Date: Feb 11
Patient: Mrs. W
Room: 430-1
Age: 85
BCIT Level 2 Nursing Care Plan
Diagnosis: heparin induced thrombocytopenia
Treatments:
PMHx: : atrial fib, HTN, crf, PE;s. Had an IVC filter
removed on Tuesday. Here for bridging. Husband died
last week in a care facility
Date of Surgery: heparin
induced thrombocytopenia
Medications, metoprolol, amlodipine, clonidine, lasix,
fondaparinux, lasix
PRN Medications: : Tylenol, Gravol
Diet:
Type of Surgery:
Activity:
Potential Problems
What are the anticipated problems for
this patient and what is potentially
causing these problems. (due to or
related to)
Is an occlusion in vein caused by
a thrombus or embolism of
another substance
Steps in thrombus formation:
1. Platelets aggregate
( as a result of turbulent
flow and endothelial
injury in valve pocket
2. WBC- adhere to
platelets
3. Platelets release clotting
factors and the thrombus
grows by adding a clot
( RBCs and fibrin)
PE: DVT breaks loose travels to
right side of the heart and into
pulmonary artery
- occludes blood flow to the part
of the lung and impairs gas
exchange
- affected portion -> necrotic ->
decreased oxygen delivery to
vital organs
- 90% comes from thrombi in
popliteal vein.
*factors contribute to DVT:
VALIDATION PROCESS
ASSESSMENT
EVIDENCE
Wednesday PM – How will I assess
each problem?
*** palpation could dislodge
causing PE
PE:
*Assess for respiratory rate and
depth
* Assess for increase WOB, SOB
, use of accessory muscles
*Assess arterial blood gases
(ABGs) and note changes
*Monitor O2 sat
* assess characteristics of pain
* assess acid-base balance
Assess for :

a cough that begins
Thursday PM – Data collected to
indicate a valid problem
INTERVENTIONS
Wednesday PM – What will I do for each
of the potential problems – both nursing
interventions and medical interventions?
* position patient with proper
alignment
Tachypnea is typical of PE.
Rapid, shallow respirations result
from hypoxia.
* changes in character of rep may
signal deterioration
*ABGS of PE patient typically
exhibit hypoxemia and
respiratory alkalosis.
Development of Respiratory
acidosis indicated resp failure
and immediate ventilator support
is indicated
* should be greater than 92% on
RA
* pain may result from shallow
breathing
* metabolic acidosis results from
a lactic acid build up from tissue
hypoxia
EVALUATION/FOLLOW
UP
Thursday PM – What will I do Friday
for each valid problem
* If not contraindicated, sitting
position allows good lung
excursion and chest expansion
*facilitates movement and
drainage of secretions
Change position Q2h –
*Airways opening by clearing
secretions
*Assist with deep breathing and
coughing
*Anticoagulant therapy
Fondaparinux
- prevention of deep vein thrombus
- treatment of acute PE with
warfarin
ACTION: anticoagulant activity
due to selective inhibition of factor
Xa which is required for the
formation of thrombin ( factor IIa) in
* coagulation cascade
- involves a series of chemical
reactions in which
fibrinogen(soluble) is converted
to fibrin(insoluble)
Clotting Factors
= enzymes that cleave bonds
and expose active sites
- mainly produced in the liver (
some found in platelets and
endothelial cells
- circulate in the plasma in an
inactive form->activated ina
hypercoagulbility of the blood,
venous wall damage, stasis of
blood flow

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

suddenly, and may
produce bloody sputum
(mucus): significant
amounts of visible blood
or lightly blood streaked
sputum (phlegm)
sudden onset of
shortness of breath at
rest or with exertion
splinting of ribs with
breathing (for example,
bending over or holding
the chest)
fainting
dizziness
sweating
anxiety
rapid breathing
rapid heart rate
chest pain:
Diagnostic Tests for PE:
Electrocardiogram
ultrasound examination of the
legs, or a lung perfusion scan
*CT angiogram is a type of
computed tomography (CT) scan.
It is fast, noninvasive, and fairly
accurate, particularly for large
clots. In this test, contrast
material is injected into a vein.
The contrast material travels to
the lungs, and a CT scanner
generates images of blood in the
arteries to determine if a
pulmonary embolism is blocking
blood flow. A CT angiogram is
the imaging test most often used
to diagnose pulmonary embolism.
the coagulation cascade
Warfarin
-Treatment of thromboembolic
complications associated with
atrial fibrillation
-treatment of venous thrombosis,
pulmonary embolism
Action: Coumarin anticoagulants
inhibit synthesis of prothrombin
- interfering with action of vitamin
K
Intrinsic Pathway (contact
activation pathway)
- occurs more slowly
-All components are within the
blood
-initiated when factor XII (clotting
factor) is activated by the contact of
blood with subendothelia collagen
damage or an artificial surface
Thrombin is the final activated
clotting factor and converts
fibrinogen to fibrin
fixed sequence
- the activated clotting factor
acts on the next precursor
- because a single activated
product can act on many
precursors-> amplification
- must reach a certain
concentration before clotting
can occur
_ there are two pathways that
lead to the activation of clotting
factor X and the synthesis of
prothrombinase ( factor Xa)
! Extrinsic pathway ( tissue
pathway)
- primary pathway
-occurs rapidly ( within
seconds of trauma)
-initiated by tissue factor (
extrinsic to the blood) (–
protein that is the primary
cellular initiator of blood
coagulation)
- on the surface of
subendothelial cells (
fibroblasts)
- released by damage
endothelial cells
Chronic Renal Failure
Results in the loss of renal cells
with progressive deterioration of
glumerular filtration, tubular
reabsorptive capacity and
endocrine functions of the
kidney.
- characterized by the reduction
in the GFR( glomerular filtration
rate), reflecting a corresponding
reduction in the number of
functional nephrons.
* monitor creatine
BUN
GRF
Urea
*Assess for signs of fluid volume
excess: elevated BP, tachypnea,
edema, weight gain, distended
neck veins, distended neck veins,
orthopnea
*Ausculate for crackles
Progression of chronic renal
failure in 4 stages
*Diminished renal reserve
- occurs when GFR drops to
approx. 50% of normal
- serum BUN and creatine levels
are still normal and no symptoms
of impaired renal function are
evident
*Renal insufficiency
-represents a reduction in the
GRF to 20%- 50% of normal
As nephrons are destroyed , the
remaining nephrons undergo
changes to compensate for the
loss. Each of the remaining
nephrons must filter more solute
particles from the blood
*Assess the amount of peripheral
edema by palpating area over the
tibia, ankles, sacrum, and back
*Renal failure
- GFR is less than 20% to 25% of
normal.
- kidneys can no longer regulate
the volume and solute
composition of the extra cellular
fluids. Edema, metabolic acidosis
and hyperkalemia begin to
appear.
*End-stage renal failure
- occurs when GFR is less than
5% of normal- reduction in renal
capillaries and scarring in the
* increased resp rate
* presence of fluid in the alveoli
impairs gas exchange
Monitor signs and symptoms of
excess fluid volume
Hypertension
* excess circulatory volume
contributes to an increase in BP
Lung crackles upon auscultation
- movement from pulmonary
circulation into alveolar spaces
* causes adventitious lung
sounds
Signs of fluid volume excess are
a result of sodium retention and
increased intracellular fluid
volume
* crackles signify the presence of
fluid in small airways
For potential fluid overload –
educate regarding restricting
dietary sodium
-sodium intake produces a
feeling of thirst. Restricting
sodium intake the amount of
fluid a patient drinks can be
reduced.
* to relieve dry mouth- ice –chips
as needed
- sugar free hard candy
- alleviated dry mouth
* Have patient sit up if complains of
SOB- optimal position for air
exchange
* advise to elevate feet when sitting
down
- prevents fluid accumulation in
lower extremities
Administer antihypertensive
medications
Lasix - promoted excretion of
water, Na+, Cl-, K+ by inhibiting
tubular reabsorption especially in the
medullary cortical portions of
ascending limb of loop of Henle
* Antihypertensive activity due to
decreased peripheral vascular
resistance.
- lowes BP
Expect: increased urine output.
glomeruli- atrophy and fibrosis
are evident in the tubules
- mass of the kidneys are usually
reduced
-accumulation of nitrogenous
wastes
- alters regulation of potassium,
phosphate, calcium, and
magnesium
-treatment with dialysis or
transplantation is necessary
Atrial Fibrillation
- is the result of disorganized
current flow within the atria.
Fibrillation interrupts the normal
contraction of the atria.
- is characterized by rapid,
chaotic atrial depolarization from
a reentrant pathway.
At extremely rapid rates the
entire atrium may not be able to
recover from one depolarization
wave before the next one begins,
resulting in mechanical and
electrical disorganization of the
atria without effective atrial
contraction.
- The AV node is bombarded
with more impulses than it can
conduct so a rapid ventricular
response comparable to the atrial
rate cannot occur.
- Because of the atrial
disorganization the “atrial kick”
is lost -> decreases cardiac out
put by 30%.
- With increasing ventricular
rates allowing less filling time,
cardiac output declines even
further and may result in
dyspnea, angina pectoris, heart
failure, and shock
-may be a pulse difference
*
Ausculate the heart for
tachycardia ( greater than
100beats) and bradycardia ( less
than 60 beats)
* assess for signs of reduced
cardiac output: rapid, slow, or
weak pulse, hypotension,
dizziness, syncope, SOB,
restlessness, chest pain, fatigue
* instruct patient to avoid intake of
stimulants: caffine, alcohol, tabacco
* I need some interventions but
patho is done
* stimulants increase the
automaticity of the heart
which can precipitate
dysrhythmias.
between apical and radial pulses.
* blood pools in the atria because
of lack of adequate contraction of
atrial appendages. Pooling blood
is prone to clot, forming a mural
thrombus, which increases the
risk of cerebral and peripheral
vascular emboli>
Discharge/coping
Nausea ( actual)
-due to medication
-pain
Nausea and vomiting
- controlled by the vomit center
(VC) in the medulla of the brain.
Assess her supports
- what family does she have
visiting her
- where has she been living?
-what are does she live in?
- where will she go after she
leaves the hospital?
- who will be taking care of her
when she leaves
-does she have a thermometer at
home
- does she have someone that can
go grocery shopping for her
before she goes home
- did she live with her husband in
the care facility
- has she seen the social worker?
- how has she been coping with
the loss of her husband?
- how is she coping with being in
the hospital
- is there anyone that I can call to
come and visit her
- Is she interested in knowing
about grief counselling/ seeing a
grief counsellor?
Meals on Wheels (Vancouver)
604-732-7638
* assess History, duration,
frequency, severity, precipitating
factors, medication, measures
used to alleviate the problem
*Assess skin colour, pale/cool
and clammy, green, temperature
and moisture
* Help Pt into a comfortable position
(often side-lying)
*small sips of water, ice chips,
ginger ale
* offer crackers
* administer cold cloth
* oral care to freshen mouth
Living through Loss Society of BC
604-873-5013
Does VGH have grief counselling?
GI sensory receptors send nerve
impulses to the brain in response
to abdominal distention/irritation.
VC returns impulses that trigger
abdominal contraction and
reverse peristalsis-induce
vomiting
- Also triggered by unpleasant
olfactory, visual stimuli, pain,
emotional factors, ICP, migraine
headache, inner ear
- can also be stimulated when the
CTZ is stimulated by drugs,
chemicals, toxins, radiation,
disease and metabolic states
During chemotherapy –release of
serotonin from small intestine
that stimulates NKI ((tachykinin
neurokinin receptor found
throughout central and peripheral
systems and in gut) stimulates
vomiting
-increased activity of
neurotransmitters – dopamine in
CTZ and acetylcholine VCinduces vomiting
*Assess for loss of or decreased
appetite
*Assess bowel sounds x4
* Assess pt. for dehydration (ie,
skin integrity, increased thirst,
decreased urine output of
<30cc/hr, increased respirations
and heart rate, fatigue, dark
coloured urine
*Assess pt. last dose of Antiemetic and route given
*Assess if pt. has excessive
saliva due to nausea
*Assess for reports of nausea
*pulse rate, >100 beats/min,
assess trend and baseline
* ambulate –patient verbalized this
was helpful
* keep emesis basin within easy
reach
* instruct patient to change positions
slowly
-sudden or gross movements may
increase nausea
* Administer antiemetic as
prescribed. \
Gravol Antihistaminics with similar
effects to the 5-HT3 receptor
antagonists. Efficacy is through high
concentrations of histamine and
muscarnic cholinergic receptors
within the vestibular system
(dimenhydrinate)
Will cause drowsiness.
Patho
*Hypertension increases the
workload of the left ventricle by
increasing the pressure against
which the heart must pump as it
ejects blood into the systemic
circulation. As workload
increases the L ventricular wall
hypertrophies to compensate for
the increased pressure work.
*Renal HTN: Renovascular
HTN: caused by reduced renal
blood flow. Reduced renal blood
flow causes the affected kidney
to release excessive amounts of
renin, increasing circulating
levels of angiotension II. ->acts
as vasoconstrictor to increase
peripheral vascular resistance-
Assess BP
*Over 140 mmHg Systolic
*Over 90 mmHg Diastolic
Assess urine output
 Decreased urine output
is a symptom
Assess heart rate – tachycardiaover 100
*Observe skin, colour, temp, and
cap refill time and diaphoresis
(excessive sweating)
-peripheral vasoconstriction may
result in pale, cool, clammy skin
with prolonged capillary refill
Support patient moving - no sudden
changes in sitting up or standing up
quickly – reduces risk of orthostatic
hypotension – this is a risk in older
patients
-educate regarding sodium intake
Age
Adequate
upper limit
19-50
1500
2300
51-70
1300
2300
Over 70 1200
2300
-Offer resource for information
-Offer fluids 200 cc per hour
* Metoprolol ( beta adrenergic
blocker)
- treatment of HTN as sole agent / in
>increases aldosterone levels and
sodium retention.
*Age – elastin fibers in walls of
arteries replaced by collagen
fibers that cause the vessels to be
stiffer and less compliant. Aorta
and lg arteries less able to buffer
the increase in systolic pressure
that occurs as blood is ejected
from the left heart and less able
to store the energy needed to
maintain diastolic pressure.
Systolic increases and diastolic
decreases or remains the same.
combination of antiHTN
Blocks the catecholamines
neurotransmitter beta 1 receptors
located in the heart
- blocks epinephrine from taking its
affect and therefore decreases
contractility in the heart
- decreases heart rate
* Clonidine hcl (a2 agonist)
- treatment of hypertension as a sole
agent/ in combination with other
antHTN
- decreases BP
* amlodipine ( calcium blocker)
Antianginal/antihypertensive effects
due to inhibition of extracellular
calcium-ion transmembrane
migration in cardiac/vascular
smooth muscle via the slow channel
pathway resulting in coronary
dilation and a decrease in peripheral
vascular resistance.
-blocks Ca2+ from crossing cell
membrane to muscle cell and
muscles need Ca2+ to contract.
Therefore, Ca2+ decreases
contractility. Can also cause AV
node block