Transcript Cardiovascular Disorders in Children

NURSING CARE OF THE
CHILD WITH A
CARDIOVASCULAR
DISEASE
ASSESSMENT OF HEART
DISORDERS IN CHILDREN
• History
• Physical
assessment
– general
appearance
– pulse, blood
pressure, &
respirations
Transition from fetal to
pulmonary circulation
•
•
•
•
•
•
•
the umbilical cord is cut
systemic vascular resistance is increased
pressure in the L side of the heart increases
foramen ovale closes
breathing is initiated
pulmonary vascular resistance falls
blood that was shunted through the PDA
now goes to the lungs.
FIGURE 26–1 Fetal circulation. Blood leaves the placenta and enters the fetus through the umbilical vein. The ductus venosus, the
foramen ovale, and the ductus arteriosus allow the blood to bypass the fetal liver and lungs. After circulating through the fetus, the blood
returns to the placenta through the umbilical arteries. From Ladewig, P. W., London, M. L., Moberly, S., & Olds, S. B. (2002).
Contemporary Maternal-Child Nursing Care (8th ed,. p. 51 ). Upper Saddle River, NJ: Prentice Hall.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–2 A, Fetal (prenatal) circulation. B, Pulmonary (postnatal) circulation. LA, left atrium; LV, left ventricle; RA, right atrium;
RV, right ventricle.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Ductus Arteriosus
• an opening in fetal circ. between the
pulmonary artery (PA) and aorta (Ao).
• in fetal circulation, most of the blood
bypasses the lungs and returns to systemic
circulation by way of the PDA (PA to Ao).
• In transition to pulmonary circulation, the
PDA constricts over 10-15hrs; permanent
closure should occur by 3wks of age,
UNLESS SATURATION REMAINS LOW
Normal pressure gradients and oxygen saturation levels in the heart chambers and great
vessels. The ventricle on the right side of the heart has a lower pressure during systole than the left
ventricle because less pressure is needed to pump blood to the lungs than to the rest of the body.
FIGURE 26–3
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Hypoxemia in the infant
• below 95% pulse oximetry.
• cyanosis results from hypoxemia
• perioral cyanosis indicates central
hypoxemia
• acrocyanosis does not.
Response to Hypoxemia
• acute: HR increases
• chronic: bone marrow produces more RBC
to increase the amount of Hgb available for
oxygen transport.
• Hct>50 is called polycythemia.
• increased blood viscosity increases risk of
thromboembolism.
Cardiac Functioning
• 02 requirements are high the first few weeks
of life
• normally, HR increases to provide adequate
oxygen transport
• infant has little cardiac output reserve
capacity
• cardiac output depends almost completely
on HR until the heart is fully developed
(age 5 yr).
Compliance in the infant
• in infancy, muscle fibers are less developed
and organized
• results in less functional capacity or less
compliance
• less compliance means the infant is unable
or less able to distend or expand the
ventricles to achieve an increase stroke
volume in order to compensate for
increased demands.
Severe Hypoxemia
• children respond with bradycardia
• cardiac arrest generally results from
prolonged hypoxemia related to respiratory
failure or shock
• in adults, hypoxemia usually results from
direct insult to the heart.
• therefore, in children, bradycardia is a
significant warning sign of cardiac arrest.
• approp Rx for hypoxemia reverses brady.
ASSESSMENT OF HEART
DISORDERS IN CHILDREN
• Diagnostic tests
–
–
–
–
Electrocardiogram
Radiography
Echocardiography
Phonocardiography & magnetic resonance
imaging
– Exercise testing
– Laboratory tests
CONGENITAL HEART
DISEASE
• Defects with increased
pulmonary blood flow
– Ventricular Septal
Defect
• Opening between
ventricles
• S/S
– 4-8 weeks, fatigue and
harsh murmur
• Therapeutic management
– Most close spontaneously,
those that don’t require
open heart surgery
Ventricular Septal Defect; VSD
•
•
•
•
opening in the ventricular septum
shunts L to R; increases pulmonary bld flow
most common: accounts for 20% CHD
only 15% large enough to generate
symptoms: tachypnea, dyspnea,, FTT,
reduced fluid intake, CHF, PHT.
• systolic murmur ; LLSB
• most small VSD close spontaneously
Treatment of VSD
• if no sx CHF or PHT, treatment is
conservative
• surgical patching during infancy if FTT
• closure by transcatheter device during CC
for some defects: Rashkind procedure.
• prophylaxis for infective endocarditis is
required
• high risk for surgical repair in first few
months of life
• Defects with
increased
pulmonary blood
flow
– Atrial Septal Defect
• Opening between
the atria
• S/S
– Murmur, second
heart sound
splitting
• Management
– Surgery
Treatment of ASD
• Echo shows RV overload and shunt size
• cxray and EKG may be normal unless a
large shunt
• surgery to close or a patch via catheter
during Cardiac Cath.
• atrial arrhythmias can be a late sx or
associated with a large ASD involving
conduction system in the septum
FIGURE 26–7 A, Septal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect
(VSD). B, Coil used to close a patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when
a thrombus forms in the mass of fabric and wire.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–8 A child with atrial septal defect repair. Surgery is performed with this type of defect to prevent pulmonary vascular
obstructive disease as an adult.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
– Patent Ductus
Arteriosus
• Fetal structure that
should begin closing
with the first breath
and should complete
by 3 months
• S/S
– Wide pulse pressure
and continuous
murmur
• Management
– Administration of
indomethacin
– Cardiac
Catheterization
– Surgery
Obstructive Congenital Defects
• due to abnormally small pulmonary vessels
• which restrict flow of blood, so the heart
hypertrophies to work harder to provide the
blood flow to organs.
• however, CO increases initially but
eventually hypertrophied muscle becomes
ineffective.
• initially R sided failure, progressing to L
sided and eventual bilateral failure
NURSING CARE OF THE CHILD
WITH A HEART DISORDER
• Obstructive defects
– Pulmonic Stenosis
• Narrowing of the
pulmonary valve or
artery causing the right
ventricle to hypertrophy
• S/S
– Mild right sided heart
failure
– Cyanosis
– SEM
• Therapeutic
Management
– Balloon angioplasty to
relieve the stenosis
-Aortic Stenosis
• Stenosis of the aortic
valve prevents blood
from passing from the
left ventricle into the
aorta, leading to
hypertrophy of the left
ventricle
• S/S
– Usually asymptomatic but
with murmur
– May have chest pain and
even sudden death
• Therapeutic
Management
– Stabilization with a Beta
Blocker or Calcium
Channel Blocker
– Balloon valvuloplasty
– Valve replacement
– Coarctation of
the Aorta
• Narrowing of the
lumen of the
aorta
• S/S
– Absence of
palpable femoral
&/or brachial
pulses;
headache,
vertigo,
nosebleeds,
CVA; leg pain
• Therapeutic
Management
– Surgery or
angiography
• Defects with decreased
pulmonary blood flow
– Tricuspid Atresia
• The tricuspid valve is
closed, blood flows
through the patent
foramen ovale into the
left atrium, bypassing
the lungs. Then it is
shunted back through a
PDA into the lungs.
When these structures
close, cyanosis,
tachycardia, and
dyspnea occur.
Surgery must correct.
• Treatment: IV infusion
of PGE until surgery
Clinical Manifestations of
Cyanotic Heart Disease
• chronic hypoxemia causes fatigue,
clubbing, exertional dyspnea, delayed
milestones, tire easily with feeding, reduced
growth, CHF
• hypercyanotic (hypoxic) spells: incr rate
and depth of respir, incr cyanosis, incr HR,
pallor and poor perfusion, agitation and
irritability.
FIGURE 26–13 Clubbing of the fingers is one manifestation of a cyanotic defect in an older child. What neurologic signs may be
associated with such a defect?
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Cyanotic Spell
• most signif prob to develop in infants and
toddlers with cyanotic heart disease
• brought on by crying, feeding, exercise,
warm bath, or straining to defecate
• during a hypoxic spell, child will often
squat knee to chest to decrease venous
return (by incr systemic vascular resistance)
from LE which decr CO and relieves the
cyanotic spell.
• Defects with decreased
pulmonary blood flow
– Tetralogy of Fallot
• Four anomalies
–
–
–
–
Pulmonary stenosis
VSD
Dextroposition of the aorta
Hypertrophy of right
ventricle
• S/S
– Cyanosis
– Polycythemia (increase in
number of RBC)
– Dyspnea, growth
restriction, clubbing of
fingers
• Therapeutic Management
– Surgery
Tetralogy of Fallot
• combination of four defects
–
–
–
–
•
•
•
•
pulmonary stenosis: degree determines severity
VSD
over-riding of the aorta
RVH
accounts for 10% of CHD
elevated R sided pressures: R to L shunt
xray: boot shaped heart d/t RVH
risk for metabolic acidosis and syncope.
Treatment of TOF
• total repair is done by 6 mo if cyanotic
spells
• surgery is not necessarily currative, but
most have improved quality of life and
improved longevity
• residual problems: arrhythmias and RV
dysfunction
• lifelong SBE required
FIGURE 26–9 This infant has a congenital heart defect with decreased blood flow. What is the
prognosis for an infant who has either of the most common malformations—tetralogy of Fallot or
transposition of the great vessels?
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–10 A child with a cyanotic heart defect squats (assumes a knee–chest
position) to relieve cyanotic spells.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–12 Place the infant who has a hypercyanotic spell in the knee–chest
position. This position increases systemic vascular resistance in the lower extremities.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Surgical treatment
• cardiac catheterization, which may include
procedural treatment in the cath lab
• valve replacement
• conduit placement
• cardiac transplant
FIGURE 26–6
Interventional catheterization, balloon valvuloplasty to open the pulmonary valve.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
ACQUIRED HEART DISEASE
• Congestive Heart Failure
– S/S
• Tachycardia, tachypnea
• Right sided: increased venous
pressure, hepatomegaly
• Left sided: dyspnea, crackles
(rales), cyanosis, and, eventually,
ride sided failure
– Therapeutic management
• Reduce workload of the heart
using diuretics, inotropics, and
vasodilators
Congestive Heart Failure
• cardiac output is inadequate to meet the
body’s needs
• may result from:
– congenital heart defect that causes increased
pulmonary blood flow or obstruction of blood
outflow tract
– problems with heart contractility
– pathology that requires a high cardiac output
(severe anemia, acidosis, respiratory disease).
CHF in the infant
•
•
•
•
•
can be subtle
good assessment skills are a must
tires easily, especially during feeding
(initial) weight loss
diaphoresis, irritability, frequent infection.
FIGURE 26–4
failure.
Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
CHF in older children
•
•
•
•
exercise intolerance
dyspnea
abdominal pain or distention
peripheral edema.
Symptoms of progressive disease
• tachycardia, tachypnea, pallor or cyanosis,
F/G/R, cough, crackles.
• fluid volume overload: periorbital and facial
edema, JVD, hepatomegaly, ascites.
• not mentioned in the book: increased weight
gain, bounding pulses, edema of dependent
body parts.
FIGURE 26–4
failure.
Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–5 Infants with cardiac conditions often require supplemental feedings to provide sufficient calories for growth and
development. The parents of this infant girl have been taught how to give her nasogastric feedings at home.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Cardiomegaly
• occurs at the heart attempts to maintain CO
• if CHF is not adequately treated, precursors
of Cardiogenic Shock arise: cyanosis, weak
peripheral pulses, cool extremities,
hypotension, heart murmurs
• clarification: not all heart murmurs are
heralding cardiogenic shock.
Clinical diagnosis
• based upon clinical assessment: tachycardia,
respiratory distress, crackles.
• cxray could show cardiac enlargement,
venous congestion, PE, atelectasis.
• cardiac echo: defects or dysfunction
• EKG: tachycardia, bradycardia, ventricular
hypertrophy
Goals of Management
• make the heart work efficiently
• remove excess fluid
• improve systemic circulation without
overloading the pulmonary circulation
Medication therapy
• positive inotropic effect and afterload reducing agents
– Digitalis
• Digoxin
– ACE inhibitors (Angiotensin-converting
enzyme inhibitors)
• Lisinopril
– Beta Blockers
• Indural (Propranolol)
– Diuretics: Lasix, HCThiazide, aldactone.
Supportive treatment
• oxygen
• fluids, as indicated( in CHF, fluids may be
restricted).
• increased calories or concentrated
formula(prescribed)
• air way support/management
• rest and spacing of activity/rest periods
• Rheumatic fever
– S/S
• Systolic murmur
• Chorea (sudden involuntary
movement of the limbs)
• Macular rash on the trunk
• Swollen and tender joints, SQ
nodules on tendon sheaths
• Positive ASO titer and increased
ESR and C-reactive protein
– Therapeutic management
• Bedrest
• Antibiotics to eliminate Group A
Beta hemolytic Strept
• Prognosis depends on how much
heart involvement
Rheumatic Fever
• inflammatory connective tissue disorder
that follows initial infection by group A
beta-hemolytic streptococci
• may lead to permanent mitral or aortic valve
damage
• sx: migratory polyarthritis, subcutaneous
nodules, erythema marginatum, fevers, St.
Vitus dance (chorea movements)
• dx: Jones criteria and an elevated ASO
Treatment for Rheumatic Fever
• antibiotics to treat the strept infection: pcn,
erythromycin
• asa for joint pain and fever
• monitored by cardiac echo (serial)
• steroids for severe carditis with CHF
• SBE prophylaxis
• long term antibiotics until adulthood
– daily oral or 1x/mo IM (Pen G)
Infective Endocarditis
• inflammation of the lining, valves, and
arterial vessels of the heart
• caused by bacterial, enterococci and fungal
infections
• significant M&M for children with CHD,
prosthetic valves and shunts, and in
immunocompromised children with long
term central venous catheters.
SBE Prophylaxis
• Prophylaxis for infective bacterial
endocarditis
• aka SBE prophylaxis ;systemic bacterial
endocarditis prophylaxis
• see Table 14-4 p 489 in B&B
• commonly given before dental procedures
to prevent oral bacteria from entering the
blood stream and seeding in the area of
defect, causing a bacterial endocarditis
• Kawasaki disease
– S/S (early)
• High fever that doesn’t respond to
therapy
• Swollen hands and feet, enlarged
joints
• Strawberry tongue, red lips,
conjunctiva
• Enlarged cervical lymph nodes
– S/S (late)
• Skin desquamation
• Platelet count increases
• aneurysms
– Therapeutic management
• Administration of Ibuprofen for
inflammation and platelet
aggregation
• IV immunoglobulin to decrease
immune response
• Most children recover fully but
some will need heart surgery to
repair damage
Kawasaki Syndrome
• acute systemic inflammatory disease
• aka mucocutaneous lymph node syndrome
• most common cause of acquired heart
disease
• etiology unknown
• 3 stages:
– acute, subacute and convalescent
• dx based upon clinical signs
Diagnostic Criteria for Kawasaki
Syndrome
• fever > 102.2 x 5 days plus 4 of the
following:
• bilateral conjunctivitis
• strawberry tongue; cracks/fissures of lips
• palmar/plantar erythema, induration,then
desquamation
• maculopapular rash on trunk
• acute cervical lymphadenitis
FIGURE 26–14
This child shows many of the signs of the acute stage of Kawasaki syndrome.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Treatment of Kawasaki
Syndrome
• high dose ASA and IgG given early
significantly decreases the risk of cardiac
involvement
• greatest risks are coronary artery lesions
and cardiac aneurysms
• monitor for cardiac involvement for
months: aneurysms, early atherosclerosis,
arrhythmias, CHF, coronary stenosis, MI
and potential death.
FIGURE 26–15 This child has returned for one of her frequent follow-up visits to assess her cardiac status after treatment for Kawasaki
syndrome. Notice the lips that show the inflammation and cracking.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Dyslipidemia
• fam hx incr risk of CAD d/t high levels of
LDL and cholesterol
• total lipid panel, nutritional history and life
style needs to be considered.
• children need fats to grow, metabolize
vitamins and produce hormones
• high fat/sat fat diet is not recommended.
• long term studies of effect of childhood
lipid levels on life span inconclusive
Hypertension
• 1-3% of the pedi population
• unknown cause = essential or primary HTN
• underlying kidney or cardiac
disease=secondary HTN
• children’s BP in >90th at incr risk for adult
HTN
• HTN in adol correlates with obesity and
elevated serum lipid level
Shock in Children

A clinical syndrome characterized by
prostration and insufficient perfusion to
meet the metabolic demands of tissues

Hypotension is not part of the definition
in children
Shock vs. Hypotension

Shock
– State of insufficient perfusion to meet the
metabolic demands of tissues

Hypotension
– Physical sign characterized by a fall in systolic
blood pressure (BP below normal values)
– Hypotension is a late sign of shock in children and
it’s presence in children implies profound
cardiovascular compromise
Pathophysiology

Hypovolemic shock
– Hemorrhage
– Dehydration

Distributive shock
– Neurogenic / Spinal
– SIRS / Sepsis
– Anaphylaxis

Cardiogenic
– Pump failure
– Obstructive
Help!

Excuse me, I
believe that my
child is in a state
of inadequate
tissue perfusion!
Recognition of shock

Early recognition is key
– The longer you wait, the higher the
mortality!!!!

Key parameters to assess:
– L.O.C.
– Respiratory rate
– Heart rate
– Peripheral perfusion
• Skin color and temp.
• Capillary refill
Heart Rate

Tachycardia
– Above higher normal limit
• (age x 5 minus 150)
– 4yr X 5 = 20 – 150 = 130
• Too fast
– Infant > 220
– Child > 180
• Too slow
– < 60
– Sustained
– Decompensated shock
• Slowing or Bradycardia
Level of Consciousness (L.O.C.)
(Key)

Changes in L.O.C. occur early
– Irritable
– Does not interact with parents
– Stares vacantly into space
– Poor response to pain
– Asleep/sleeping a lot
• Difficult to arouse
– Unresponsive
Peripheral Perfusion (Key)


Decreased or
bounding pulses
Volume discrepancy
– Central vs peripheral
pulses
• Poor or brisk capillary
refill
• Cool or mottled or red
and warm extremities
• Decreased urine
output
Respiratory Rate

Compensated shock
– Tachypnea
• Elevated for age
• “Quiet respirations”
– Think of DKA or Hypovolemia
• Retractions
– Sepsis
• Decompensated shock
– Bradypnea or apnea
Compensated (Early) Shock

Vital organ function is maintained by
intrinsic compensatory mechanisms;
blood flow is usually normal or
increased but generally uneven or
maldistributed in the microcirculation.
Compensated (Early) Shock

Normal level of consciousness
– Agitated


Quiet tachypnea
Tachycardia
– Sustained
– Difference between central and peripheral pulses


Normal or delayed capillary refill
Normal or elevated B/P
Decompensated Shock
(with hypotension)

Efficiency of the CVS gradually
diminishes, until perfusion in the
microcirculation becomes marginal
despite compensatory adjustments.
Decompensated Shock
(with hypotension)

Altered level of consciousness
– Painful stimulation or unresponsive

Delayed capillary refill
– > 5 seconds



Hypotension
Weak central pulses, absent peripheral
pulses
Bradycardia
Hypotension

Blood Pressure
– Lowest acceptable systolic blood pressure
•
•
•
•

Birth – 1 month: 60 mmhg
1 month – 1 year: 70 mmhg
1 year – 10 year: 70 + (2 X age in years)
>10 years : 90 mmhg
Normal systolic
– 80 + (2 x age in years)
– or fiftieth percentile
Irreversible (terminal) shock

Damage to vital organs such as the
heart or brain of such magnitude that
the entire organism will be disrupted
regardless of therapeutic intervention.
Death occurs even if CV measurements
return to normal levels with therapy.
Hypovolemic shock

Hypovolemia is the usual cause of
shock in the out of hospital setting
– Most common cause is blood loss
secondary to blunt force trauma
– Vomiting and diarrhea is a second leading
cause
Septic Shock



Most common form of
distributive shock
Infectious organism or
their byproducts
(endotoxins)
Triggers an immune
response
– Vasodilation
– Increase capillary
permeability
– Maldistribution of blood

Early stage
– High cardiac output, low
vascular resistance
• Tachycardia
– Bounding pulses
• Flash capillary refill
• Flush, warm skin

Later stage
– Just like hypovolemic shock
Neurogenic

Usually the result of
either head or high
spinal cord injury
(T6)
– Disrupts sympathetic
nervous system
innervention with
blood vessels and
heart
– Uncontrolled
vasodilation

Signs and
symptoms
– Hypotension with
wide pulse pressure
– Normal heart rate or
bradycardia
– Increased respiratory
rate
– Diaphragmatic
breathing
Cardiogenic Shock

Usually a problem
with stroke volume

Manifestations
– Rate is either:
– Alteration in L.O.C.
– Trouble breathing
• Too fast
• Crackles/rales
– Inadequate time for
ventricle filling
– SVT, Atrial Fib
• Too slow
– Bradycardia
• Or not at all
– Asystole
– PEA
– Trouble feeding or
not feeding well
– Large liver
– S3 gallop
Anaphylactic
Acute multisystem
allergic response
 Can occur in seconds
or minutes
– Usually within 5 – 10
minutes of exposure



• Venodilation
• Systemic vasodilation
• Pulmonary
vasoconstriction
Signs & symptoms
 – Anxiety/agitation
 – Nausea and vomiting
 – Urticaria (hives)
 – Angioedema
 – Respiratory distress
 – Hypotension
 – Tachycardia
Nursing management

Dxs:
– Ineffective breathing pattern R/T
diminished oxygen needed for impaired
tissue perfusion
– Altered tissue perfusion R/T reduced blood
flow, decreased blood volume, reduced
vascular tone
– Altered family process R/T a child in a lifethreatening condition
Nursing management


Goals:
Inc O2 to lungs
Neck in neutral
or “sniffing”
position
– Adm O2 as prescribed, position to maintain open
airway, monitor artificial airway

Promote venous return and cardiac output
– Position flat with legs elevated
– Adm. IV fluids and plasma expander, vasopressor
and cardiotonics
– Maintain opt body tempr.
The end.
Q&A?