarm stage (AS)-
fight or flight reaction
-levels of resistance are
decrease
-awareness of presence of
threat or danger
-psychological, emotional
and physical response occur
-instantaneous, short term
and life preserving.
Resistance stage(RS)
adaptation
-level of resistance are
increase
-the person moves back
to homeostasis/
resources are mobilized
-the body fights back in
response to alarm
-able to combat effects
of stressors
Exhaustion stage (ES)
prolonged/ severe
exposure to stress
-the body is unable to
adapt so tissues
surrender to stress, may
result to death unless
other adaptive
mechanisms will be
mobilized
PRICIPAL NEUROENDOCRINE PATHWAYS THAT MEDIATE THE
RESPONSE TO STRESS
STRESS
SYMPATHETIC NS
HYPOTHALAMUS
PITUITARY
ADRENAL CORTEX
ADRENAL MEDULLA
MINERALOCORTICOIDS(PROINFLAMMATORY)
Na+ RETENTIONCHON ANABOLISMNOREPINEPHRINEPERIPHERAL VASOCONSTRICTIONBLOOD TO KID
NEYRENINGLUCOCORTICOIDS(ANTIINFLAMMATORY)
CHON CATABOLISMGLUCOGENESIS
EPINEPHRINE-TACHYCARDIA
MYOCARDIAL CONTRACTILITY
BRONCHIAL DILATATION
BLOOD CLOTTING
METABOLISM
FAT MOBILIZATION
GAS
1.Alarm
2.Resistance
3.Exhaustion
Stressor
Alarm ReactionShock PhaseEpinephrine CortisoneCounter shock phase
Stage Resistance
Stage ExhaustionRest Death
Systemic Physiologic response to Stress
(Sympatho-Adreno-Medullary Responsesby: Walter Canon)
Stressor
a. physical injury
b. elevated body temperature
c. dehydration
/
HYPOTHALAMUS
/
________________________
/ /
SNS Adrenal Medulla
(norepinephrine) (epinephrine & norepinephrine)
/ /
_________________________
/
Results to different responses of body systems
 Brain: increased alertness;
restlessness
Eyes: dilated pupils; increased
visual perception
Mouth: decrease salivary
secretion,thirst and dryness
Heart: tachycardia, coronary
vasodilation; increased force of
cardiac contractility; increased
cardiac output
Lung: hyperventilation;
bronchodilation
Blood vessels: peripheral
vasoconstriction; increased BP
Skin: pallor, diaphoresis; cold
clammy skin

Liver: increased glycogenolysis and

gluconeogenesis; increased blood
glucose level
Muscles: increased glycogenolysis;
increased muscle tension
G.I.tract: decreased gastric
motility; decreased HCL secretion;
decreased peristalsis; constipation;
flatulence
Spleen: contraction; decreased
hemolysis
Pancreas: decreased secretion of
insulin and pancreatic enzymes
Urinary Bladder: relaxation of the
detrusor muscle
Local Adaptation Syndrome
a short process which takes
place with a specific
response.
a response to stress through
a particular body parts or
organ

ex: inflammation, infection,

diarrhea, backache,
headache etc.
Localized responses includes:

a. dolor(pain)
b. tumor(swelling)
c. rubor(redness)
d. calor(heat)
e. Loss of Function
Inflammatory Response:
Inflammants: Physical (thermal, radiation), mechanical, chemical, microbial and
electrical
/
tissue injury
/
1. Vascular response: transitory vasoconstriction
/
immediately followed by vasodilatation
(due to the release of histamine, bradykinin, and
prostaglandin E)
/
Increased capillary permeability
/
_____________________________________
/ /
Hyperemia: Fluid/ cellular exudates
redness (rubor) /
heat (calor) ______________________________
/ /
Edema (tumor) Exudates:
/ * serous / fibrinouspain (dolor) serosanguinous* compression of nerve endings
sanguineous / hemorrhagicby fluids purulent / pus-Injury to nerve endings mucoid
-Release of bradykinin/
Impaired function
Classification of Inflammation
According to the duration of the reaction

1. Acute-sudden onset and progresses quickly

to recovery
2. Chronic insidious onset and persist over a
period of months to years
According to the structure affected suffix itis is used for inflammation

According to the nature of the exudates

According to the causative agent this relates to

nature of inflammatory agent. The terms

traumatic, chemical, bacterial or allergic maybe
used as descriptive terms.
Health History
Goals:
Gain parents trust.
Elicit a meaningful health history
Maintain the parents and child s privacy.
ENA recommends
CIAMPEDS format:
C chief complaint
I Immunization
-Isolation
A Allergies
M -Medication
P Past health history
-Parent s impression of
the child s health
condition
E events surrounding
the illness or injury
D diet
-diapers
S symptoms associated
with the illness or injury
C
Chief Complaint
Reason for the Child s Visit
I
Immunizations
Isolation
Evaluation the child s current
immunization status
Evaluation of the child s exposure to
communicable diseases
Need for isolation of child upon arrival to
ED (chicken pox, meningitis, tuberculosis)

A
Allergies
Evaluation of child s previous allergic or
hypersensitivity reactions
M
Medications
Evaluation of prescription and over the
counter medication and supplements:
dose, time of last dose, duration of use.
P
Past Medical History
Parent s/Caregiver s
Impression of Child
Review of child s health status, prior
illnesses, prior hospitalizations, prior
surgeries, birth weight, date of last
menstrual period
Evaluation of caregiver s concerns and
observations of the child s condition
E
Events Surrounding Illness
Evaluation of the onset of the illness or
circumstances of the injury
Length of illness and any prior treatment
Mechanism of Injury
Injuries Suspected
Vital signs prior to hospital arrival
Treatment prior to hospital arrival

D
Diet
Diapers
Assessment of the child s recent oral intake
and any changes in eating pattern
Assessment of child s urine and stool
output

S
Symptoms Associated with the
illness or injury
Identification of symptoms and progression
of symptoms since the time of onset of the
illness or injury
Appearance (TICKLES)
T-one
I-nteractability
C-onsolability
L ook/gaze
S peech/cry
Tickles
Element
Explanation
Tone
Is she moving around or resisting examination vigorously and
spontaneously? Is there good muscle tone?
Interactability
How alert is she? How readily does a person, object, or sound
distract her
or draw her attention? Will she reach out, grasp and play with a
toy or new
object, like a penlight or tongue blade?
Consolability
Can she be consoled or comforted by the caregiver or by the
clinician?
Look/Gaze
Can she fix her gaze on the clinician s or caregiver s face or is
there a
nobody home, glassy-eyed stare?
Speech/Cry
Is her speech/cry strong and spontaneous? Or weak, muffled,
or hoarse?
Physical Assessment
Goals:
Minimize stress and anxiety associated with
the physical assessment.
Foster trust among child, parent and
emergency nurse.
Prepare the child as much as possible for the
physical assessment.
ENA recommends the A to
I approach to physical
examination:
A irway
B reathing
C irculation
D isability
E xposure and
environmental control
F ull set of vital sign
-amily presence
G ive comfort measures
H ead to toe assessment
I nspect posteriir surface
Airway
Observe for airway
patency
Listen for airway
obstructions (stridor)
Observe the child s
position for air entry
(tripod, neck extended,
lowered jaw

Observe for airway

obstruction
Note breathe odor
(ketones, alcohol)
Breathing
Observe the rate and pattern before the child
starts crying
Is rate too slow or too fast?
Look for retractions, nasal flaring, paradoxical
chest movement, grunting, and head bobbing.
Listen for adventitious breathe sounds.
Observe for depth of respirations
Circulation
Observe the color of the skin
Measure capillary refill.
Palpate the central and peripheral pulses for
strength and equality.
Palpate the skin with the back of the hand to
determine skin temperature.
Disability
Observe child s activity
level
Note LOC; observe the
child s ability to follow
directions
Observe the child s level
of consolability
Measure the pupillary
equality and response

Obtain GCS or AVPU

assessment:

A Alert
V response to verbal
stimuli
P response to painful
stimuli
U -unresponsive
Glasgow Coma Scale
Exposure and Environment Control
Remove the child s
clothing as needed to
continue the
assessment
Initiate measures to
maintain a
normothermic state or
to warm the child
Full Set of Vital Signs
AGE
RATE(BPM)
Newborn
35
1-11 mos.
30
2 yrs
25
4 yrs
23
6 yrs
21
8 yrs
20
10 yrs
19
12 yrs
19
14 yrs
18
16 yrs
17
18 yrs
16-18

AGE
TEMP (C)
3 mos
37.5
6 mos
37.5
1 yr
37.7
3 yrs
37.2
5 yrs
37.0
7 yrs
36.8
9 yrs
36.7
11 yrs
36.7
13 yrs
36.6

Wong s Essentials of Pediatric Nursing, 2005

Full Set of Vital Signs
AGE
RESTING(Awake)
RESTING
(Sleeping)
EXERCISE(Fever)
NB
100-180
80-160
Upto 220
1wk-
3mos
100-220
80-200
Up to 220
3mos-
2yrs
80-150
70-120
Up to 200
2yrs-
10yrs
70-100
60-90
Up to 200
10yrs-
adult
55-90
50-90
Up to 200

Wong s Essentials of Pediatric Nursing, 2005

Family Presence
Assess needs of family,
taking into
consideration cultural
variables
Support family s
involvement in child s
care
Assign a healthcare
professional to provide
explanations to the
family

Assign a staff member

to provide support
Give Comfort Measures
Initiate comfort
measures based on the
chief complaint
Evaluate presence and
level of pain
Stabilize suspected
fractures
Head to Toe
Techniques to Assess Appearance
observing from a distance, allowing the child
to remain in the caregiver's lap or arms, using
distractions such as bright lights or toys to
gauge responsiveness, and kneeling down to
be on eye level with the child.
Significance
·RBC-Decreases in RF, infective carditis, anemia
Increasesin heart diseases characterized by inadequate
oxygenation such as CHD, Polycythemia
·WBC-Increasesin infectious & inflammatory diseases of the
heart as well as MI
·Hct-Increases in Hypovolemia & excessive diuresisDecreases in anemia
·Hgb-Decreasesin various anemias Increases in Polycythemia, CHF
Can you still
remember them?
RBC: Male: 4.5 M to 5.5M
Female: 4.5M to
5.0M
WBC:5,000 to 10,000/ mm3
Platelets:200T to 400T/ mm3
Hgb:Male: 12 to 16 g/dl
Female: 14 to18 g/dl
Hct:Male: 40% to 54%
Female: 31% to 47%
hm00361_
3/12/201042
Normal Chest Xray
Chest X-ray/ CT ScanDone to
visualize the
structures of
the respiratory
systempict1
http://www.angelfire.com/ab/cardiosv/images/echo3.gif
Measures the electrical activities of the heart
Indicates changes in myocardial oxygenation
FIRST diagnostic test done when CVD is suspected.
Significance:
MI: Elevated ST segmentInverted T wavePathologic Q wave

C:\WINDOWS\Desktop\N103\ekgmove.gif
(Holter monitoring, Stress test/Treadmill)
3/12/201044
ABG Analysis Measures the
amount of oxygen
and carbon dioxide
in the blood, as well
as its acidity.

Arteri1
Use heparinized syringe
Radial artery common
site

Nursing Alert !
3/12/2010
45
Normal Chest Xray
Chest X-rayPractice the
client on how
to hold his
breath and to
do deep
breathingNursing Alert !
Respiratory Failure
TERMS
RESPIRATORY FAILURE
Inability of the respiratory apparatus to
maintain adequate oxygenation of the blood,
with or without CO2 retention.
RESPIRATORY INSUFFICIENCY
TWO situations:
1.. work of breathing but gas exchange is near
normal
2.Normal blood gas tensions cannot be sustained
.hypoxemia and acidosis! (2. to CO2
retention)
RESPIRATORY ARREST
Cessation of respiration

APNEA
Cessation of breathing for more than 20 sec or
less associated with hypoxemia or bradycardia
Signs and Symptoms
Cardinal Signs
Restlessness
Tachypnea
Tachycardia
Diaphoresis

Early but less obvious signs:

Mood changes
Headache
Altered depth pattern of
respiration
Hypertension
Exertionaldyspnea
Anorexia
Expiratory grunt

Signs of more severe

hypoxia:
Hypo/hypertension
Dimness of vision
Somnolence
Stupor
Coma
Dyspnea
Depressed respiration
Bradycardia
Cyanosis (peripheral or
central)
Therapeutic Management
Artificial Ventilation:
Manual self inflating ventilation bag with mask
and valve to prevent rebreathing. (TEMPORARY)
Mechanical Ventilation (PROLONGED
ASSISTANCE)
Either positive or negative pressure
Positive pressure: inflates the lungs by increasing
airway pressure above atmospheric pressure
Negative pressure: inflates the lungs by creating a
subatmosphericpressure around the chest wall while
airway pressure remains atmospheric
Nursing Considerations
Support of family
Keep them informed of the child s status
Help them cope with near-death experience or
actual death
During CPR, is it necessary for the family to be
inside the patient s room?
CPR General Notes
Cardiac Arrest in children is less often of cardiac
origin that from prolonged hypoxemia
Causes of CA: injuries, suffocation, smoke
inhalation, SIDS, or infection
Respiratory Arrest has been associated with
better survival that CA.
Complete apnea signals the nurse for rapid
vigorous action to prevent CA
Check emergency equipment at least once daily
CPR Procedure
Cardiopulmonary Resuscitation (CPR):
The victim should be placed on the back on a
firm, flat surface.
To open the airway, HTCL or jaw thrust maneuver
is applied.
Finger sweep any obstruction
To ventilate the lungs:
<1yr = the operators mouth is placed in such a way
that both the mouth and the nostrils are covered.
 Children > 1yr = ventilated through the mouth
while the nostrils are firmly pinched.
Apply 2 initial breaths, then the pulse is palpated
to determine heartbeat. (1stchoice carotid artery,
2ndchoice brachial)
Absence of pulse, perform chest compression with
fingers (for infant) is at a point on the lower
sternum (one fingerbreadth below the
intersection of the sternum and the nipple line).
 For 1-8 years old, compressions are applied to the
lower sternum 2 fingerbreadths above the sternal
notch
One-Rescuer CPR
ABC
OBJECTIVES
ACTIONS
CHILD(1-8 YR)
INFANT(<1 YR)
A.AIRWAY

1. Assessment.
Determine
unresponsiveness
Tap orgently shake shoulder.
Say are you OK? Speak loudly
2. Get help
Shout for help. If 2ndperson comes,
have him activate EMS
3. Positionthe
victim
Turnon back as a unit, supporting
head and neck if necessary (4-10 sec)
Open the airwayHeadtilt/child lift
ABC
OBJECTIVES
ACTIONS
CHILD (1-8 YR)
INFANT(< 1 YR)
B. BREATHING
5. Assessment.
Determine
breathlessness
Maintainopen airway. Place ear over mouth, observing
chest. Look, listen, feel for normal breathing (no more than
10 sec.)
6. Give 2
rescue breaths
Maintainopen airway
Pinch nose, seal mouthto mouth
Mouthto nose and
mouth
Give 2slow effective breaths. Observe chest rise. Allow
lung deflation between breaths
1 to 1 ½ sec each
7. Option for
obstructed
airway
Reposition victim s head. Try again to give rescue breaths
Activate EMS
Give 5 subdiaphragmaticabdominal thrusts (Heimlich
maneuver)
Give5 back blows
Give 5 chest thrusts
Tongue-jaw lift, but finger sweep only if you see a foreign
object
If unsuccessful, repeat above until successful
One-Rescuer CPR
ABC
OBJECTIVES
ACTIONS
CHILD (1-8 YR)
INFANT(< 1 YR)
C.CIRCULATION
8. Assessment:
determine
pulselessness
Feel for carotid
pulse with one
hand; maintain
head-tilt with
other hand(no
more than 10 sec)
Feel for brachial
pulse: keep head
tilt
ABC
OBJECTIVES
ACTIONS
CHILD (1-8 YR)
INFANT(< 1 YR)
CPR
Pulseabsent: begin
chest compres ns:
9. Landmark check
Use 2-3 fingers to locatelower margin
of rib cage. Follow rib margin to base of
sternum (xiphoidprocess)
Imagine a line drawn
between the nipples
10. Handposition
Place one hand above fingersof first
hand on lower half of the sternum
Place 2 fingers on
sternum 1 finger swidth
below line. Depress 1/2
1 in.
Use heel of one hand. Depress 1-1 ½ in.
11. Compres nrate
100per min
At least 100 per min
12. Compres nto
breaths
1 breath to every 5 compressions
13. No. of cycles
20 (approx.1 min)
14. Reassessment
Feel for carotidpulse
Feel for brachialpulse
If alone, activate EMS. If no pulse,resume CPR, starting with
compressions
Pulse present;not
breathing: begin
rescue breathing
1 breathevery 3 sec (20 per min)
Drugs for Pediatric CPR
DRUG
ACTION
NURSINGIMPLICATION
EPINEPHRINE
Adrenergic; acts on both .
and .receptor sites
Most useful drugin cardiac arrest;
disappears rapidly from the
bloodstream after injection; may be
given via ET
SODIUM
BICARBONATE
Alkanizer, buffers pH
Infuse slowlyand when ventilation is
adequate; flush with saline before
and after
ATROPINE
SULFATE
Anticholinergic-
parasymphatolytic; .CO,
HR by blocking vagalstimulation
Usedto treat bradycardia; always
provide ventilation and monitor
O2sat; produces pupillarydilation
CALCIUM
CHLORIDE 10%
Electrolytereplacement,
needed for normal cardiac
contractility
Used only for hypocalcemia, calciumblocker overdose, hyperkalemiaor
hypermagnesemia; administer very
slowly via central vein
Drugs for Pediatric CPR
DRUGACTION
NURSINGIMPLICATION
LIDOCAINE HCL
Antidysrhythmic
Used for ventriculararrhythmias
only
AMIODARONE
Antidysrhythmicagent;
inhibits adrenergic
stimulation, prolongs action
potential and refractory
period in myocardial tissues
First choice for shock-refractory
V.tach
ADENOSINE
Antidysrhythmic;for
supraventriculartachcardia
Givenby rapid push followed by
NSS flush
NALOXONE
Reversesrespiratory arrest
due to overdose of opiates
Evaluatelevel of pain
MAGNESIUM
Inhibitscalcium channel and
cause smooth muscle
relaxation
Given by rapid IV infusion;have Ca
gluconateIV available as antidote
CARE OF THE CLIENTS
IN
Shock Syndrome
a condition of profound hemodynamic and
metabolic disturbance due to inadequate
blood flow and oxygen delivery to the
capillaries and tissues of the body
a systemic condition in which the peripheral
blood flow is inadequate to provide sufficient
blood to the heart for normal function and
transport of oxygen to all organs and tissues
EXCEPT
Factors Affecting Maintenance of Tissue Perfusion:
Cardiac Output:
this depends on the ability of
the heart to pump
Circulating Volume:
there should be an adequate
amount of blood for the heart to
pump around the body
Systemic Vascular Resistance:
Blood vessels with good tone, able to
constrict and dilate to maintain normal
pressure
Autonomic Response:
The SNS promotes vasoconstriction
through secretion of norepinephrine
Hormones:
Catecholamines
Promote vasoconstriction and adequate
pump action of the heart

RAA
Promotes vasoconstriction and retention of
Na and water

ADH
Causes retention of water
Common Cause of Shock
Syndrome
Any factors that affect blood volume, blood
pressure or cardiac function such as;
Hemorrhage
Drug reaction
Trauma
Pulmonary embolism
MI
Dehydration
Heat stroke
Infection
2 Classification of Shock
Syndrome
Traditional
Cardiogenic
Neurogenic
Anaphylactic
Septic
Hypovolemic

Functional
Hypovolemic
Obstructive
Cardiogenic
Transport
Anaphylactic
Neurogenic
Septic
TYPES OF SHOCK
TYPE
CHARACTERISTICS
FREQUENTCAUSES
HYPOVOLEMIC
Reduction insize
of vascular
compartment
Falling BP
Poor capillary
refill
Low CVP

Blood loss(Hemorrhagic
shock) trauma, GIB, IC
hemorrhage
Plasma loss inc.capillarypermeability sepsis,
acidosis, hypoproteinemia,
burns, peritonitis
Extracellular fluid loss
vomiting, diarrhea,
glycosuricdiuresis,
sunstroke
TYPES OF SHOCK
TYPECHARACTERISTICS
FREQUENTCAUSES
DISTRIBUTIVE
Reduction in PVR
Profoundinadequate tissue
perfusion
Increase venous
capacity and
pooling
Acute reduction in
return of blood to
the heart
Diminished CO

Anaphylaxis(Anaphylactic
Shock)
Sepsis (Septic, Bacteremic,
EndotoxicShock)
Loss of neural control
(NeurogenicShock) spinal
cord injury
Myocardial depression and
peripheral dilation
anesthesia, barbiturates,
tranquilizers, opioids,
antiHPN, ganglionicblocking agents.
TYPES OF SHOCK
TYPECHARACTERISTICS
FREQUENTCAUSES
CARDIOGENIC
DecreasedCO

Post surgery forcongenital HD

Primary pump failure
myocarditis, myocardial
trauma, CHF
Dysrhthmias
supraV.Tach, AV block, V.
dysrhythmias
The Four Stages Of The Shock
Syndrome
INITIAL STAGE
Marked by decreased cardiac output and impaired
tissue perfusion

COMPENSATORY STAGE
Homeostatic mechanism in the body is initiated

PROGRESSIVE STAGE
cellular damage

REFRACTORY STAGE
condition is irreversible
CLINICAL MANIFESTATIONS
OF SHOCK
COMPENSATED

Apprehensiveness
Irritability
Unexplained tachycardia
Normal BP
Narrow pulse pressure
Thirst
Pallor
Diminished urine output
Reduced perfusion of
extremities

UNCOMPENSATED

Confusion and somnolence

Tachypnea
Moderate metabolic acidosis
Oliguria
Cool, pale extremities
Decreased skin turgor
Poor capillary filling

IRREVERSIBLE

Thready, weak pulse

Hypotension
Periodic breathing or apnea
Anuria
Stupor or coma
TRADITIONAL CLASSIFICATION OF SHOCK
DEFINITION
ETIOLOGY
MANAGEMENT
HYPOVOLEMIC SHOCK
Occur when there is a lack of
circulating fluid in the intravascular
space.
Most common type of shock
CAUSES
DHN
vomiting and diarrhea in case of AGE

Severe burn injuries

Vasodilation
due to neurogenic shock ( loss of sympathetic tone),
Anaphylactic shock ( release of histamine), Septic shock ( release
of endotoxin)

Other factor such as:

Nasogastric suctioning
Diuretic therapy
Diabetes insipidus
Trauma
Surgery
Hyperglycemic osmotic diuresis
HYPOVOLEMIC SHOCK
Pathophysiology:

AbsoluteHypovolemia
Relative
Hypovolemia
Third Spacing
Venous return to the heart
Cardiac OutputInadequate O2 supply to
Body tissues
Assessment with clinical manifestation
PR/HR -Tachycardia
BP -Pulse pressure narrows as the diastolic increases
RR -Tachypnea and increase in depth of respiration ( may gasps
for breath)
I & O -Decline in urine output
Skin pale, cool, delayed capillary refill
Jugular veins appear flat
Decreased cerebral perfusion ( lead to change in LOC):
Disorientation
Confused
Restless
Anxious
Irritable
Management of Hypovolemic
Shock
The nurse should:
Implement measures to minimize fluid loss
Fluid replacement cc/cc

Monitor V/S and CVP reading

Position the patient to modified T-burg position

( leg elevated , trunk flat, head & shoulder above

the chest)
Monitor RR -to determine fluid overload ( distress,
crackles & rhonchi, changes in the heart sounds &
HR)
Monitor lab results CBC (alteration in coagulation
process, WBC level for infection, Hgb and Hct level)
Mgnt. Cont ..
Observed for signs of infection chills & fever
Monitor mental status indicator of decreased
cerebral perfusion
Administer analgesics
Provide calm environment
Provide position for comfort
Limit activity to decrease demand and
conserve O2
Educate patient and family for measures to
reduce anxiety
PARAMETERS FOR ASSESSING STATUS OF
CLIENT IN SHOCK:
Hemodynamic Monitoring
blood pressure
pulse
central nervous system
cardiac output
ECG

Respiratory Monitoring
rate, depth, rhythm, effort
breath sounds
blood gases (pH, pO2, pCO2)

Fluids and Electrolytes Monitoring

serum electrolytes
intake and output
weight
BUN, Creatinine
Urine specific gravity
Neurologic Monitoring
alertness
orientation
Confusion

Hematologic Monitoring
CBC
PT,PTT, clotting time

Other monitoring
bowel sounds
skin temperature
COLLABORATIVE MANAGEMENT:
Promoting Fluid balance and Cardiac Output:
whole blood and blood products
colloid solutions (albumin, plasma protein factor)
Plasma expanders (dextran, mannitol)
Crystalloid Solutions(hypotonic: 45%NSS, 5%
D5W)
Crystalloid solutions(Isotonic: NSS, LR,RS)

Assisting with Cardiac Support:

Intraaortic Balloon Pump
Medical anti-shock trouser(MAST)
Modified T-burg position
 Assisting with Respiratory Support:
oxygen therapy
mechanical ventilator(Positive End-Expiratory pressure
for ARDS)
DBE, Coughing exercise
Suction as necessary

Assisting with Renal support:

Monitor urine hourly, BUN, Creatinine
Diuretics administration such as furosemide,mannitol

Assisting with G.I. Support (prevent stress ulcer)

NGT to suction
Histamine blockers
Antacids
 Promoting Safety
soft restraints if restless and
attempts to remove life-saving
equipment
practice strict asepsis
prevent complication of immobility
protect from chills which causes
sludging of blood in microcirculation
Help Stamp Out Shock
Solutions
Hemodynamic changes
CVP,BP

Oxygen to saturate those RBC

Checking the skin is often cold & clammy
Kick em up
Elevate leg. Don t put head down

j0240719
DRUG THERAPY
IN
SHOCK:
j0216724
Vasocontrictors
Norepinephrine (Levarterenol)
Metaraminol (Aramine)
Epinephrine
Dopamine
Dobutamine

Vasodilators
Nitroprusside (Nipride)
Nitroglycerine, Isosorbide
Phentolamine(Regitine)
Prasozin(Minipress)
Hydralazine(Apresoline)
Others
Na Bicarbonate to reverse acidosis
Antibiotics to control sepsis
Heparin to treat DIC
Steroids to produce anti inflammatory effect
Cimetidine to decrease stress ulcer
Glucose 50% to meet increased demand for energy
during shock
Naloxone(Narcan) to block endorphin-mediated
hypotension
Diphenhydramine for anaphylaxis
Narcotics to relieve pain
Cardiotonic Medications
to treat dysrhythmias
lidocaine
bretylium
Quinidine
procainamide

To treat Bradycardia
isoproterenol
atropine sulfate
ORGAN DAMAGE IN PROGRESSIVE SHOCK:
Kidneys> renal failure
Brain> altered LOC
Heart> dysrhythmias

>Cardiac arrest
Lungs> decrease surfactant production lead
to atelectasis

> respiratory acidosis

Gastrointestinal Tract
»decrease peristalsis
»septic shock due to lysis of colonic
microorganisms

Liverseptic shock due to destruction of

Kupffer cells
Blood> DIC

> Hemorrhage
Emergency Treatment of SHOCK
Ventilation
Establish airway be prepared for intubation
Administer O2, usually 100% by mask

Fluid administration
Obtain vascular access
Restore fluid volume as ordered

Cardiovascular support
Administer vasopressors, esp. epinephrine
May repeat every 3-5 minsin cardiac arrest
Emergency Treatment in SHOCK
General support
Continuous ECG monitoring
Monitor pulse oxymetry
Keep child warm and calm

In addition:
Septic Shock: administer broad-spectrum
antibiotics
Anaphylaxis: remove allergen, IM Epior
corticosteroids as ordered
poisoning
Most common frequently ingested poison:
Cosmetics and personal care products
Cleaning products
Plants
Foreign bodies
Hydrocarbons

> 90% of poisoning occurs at home

Poisoning
Emergency stabilization of the patient comes first.
Phases of Poisoning Management.
First, treat the patient, not the poison!!
ABC's of resuscitation then add D for:

Disability;
1. Perform a brief neurologic exam, establish the level of
consciousness (Glasgow Coma Scale), and determine
pupillary size and reactivity.
2. Anticipate drug therapy: oxygen, dextrose, and naloxone
as indicated.
3. Consider decontamination: ocular, dermal, GI, etc.
 Clinical evaluation:
A.Symptom complexes (toxidromes) may give clues to an
unknown poisoning.
B.History -focused and complete.
-Substance or substances -including ingredients. Meds in house.
-Maximum possible amount
-Estimate ingestion
-Estimated time of ingestion
-Symptoms
-Home treatment
-Significant Past Medical History
 PE
Vital signs
level of consciousness
(GCS)
motor function
Eyes (pupils, EOM)
mouth (lesions, odors)

heart (rate, rhythm)

Lungs (rate, pattern)
Skin
odors (breath, clothing)
Intervention:
Gastric emptying:
Syrup of Ipecac -usually used at home, rarely used
after presenting to medical facility.

Dose : < 1 year = 1 cc/kg

1 to 12 years = 15 ml
> 12 years = 30 ml
Follow with water or juice (induction of emesis will be
delayed if given with milk)
may repeat once if no emesis in 30 minutes.
Keep emesis for analysis.
 Contraindications:
lost gag reflex
decreased level of consciousness
seizures
ingestion of agent that rapidly depresses mental
status (cyclic antidepressants, hypnotics,
strychnine)
ingestion of caustic agent
< 6 months of age
 Gastric Lavage:
usually used for extremely toxic substances, in
cases of unknown ingestions or when loss of
consciousness is present.
Check lavage for pill fragments.
Contraindications:
alkalis, sharp objects, pills larger than lavage hose,
drug packets/vials, nontoxic ingestions.
 Activated Charcoal:
Almost irreversibly absorbs drugs and chemicals,
preventing absorption.
Consider for all significant toxic ingestions; poorly binds Fe
and Lithium, not to be used in caustic ingestions (mineral
acids or bases, solvents, hydrocarbons) because of poor
binding
Ideally, the dose of charcoal is given within 1-2 hours of
the ingestion. However, it may be given up to 12-24 hours
after the ingestion in the case of anticholinergic, narcotic,
or sustained release/enteric coated preparations
ingestions.
 ADVERSE EFFECTS: Nausea, vomiting and
constipation are the most common.
Pulmonary aspiration of charcoal is the most
serious complication (usually seen with
hydrocarbon ingestions).

REMEMBER: Airway protection before

administration!!!!!
Near Drowning
 Drowning ranks 2ndas a cause of accidental
death in children.
Accidental drowning occurs 5x in males than
females.
Pathophysiology
Pulmonary changes that occur in drowning is
directly related to the length of submersion,
the physiologic response of the victim and the
development and degree of immersion
hypothermia.
Cerebral recovery depends on the
effectiveness of initial resuscitation and
subsequent critical care measure to support
cerebral salvage.
 Problems:
Hypoxia: primary problem because it results in global
cell damage. Neurons, especially cerebral cell, sustain
irreversible damage after 4-6 minutes of submersion.
Heart and lungs can survive up to 30 mins.
Aspiration: results in pulmonary edema, atelectasis,
airway spasm and pneumonitis.
Hypothermia: may make resumption or maintenance
of cardiac function possible if body temp is less than
30C.
Therapeutic Management
Resuscitative measures should begin at the
scene.
Priority is to restore delivery of oxygen to the
cells.
Aspiration pneumonia is a frequent
complication that occurs 48-72 hours after the
episode.
Renal failure
Acute Renal Failure
Sudden interruption of kidney function resulting
from obstruction, reduced circulation, or disease of
the renal tissue
Results in retention of toxins, fluids, and end
products of metabolism
Usually reversible with medical treatment
May progress to end stage renal disease, uremic
syndrome, and death without treatment
Acute Renal Failure
Persons at Risks
Major surgery
Major trauma
Receiving nephrotoxic medications
Elderly
Acute Renal Failure
Causes
Prerenal
Hypovolemia, shock, blood loss, embolism, pooling of fluid d/t
ascites or burns, cardiovascular disorders, sepsis

Intrarenal
Nephrotoxic agents, infections, ischemia and blockages, polycystic
kidney disease

Postrenal
Stones, blood clots, BPH, urethral edema from invasive procedures
Acute Renal Failure
Stages
Onset 1-3 days with ^ BUN and creatinine and possible
decreased UOP
Oliguric UOP < 400/d, ^BUN,Crest, Phos, K, may last up
to 14 d
Diuretic UOP ^ to as much as 4000 mL/d but no waste
products, at end of this stage may begin to see
improvement
Recovery things go back to normal or may remain
insufficient and become chronic
Acute Renal Failure
Subjective symptoms
Nausea
Loss of appetite
Headache
Lethargy
Tingling in extremities
Acute Renal Failure
Objective symptoms
Oliguric phase
vomiting
disorientation,
edema,
^K+
decrease Na
^ BUN and creatinine
Acidosis
uremic breath

CHF and pulmonary

edema
hypertension caused by
hypovolemia, anorexia
sudden drop in UOP
convulsions, coma
changes in bowels
Acute Renal Failure
Objective systoms
Diuretic phase
Increased UOP
Gradual decline in BUN and creatinine
Hypokalemia
Hyponaturmia
Tachycardia
Improved LOC
Acute Renal Failure
Diagnostic tests
H&P
BUN, creatinine, sodium, potassium. pH, bicarb. Hgb and
Hct
Urine studies
US of kidneys
KUB
ABD and renal CT/MRI
Retrograde pyloegram
Acute Renal Failure
Medical treatment
Fluid and dietary restrictions
Maintain E-lytes
D/C or change cause
May need dialysis to jump start renal function
May need to stimulate production of urine with IV
fluids, Dopomine, diuretics, etc.
Acute Renal Failure
Medical treatment
Hemodialysis
Subclavian approach
Femoral approach

Peritoneal dialysis
Continous renal replacement therapy (CRRT)
Can be done continuously
Does not require dialysate
Acute Renal Failure
Nursing interventions
Monitor I/O, including all
body fluids
Monitor lab results
Watch hyperkalemia
symptoms: malaise, anorexia,
parenthesia, or muscle
weakness, EKG changes
watch for hyperglycemia or
hypoglycemia if receiving TPN
or insulin infusions

Maintain nutrition
Safety measures
Mouth care
Daily weights
Assess for signs of heart
failure
GCS and Denny Brown
Skin integrity problems
Chronic Renal Failure
Results form gradual, progressive loss of renal
function
Occasionally results from rapid progression of acute
renal failure
Symptoms occur when 75% of function is lost but
considered cohrnic if 90-95% loss of function
Dialysis is necessary D/T accumulation or uremic
toxins, which produce changes in major organs
Chronic Renal Failure
Subjective symptoms are relatively same as acute
Objective symptoms
Renal
Hyponaturmia
Dry mouth
Poor skin turgor
Confusion, salt overload, accumulation of K with muscle weakness
Fluid overload and metabolic acidosis
Proteinuria, glycosuria
Urine = RBC s, WBC s, and casts
Chronic Renal Failure
Objective symptoms
Cardiovascular
Hypertension
Arrythmias
Pericardial effusion
CHF
Peripheral edema

Neurological
Burning, pain, and itching,
parestnesia
Motor nerve dysfunction
Muscle cramping
Shortened memory span
Apathy
Drowsy, confused, seizures,
coma, EEG changes
Chronic Renal Failure
Objective symptoms
GI
Stomatitis
Ulcers
Pancreatitis
Uremic fetor
Vomiting
consitpation

Respiratory
^ chance of infection
Pulmonary edema
Pleural friction rub and
effusion
Dyspnea
Kussmaul s respirations
from acidosis
Chronic Renal Failure
Objective symptoms
Endocrine
Stunted growth in children
Amenorrhea
Male impotence
^ aldosterone secretion
Impaired glucose levels R/T
impaired CHO metabolism
Thyroid and parathyroid
abnormalities

Hemopoietic
Anemia
Decrease in RBC survival
time
Blood loss from dialysis and
GI bleed
Platelet deficits
Bleeding and clotting
disorders purpura and
hemorrhage from body
orifices , ecchymoses
Chronic Renal Failure
Objective symptoms
Skeletal
Muscle and bone pain
Bone demineralization
Pathological fractures
Blood vessel calcifications
in myocardium, joints,
eyes, and brain

Skin
Yellow-bronze skin with
pallor
Puritus
Purpura
Uremic frost
Thin, brittle nails
Dry, brittle hair, and may
have color changes and
alopecia
Chronic Renal Failure
Lab findings
BUN indicator of glomerular filtration rate and is affected
by the breakdown of protein. Normal is 10-20mg/dL.
When reaches 70 = dialysis
Serum creatinine waste product of skeletal muscle
breakdown and is a better indicator of kidney function.
Normal is 0.5-1.5 mg/dL. When reaches 10 x normal, it is
time for dialysis
Creatinine clearance is best determent of kidney function.
Must be a 12-24 hour urine collection. Normal is > 100
ml/min
Chronic Renal Failure
K+ -
The kidneys are means which K+ is excreted. Normal is 3.5-
5.0 ,mEq/L. maintains muscle contraction and is essential
for cardiac function.
Both elevated and decreased can cause problems with
cardiac rhythm
Hyperkalemia is treated with IV glucose and Na Bicarb
which pushes K+ back into the cell
Kayexalate is also used
Chronic Renal Failure
Ca
With disease in the kidney, the enzyme for utilization of Vit
D is absent
Ca absorption depends upon Vit D
Body moves Ca out of the bone to compensate and with
that Ca comes phosphate bound to it.
Normal Ca level is 4.5-5.5 mEq/L
Hypocalcemia = tetany
Treat with calcium with Vit D and phosphate
Avoid antacids with magnesium
Chronic Renal Failure
Other abnormal findings
Metabolic acidosis
Fluid imbalance
Insulin resistance
Anemia
Immunoligical problems
Chronic Renal Failure
Medical treatment
IV glucose and insulin
Na bicarb, Ca, Vit D, phosphate binders
Fluid restriction, diuretics
Iron supplements, blood, erythropoietin
High carbs, low protein
Dialysis -After all other methods have failed
Chronic Renal Failure
Hemodialysis
Vascular access
Temporary subclavian or femoral
Permanent shunt, in arm
Care post insertion

Can be done rapidly

Takes about 4 hours
Done 3 x a week
Chronic Renal Failure
Peritoneal dialysis
Semipermeable membrane
Catheter inserted through
abdominal wall into
peritoneal cavity
Cost less
Fewer restrictions
Can be done at home
Risk of peritonitis
3 phases inflow, dwell and
outflow

Automated peritoneal
dialysis
Done at home at night
Maybe 6-7 times /week

CAPD
Continous ambulatory
peritoneal dialysis
Done as outpatient
Usually 4 X/d
Chronic Renal Failure
Nursing care
Frequent monitoring
Hydration and output
Cardiovascular function
Respiratory status
E-lytes
Nutrition
Mental status
Emotional well being

Ensure proper
medication regimen
Skin care
Bleeding problems
Care of the shunt
Education to client and
family
Chronic Renal Failure
Nursing diagnosis
Excess fluid volume
Imbalanced nutrition
Ineffective coping
Risk for infection
Risk for injury
Chronic Renal Failure
Transplant
Must find donor
Waiting period long
Good survival rate 1 year 95-97%
Must take immunosuppressant s for life
Rejection
Watch for fever, elevated B/P, and pain over site of new
kidney
3815
Chronic Renal Failure
Post op care
ICU
I/O
B/P
Weight changes
Electrolytes
May have fluid volume deficit
High risk for infection
Transplant Meds
Patients have decreased resistance to infection
Corticosteroids anti-inflammarory
Deltosone
Medrol
Solu-Medrol

Cytotoxic inhibit T and B lymphocytes

Imuran
Cytoxan
Cellcept

T-cell depressors -Cyclosporin

BURNS
BURNS
Types
Thermal :flame, flash, scalding and contact
with hot objects
Smoke inhalation: causes respiratory
damage
Chemical:caused by tissue contact,
ingestion, inhalation of acids or alkalis
Electrical: produces direct damage to
nerves
Burn
Superficial partial thickness
(1st degree)
Involves epidermis

painful; with erythema,

blanching on pressure, no
vesicles
Caused by sunburn, splashes
of hot liquid
Rapid healing 3-5 days
Burn
Partial thickness ( 2ndegree)
Involves epidermis and
dermis
Skin appearing red to pale
ivory and moist.
Formation of wet, thin-walled
blisters immediately after
injury
Intact pain sensation
Heal in 21-28 days with
variable scaling
Second degree Burn
Full-thickness (3rd and 4th degree)
Involves all skin layers and nerve endings, may
involve muscles, tendons and bones;
Wound is dry, white, leathery, hard due to loss of
epidermal elasticity
Caused by flame, chemicals, scalding, electric
current
Painless to touch because of destruction of all
superficial nerve endings
Marked edema
Full-thickness (3rdand 4th degree)
Full-thickness (3rd and 4th degree)
Assessment
Extent of injury by Rule of Nines
Head and neck (9%)
Each arm (9%)
Each leg (18%)
Trunk (front 18%, back 18%)
Genitalia (1%)
Severity of Burn
Major: partial thickness greater than
25%, full thickness > or = 10%;
involves the eyes, ears, hands, face,
feet or perineum;
involves electrical or inhalational
injury; client is > 60 years old or
other injuries evident or with chronic
illness
Stages
Emergent phase
Remove person form source of burn: stop,
drop and roll; wash off chemicals with
copious amounts of water
Manage any problems in airway
Emergent phase
Wrap burned area in dry, clean sheet or
blanket to prevent further contamination of
wound and provide warmth
Assess how and when burn occurred
Transport to ER
Shock phase (first 24-48 hours)/Fluid
Accumulation Phase
Shift of fluid from intravascular to interstitial
phase
WOF: dehydration and shock (tachycardia,
oliguria)
Labs:.
hyperkalemia (released from damaged cell)
hyponatremia(trapped in the edema fluids),
elevated hematocrit, due to hemoconcentration
because liquid components of blood is lost in the IS
metabolic acidosis
Fluid remobilization or diuretic phase (2-5 days post-
burn)
Return of fluid into the intravascular space
WOF: elevated BP, increased urine output
Labs: hypokalemia, hyponatremia, metabolic
acidosis
Diuresis because of increase renal perfusion,
decrease Aldosterone and ADH
Convalescent (Rehabilitation) phase5thDay onwards
Starts when diuresis is completed and wound
healing begin
Dry, waxy-white appearance of full-thickness
burns changing to dark brown; wet, shiny and
serous exudates in partial thickness
Labs: hyponatremia, hypo Ca due to lost in
exudates and is utilized in granulation tissue
formation
Medical Management
Supportive therapy
Fluid management

Parkland Formula (4 ml(LR) X wt (kg) X % BSA

burned)
Fluid: Lactated Ringer s
Day 1: Half to be given on the first 8 hours, half to
be given on the next 16 hours
Day 2: Varies, colloid added
Catheterization : monitor urine output
Medical Management
Wound care
Hydrotherapy, debridement
Drug therapy
Topical antibiotics
Systemic antibiotics
Tetanus toxoid and tetanus
immunoglobulin
Analgesics( morphine SO4)
Surgery
Excision and grafting

C:\Pictures\disasater\brs_burns_epd_01.jpg
Nursing Management
Provide relief/control of pain
Administer IV morphine sulfate
Administer analgesics 30 minutes before
wound care
Position burned areas in proper
alignment

Monitor alteration in fluid and electrolyte

balance
Nursing Management
Assess for signs of fluid and electrolyte
imbalance
Administer IV fluids as ordered
Weigh daily
Nursing Management
Promote maximal nutritional status

Tube feedings/ TPN as necessary

Diet: High calorie, high protein, high
carbohydrate, vitamin/mineral supplements
Vit A for skin and mucuos integrity
Vit B for metabolism
Vit C for increase resistance to tissue infection
Avoid oral fluids for the 1st48 hours

> paralytic ileus

> gastric dilatation
> water intoxication
Nursing Management
Prevent wound infection

Hydrotherapy for no more than 30 minutes to

remove debri, improves circulation and relieves pain
Mafenide (Sulfamylon): monitor acid-base status
and renal function
Silver sulfadiazine: WOF hypersensitivity
Silver nitrate: leaves black stain on clothing, keep
dressings wet since dryness increases concentration
Gentamicin: monitor hearing and renal function
Nursing Management
Prevent GI complications

Assess for ileus, may insert NGT

Prevent Curling s ulcer: give antacids and H2
blockers
Provide client teaching and discharge planning

Care of healed burned wound

Exercises to prevent contractures
Methods of coping and resocialization
FLUID REPLACEMENT:
Evan s Formula:

> Colloid: 1ml x % Burns x KgBW

> Electrolyte: 1ml x %burns x KgBW
> Non-Electrolyte: 2000ml(d5W)
Brook s Formula:
> C: 0.5ml x %burnsx KgBW
>E: 1.5ml x % burns xKgBW
>N: 2000ml
Moore s Burn Budget:
> 75 ml plasma,75ml Elect/ 1%BSA, 2000D5
End of Life
Palliative care :
focuses on caring
interventions and
symptom management
rather than cure for
diseases that no longer
respond to treatment
A pain controlled or
symptom controlled
environment is
established
 Near death physiological manifestation:
Reduced metabolism
Cheyne stokes respiration
Decreased HR and BP
Decreased UO
Cosntipation, gas formation and abdominal
distention
Death rattle
Bodily Changes after Death:
Rigor mortis
limbs of the corpse to
become stiff

Algor mortis
reduction in body
temperature following
death
generally a steady decline
until matching ambient
temperature
2°Celsius during the first
hour and 1°Celsius per
hour until the body nears
ambient temperature

Livor mortis
settling of the blood in
the lower (dependent)
portion of the body
starts 20 minutes to 3
hours after death