Acute Biologic Crisis

Historical Theories
• Claude Bernard: • Rene Jules Dubos (1965)
– 19th century French – Homeostasis and adaptation
physiologist – Acceptable ranges of
– There must be a response to stimuli existed
consistency or fixity of the and that this responses
internal milieu varied for different individual
• Walter Canon:
– Used the term
homeostasis
 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 so that
the person is again in equilibrium and has that
energy and ability to meet new demands.
• 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 • Experiences w/ a
• Perception of the stressor comparable stressors
• Number of simultaneous • Age
stressors • Support people
• Duration of exposure to
the stressor
 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
 Physiologic Response to Stress:
The General Adaptation Phases:
Syndrome (Selye, 1963) – Alarm stage (AS)-
first described a syndrome
consisting of enlargement “ fight or flight reaction”
of the adrenal cortex; - levels of resistance are
shrinking of the thymus, decrease
spleen, lymph nodes and - awareness of presence of
other lymphatic structures. threat or danger
And the appearance of - psychological, emotional
deep, bleeding ulcer in the and physical response occur
stomach and duodenum. - instantaneous, short term
and life preserving.
Resistance stage (RS) Exhaustion stage (ES)
– adaptation – prolonged/ severe
- level of resistance are exposure to stress
increase - the body is unable to
- the person moves back adapt so tissues
to homeostasis/ surrender to stress, may
resources are mobilized result to death unless
- the body fights back in other adaptive
response to alarm mechanisms will be
- able to combat effects mobilized
of stressors
PRICIPAL NEUROENDOCRINE PATHWAYS THAT MEDIATE THE
RESPONSE TO STRESS

STRESS

SYMPATHETIC NS

HYPOTHALAMUS

PITUITARY

ADRENAL CORTEX ADRENAL MEDULLA

MINERALOCORTICOIDS NOREPINEPHRINE
(PROINFLAMMATORY) PERIPHERAL VASOCONSTRICTION
Na+ RETENTION BLOOD TO KIDNEY
CHON ANABOLISM RENIN

EPINEPHRINE-TACHYCARDIA
GLUCOCORTICOIDS
MYOCARDIAL CONTRACTILITY
(ANTIINFLAMMATORY)
BRONCHIAL DILATATION
CHON CATABOLISM
BLOOD CLOTTING
GLUCOGENESIS
METABOLISM
FAT MOBILIZATION

GAS

1. Alarm
2. Resistance
3. Exhaustion
 Stressor

Alarm Reaction

Shock Phase

Epinephrine Cortisone

Counter shock phase

Stage Resistance

Stage Exhaustion

Rest Death
 Systemic Physiologic response to Stress
(Sympatho-Adreno-Medullary Responses
by: 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 • Localized responses includes:
place with a specific a. dolor (pain)
response. b. tumor (swelling)
• a response to stress through c. rubor (redness)
a particular body parts or
organ d. calor (heat)
e. Loss of Function
ex: inflammation, infection,
diarrhea, backache,
headache etc.
 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 / fibrinous
pain (dolor) serosanguinous
* compression of nerve endings sanguineous / hemorrhagic
by 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 P – Past health history
CIAMPEDS format: - Parent’s impression of
C – chief complaint the child’s health
I – Immunization condition
- Isolation E – events surrounding
A – Allergies the illness or injury
M - Medication D – diet
- diapers
S – symptoms associated
with the illness or injury
C Chief Complaint Reason for the Child’s Visit
I Immunizations •Evaluation the child’s current
immunization status
Isolation •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 •Review of child’s health status, prior
illnesses, prior hospitalizations, prior
Parent’s/Caregiver’s surgeries, birth weight, date of last
Impression of Child 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 •Assessment of the child’s recent oral intake
and any changes in eating pattern
Diapers •Assessment of child’s urine and stool
output
S Symptoms Associated with the Identification of symptoms and progression
illness or injury 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
 Explanation
Element
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: F – ull set of vital sign
A – irway - amily presence
B – reathing G – ive comfort measures
C – irculation H – ead to toe assessment
D – isability I – nspect posteriir surface
E – xposure and
environmental control
 Airway
• Observe for airway • Observe for airway
patency obstruction
• Listen for airway • Note breathe odor
obstructions (stridor) (ketones, alcohol)
• Observe the child’s
position for air entry
(tripod, neck extended,
lowered jaw
 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 • Obtain GCS or AVPU
level assessment:
• Note LOC; observe the A – Alert
child’s ability to follow V – response to verbal
directions stimuli
• Observe the child’s level P – response to painful
of consolability stimuli
• Measure the pupillary U - unresponsive
equality and response
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 TEMP (C) AGE RATE (BPM)
3 mos 37.5 Newborn 35
6 mos 37.5 1-11 mos. 30
1 yr 37.7 2 yrs 25
3 yrs 37.2 4 yrs 23
5 yrs 37.0 6 yrs 21
7 yrs 36.8 8 yrs 20
9 yrs 36.7 10 yrs 19
11 yrs 36.7 12 yrs 19
13 yrs 36.6 14 yrs 18
16 yrs 17
18 yrs 16-18
Wong’s Essentials of Pediatric Nursing, 2005
 Full Set of Vital Signs
AGE RESTING RESTING EXERCISE
(Awake) (Sleeping) (Fever)
NB 100-180 80-160 Up to 220
1wk- 100-220 80-200 Up to 220
3mos
3mos- 80-150 70-120 Up to 200
2yrs
2yrs- 70-100 60-90 Up to 200
10yrs
10yrs- 55-90 50-90 Up to 200
adult

Wong’s Essentials of Pediatric Nursing, 2005

 Family Presence
• Assess needs of family, • Assign a staff member
taking into to provide support
consideration cultural
variables
• Support family’s
involvement in child’s
care
• Assign a healthcare
professional to provide
explanations to the
family
 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.
 Can you still
remember them?
RBC: Male: 4.5 M to 5.5M
Female: 4.5M to
Significance 5.0M
· RBC- Decreases in RF, infective carditis, anemia
WBC: 5,000 to 10,000/ mm3
Platelets:
Increases in heart diseases characterized by200T to 400T/ mm3
inadequate
Hgb:
oxygenation such as CHD, Polycythemia Male: 12 to 16 g/dl
Female: 14 to18 g/dl
· WBC - Increases in infectious & inflammatory diseases of the
Hct: Male: 40% to 54%
heart as well as MI
Female: 31% to 47%
· Hct - Increases in Hypovolemia & excessive diuresis Decreases in anemia
· Hgb- Decreases in various anemias Increases in Polycythemia, CHF
 Chest X-ray/ CT Scan

Done to
visualize the
structures of
the respiratory
system

3/12/2010 42
 (Holter monitoring, Stress test/Treadmill)

•Measures the electrical activities of the heart

•Indicates changes in myocardial oxygenation
•FIRST diagnostic test done when CVD is suspected.

•Significance:
MI: Elevated ST segment
Inverted T wave
Pathologic Q wave
 ABG Analysis • Measures the
amount of oxygen
and carbon dioxide
in the blood, as well
as its acidity.

• Use heparinized syringe

• Radial artery – common
site
3/12/2010 44
 Chest X-ray

Practice the
client on how
to hold his
breath and to
do deep
breathing
3/12/2010 45
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! (2ᵒ 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 • Signs of more severe
– Restlessness hypoxia:
– Tachypnea – Hypo/hypertension
– Tachycardia – Dimness of vision
– Diaphoresis – Somnolence
• Early but less obvious signs: – Stupor
– Mood changes – Coma
– Headache – Dyspnea
– Altered depth pattern of – Depressed respiration
respiration – Bradycardia
– Hypertension – Cyanosis (peripheral or
– Exertional dyspnea central)
– Anorexia
– Expiratory grunt
 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
subatmospheric pressure 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. (1st choice carotid artery,
2nd choice 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. Tap or gently shake shoulder.
Determine
unresponsiveness
Say “are you OK?” Speak loudly
2. Get help Shout for help. If 2nd person comes,
have him activate EMS
3. Position the Turn on back as a unit, supporting
victim head and neck if necessary (4-10 sec)
Open the airway Head tilt/child lift
 ABC OBJECTIVES ACTIONS
CHILD (1-8 YR) INFANT (< 1 YR)
B. BREATHING 5. Assessment. Maintain open airway. Place ear over mouth, observing
Determine chest. Look, listen, feel for normal breathing (no more than
breathlessness 10 sec.)
6. Give 2 Maintain open airway
rescue breaths Pinch nose, seal mouth to mouth Mouth to nose and
mouth
Give 2 slow effective breaths. Observe chest rise. Allow
lung deflation between breaths
1 to 1 ½ sec each
7. Option for Reposition victim’s head. Try again to give rescue breaths
obstructed Activate EMS
airway
Give 5 subdiaphragmatic Give 5 back blows
abdominal thrusts (Heimlich Give 5 chest thrusts
maneuver)
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: Feel for carotid Feel for brachial
determine pulse with one pulse: keep head
pulselessness hand; maintain tilt
head-tilt with
other hand (no
more than 10 sec)
ABC OBJECTIVES ACTIONS
CHILD (1-8 YR) INFANT (< 1 YR)
CPR Pulse absent: begin Use 2-3 fingers to locate lower margin Imagine a line drawn
chest compres’ns: of rib cage. Follow rib margin to base of between the nipples
9. Landmark check sternum (xiphoid process)

10. Hand position Place one hand above fingers of first
hand on lower half of the sternum
Use heel of one hand. Depress 1-1 ½ in.
Place 2 fingers on
sternum 1 finger’s width
below line. Depress 1/2
– 1 in.

11. Compres’n rate 100 per min At least 100 per min
12. Compres’n to 1 breath to every 5 compressions
breaths
13. No. of cycles 20 (approx. 1 min)
14. Reassessment Feel for carotid pulse Feel for brachial pulse
If alone, activate EMS. If no pulse, resume CPR, starting with
compressions
Pulse present; not 1 breath every 3 sec (20 per min)
breathing: begin
rescue breathing
 Drugs for Pediatric CPR
DRUG ACTION NURSING IMPLICATION
EPINEPHRINE Adrenergic; acts on both ᵅ Most useful drug in cardiac arrest;
and ᵅreceptor sites disappears rapidly from the
bloodstream after injection; may be
given via ET
SODIUM Alkanizer, buffers pH Infuse slowly and when ventilation is
BICARBONATE adequate; flush with saline before
and after
ATROPINE Anticholinergic- Used to treat bradycardia; always
SULFATE parasymphatolytic; ↑ CO, provide ventilation and monitor
HR by blocking vagal O2sat; produces pupillary dilation
stimulation
CALCIUM Electrolyte replacement, Used only for hypocalcemia, calcium
CHLORIDE 10% needed for normal cardiac blocker overdose, hyperkalemia or
contractility hypermagnesemia; administer very
slowly via central vein
 Drugs for Pediatric CPR
DRUG ACTION
LIDOCAINE HCL Antidysrhythmic
AMIODARONE Antidysrhythmic agent;
inhibits adrenergic
stimulation, prolongs action
potential and refractory
period in myocardial tissues
ADENOSINE Antidysrhythmic; for
supraventricular tachcardia
NALOXONE Reverses respiratory arrest
due to overdose of opiates
MAGNESIUM Inhibits calcium channel and
cause smooth muscle
relaxation
NURSING IMPLICATION
Used for ventricular arrhythmias
only
First choice for shock-refractory
V.tach
Given by rapid push followed by
NSS flush
Evaluate level of pain
Given by rapid IV infusion; have Ca
gluconate IV 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 • Functional
– Cardiogenic – Hypovolemic
– Neurogenic – Obstructive
– Anaphylactic – Cardiogenic
– Septic – Transport
– Hypovolemic • Anaphylactic
• Neurogenic
• Septic
 TYPES OF SHOCK
TYPE CHARACTERISTICS FREQUENT CAUSES
HYPOVOLEMIC •Reduction in size •Blood loss (Hemorrhagic
of vascular shock) – trauma, GIB, IC
compartment hemorrhage
•Falling BP •Plasma loss – inc.capillary
•Poor capillary permeability – sepsis,
refill acidosis, hypoproteinemia,
•Low CVP burns, peritonitis
•Extracellular fluid loss –
vomiting, diarrhea,
glycosuric diuresis,
sunstroke
 TYPES OF SHOCK
TYPE CHARACTERISTICS FREQUENT CAUSES
DISTRIBUTIVE •Reduction in PVR •Anaphylaxis (Anaphylactic
•Profound Shock)
inadequate tissue •Sepsis (Septic, Bacteremic,
perfusion Endotoxic Shock)
•Increase venous •Loss of neural control
capacity and (Neurogenic Shock) – spinal
pooling cord injury
•Acute reduction in •Myocardial depression and
return of blood to peripheral dilation –
the heart anesthesia, barbiturates,
•Diminished CO tranquilizers, opioids,
antiHPN, ganglionic
blocking agents.
 TYPES OF SHOCK
TYPE CHARACTERISTICS FREQUENT CAUSES
CARDIOGENIC •Decreased CO •Post surgery for
congenital 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
• Apprehensiveness
• Irritability
• Unexplained tachycardia
• Normal BP
• Narrow pulse pressure
• Thirst
• Pallor
• Diminished urine output
• Reduced perfusion of
extremities
• Confusion and somnolence
• Tachypnea
• Moderate metabolic acidosis
• Oliguria
• Cool, pale extremities
• Decreased skin turgor
• Poor capillary filling
• 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:
Absolute Relative Third Spacing
Hypovolemia Hypovolemia

Venous return to the heart

Cardiac Output

Inadequate 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
DRUG THERAPY
IN
SHOCK:
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
• Liver septic 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 mins in 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 Epi or
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 – heart (rate, rhythm)
– Vital signs – Lungs (rate, pattern)
– level of consciousness – Skin
(GCS) – odors (breath, clothing)
– motor function
– Eyes (pupils, EOM)
– mouth (lesions, odors)
 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 2nd as 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 • CHF and pulmonary
• disorientation, edema
• edema, • hypertension caused by
• ^K+ hypovolemia, anorexia
• decrease Na • sudden drop in UOP
• ^ BUN and creatinine • convulsions, coma
• Acidosis • changes in bowels
• uremic breath
 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 – Maintain nutrition
body fluids
– Safety measures
– Monitor lab results
– Mouth care
– Watch hyperkalemia
symptoms: malaise, anorexia, – Daily weights
parenthesia, or muscle – Assess for signs of heart
weakness, EKG changes failure
– watch for hyperglycemia or – GCS and Denny Brown
hypoglycemia if receiving TPN
or insulin infusions – 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 – Neurological
• Hypertension • Burning, pain, and itching,
parestnesia
• Arrythmias
• Motor nerve dysfunction
• Pericardial effusion • Muscle cramping
• CHF • Shortened memory span
• Peripheral edema • Apathy
• Drowsy, confused, seizures,
coma, EEG changes
 Chronic Renal Failure
• Objective symptoms
– GI – Respiratory
• Stomatitis • ^ chance of infection
• Ulcers • Pulmonary edema
• Pancreatitis • Pleural friction rub and
• Uremic fetor effusion
• Vomiting • Dyspnea
• consitpation • 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 – Skin
• Muscle and bone pain • Yellow-bronze skin with
• Bone demineralization pallor
• Pathological fractures • Puritus
• Blood vessel calcifications • Purpura
in myocardium, joints, • Uremic frost
eyes, and brain • 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
 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 (3rd and 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) phase
5th Day 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

 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 1st 48 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
– Livor mortis
• limbs of the corpse to • settling of the blood in
become stiff the lower (dependent)
portion of the body
– Algor mortis
• reduction in body • starts 20 minutes to 3
temperature following hours after death
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