Download disorder - WordPress.com

1. Give the pathophysiology, sign / symptoms and nursing care for the following disorders.
Inflammatory Heart
Disease
Rheumatic Fever/
Rheumatic Heart
Disease
Pathophysiology
Endocarditis
Inflammation of the
endocardium (can
involve any portion
of the endothelial
lining of the heart).
• Relatively
uncommon (1.5 to
6.2 cases per
100,000 people in
developed countries)
• Not fully
understood
• Thought to result
from an abnormal
immune response to
M proteins of group
A β- hemolytic
streptococcal
bacteria
• Carditis,
inflammation of the
heart, develops in
about 50% of people
with RF; usually
involve 3 layers of
the heart:
pericardium,
myocardium and
endocardium.
• As inflammatory
resolves, fibrous
scarring occurs
causing deformity
(RHD).
• Results to stenosis
and regurgitation
Sign and Symptoms
Nursing Care
• Fever and
migratory join pains
– initial
manifestation
Cardiac: chest pain,
friction rub, heart
murmur, S3, S4,
cardiomegaly,
pericardial effusion
• Musculoskeletal:
migratory
polyarthritis:
redness, heat,
swelling, pain, and
tenderness of more
than one joint;
usually affects large
joint of extremities.
• Integumentary:
erythema
marginatum:
transitory pink,
nonpruritic,
macular lesion on
trunk or inner
aspect of upper
arms or thighs;
subcutaneous
nodules over
extension or wrist,
elbow, ankle, and
knee joints
• T 39.4°C (101.5°F)
+ flulike symptoms,
accompanied by
cough, SOB, and
join pain
• Embolic
complications
• Heart murmur
(90% in infective
endocarditis); may
Healht promotion
• Prompt identification
and treatment of
streptococcal throat
infections (red, fierylooking throat, pain
with swallowing,
enlarged and tender
cervical lymph nodes,
fever rage 38.3°C to
40°C) to decrease
spread of pathogen
and the risk for
rheumatic fever.
Assessment
• Health history: assess
risk for RF (prolonged,
untreated or recurrent
pharyngitis),
complaints of sore
throat with fever,
difficulty swallowing,
and general malaise
Healht promotion
• Prevention of
endocarditis
• Education is the key
part of prevention
Assessment
• Physical examination:
V/S, apical pulse and
heart sounds; rate and
ease of respirations,
• Classified by its
acuity and disease
course
Myocarditis
• Infectious agent
infiltrate interstitial
Pericarditis
Pericardial damage
worsen or new
murmur develop
lung sound; skin color,
temperature, and
presence of petechiae
or splinter
hemorrhages.
• Depends on the
degree of
myocardial damage
of abscesses
• Chest pain
• Inflammatory
• Abnormal heart
process damage the
sound: muffled S1,
S3, murmur,
local or diffuse
pericardial friction
swelling and damage. rub
• Frequently assess for
manifestations of heart
failure: activity
intolerance, UO, heart
and breath sounds
• During acute phase:
hemodynamic
monitoring and the
ECG
• Both physical and
emotional rest are
indicated, because
anxiety increased
myocardial oxygen
demand
• Classic
manifestations:
-release of
chest pain,
pericardial friction
inflammatory
rub (characteristic
sign of pericarditis)
vasodilation,
and fever.
hyperemia, and
• Chest pain – the
edema; increase
most common is
capillary permeability abrupt onset;
-Escape of plasma
caused by
inflammation of
proteins and
nerve fibers in the
fibrinogens into the
lower parietal
pericardial space
pericardium and
- influx of WBC to the pleura covering
diaphragm. (Refer
site of injury to
to page 10 of this
destroy the causative sheet.) Relieved by
agent
sitting upright and
leaning forward as
- exudate formation
the heart moves
away from the
- inflammatory
diaphragmatic side
resolve without long- of the lung pleura.
term effects or may
• Low grade fever
Healht
promotion
• Early
identification
and treatment
of the disorder
can reduce the
risk of
complications.
• Promptly
report a
pericadial
friction rub or
othe
rmanifestations
of pericarditis
in client with
recent AMU,
cardiac
surgery, or
systemic
disease
associated with
a risk for
pericarditis.
Assessment
produce scar tissue
and adhesions
between the
pericardial layers
- restrict cardiac
function
Valvular
Heart
Disease
Mitral
Stenosis
• Dyspnea and
tachycardia
Chronic constrictive
pericarditis
• Tissue scarring of
pericardial layers
that leads contract,
restricting diastolic
filling and elevating
venous pressure.
• May follow viral
infection, radiation
therapy, or heart
surger
• Health History:
complain of acute
substernal or
precordial chest pain,
effect of movement
and breathing on
discomfort, pain
radiation, associated
symptoms; recent AMI,
heart surgery, or other
cardiac disorder;
current medications;
chronic conditions
(e.g., RF, or connective
tissue or autoimmune
disorder)
• Physical examination:
V/S; variation in
systolic BP with
respirations; strength
of peripheral pulses,
variations with
respiratory movement;
apical pulse, clarity
changes with
respiratory movement,
presence of a friction
rub; neck vein
distension; LOC, skin
color, and other
indicators of cardiac
output.
Pathophysiology
Sign and
symptoms
Nusring Care
• RHD or bacterial endocarditis;
• Typical earliest
manifestation:
dyspnea on
exertion (DOE)
• Cough,
hemoptysis,
frequent
pulmonary
infections
• Loud S1, split S2,
mitral opening
• the cardio-care six
• observe closely for
findings of heart
failure, pulmonary
edema, and reactions
to drug therapy.
• if client has had
surgery, watch for
hypotension,
arrhythmias, and
thrombus formation.
reduces blood volume to left
rising pressure in the left atrium;
calcification of the valve leaflets (due
to blo
atrial hypertrophy and pulmonary
congestion, increasing pressure in the
hypertrophy of the R ventricle and
Mitral
Regurgit
ation
allowing blood to regurgitate during
systole form L ventricle
atrial hyperthrophy and pulmonary
enlargement of the R ventricle.
Mitral
Valve
Prolapse
Excess tissue in the valve leaflets and
ventricular blood regurgitates into
the L atrium
snap, diastole
murmur: lowpitched, rumbling,
crescendodecrescendo,
heard best in the
apical region;
palpable thrill
• Atrial
dysrhythmias
• explain the need for
long-term antibiotic
therapy and the need
for additional
antibiotics before
dental care.
• report early findings
of heart failure such as
dyspnea or a hacking,
nonproductive cough.
• Fatigue,
weakness,
DOE,
orthopnea
• Murmur:
loud, highpitched,
rumbling,
and
holosystoli
c
(occurring
throughou
t systole);
accompani
ed by
palpable
thrill,
heard
most
clearly at
the
cardiac
apex
• May be
asymptom
atic
• Severe or acute
regurgitation:
pulmonary
congestion and
edema
•
Tachydysr
hythmias
causing
palpitation
• the cardiocare six
• monitor the
cardio seven
• if client has
surgery,
monitor
postoperativel
y for
hypotension,
arrhythmias
and thrombus
formation
• diet
restrictions
and drugs
• explain tests
and
treatments
• prepare
client for longterm
antibiotic and
follow-up
care.
• stress the need for
prophylactic
antibiotics during
dental care.
• Assess mental status
(Restlessness, severe
anxiety and
confusion).
s,
lightheade
dness,
syncope
•
Progressiv
e
worsening
: leads to
heart
failure,
embolizati
on may
cause
transient
ischemic
attacks
(TIAs)
• Most
common
symptom
– atypical
chest pain:
left sided
or
substernal
,
frequently
related to
fatigue,
not
exertion
• Usually
asymptom
atic
• Audible
midsystolic
ejection click or
murmur; high
pitched last
systolic murmur
Aortic
Stenosis
The increased pressure load
imposed by aortic stenosis results in
compensatory hypertrophy of the
left ventricle (LV) without cavity
enlargement (concentric
hypertrophy). With time, the
ventricle can no longer compensate,

Chest
pain:
Angina
pectoris in
patients
with aortic
1. Assist the
patient in
bathing, if
necessary.
2. Provide a
bedside
causing secondary LV cavity
enlargement, reduced ejection
fraction (EF), decreased cardiac
output, and a misleadingly low
gradient across the aortic valve
(low-gradient severe AS). Patients
with other disorders that also cause
LV enlargement and reduced EF
(eg, myocardial infarction, intrinsic
cardiomyopathy) may generate
insufficient flow to fully open a
sclerotic valve and have an
apparently small valve area even
when their AS is not particularly
severe (pseudosevere AS).
Pseudosevere AS must be
differentiated from low-gradient
severe AS because only patients
with low-gradient severe AS benefit
from valve replacement.
Elevated shear stress across the
stenosed aortic valve degrades von
Willebrand factor multimers. The
resulting coagulopathy may cause
GI bleeding in patients with
angiodysplasia (Heyde syndrome).


stenosis is
typically
precipitate
d by
exertion
and
relieved by
rest
Heart
failure:
Symptoms
include
paroxysm
al
nocturnal
dyspnea,
orthopnea,
dyspnea
on
exertion,
and
shortness
of breath
Syncope
: Often
occurs
upon
exertion
when
systemic
vasodilatat
ion in the
presence
of a fixed
forward
stroke
volume
causes the
arterial
systolic
blood
pressure
to decline
3.
4.
5.
6.
commode
because
using a
commode
puts less
stress on
the heart
than using a
bedpan.
Offer
diversional
activities
that are
physically
undemandi
ng.
Alternate
periods of
rest to
prevent
extreme
fatigue and
dyspnea.
To reduce
anxiety,
allow the
patient to
express his
concerns
about the
effects of
activity
restrictions
on his
resposibilitie
s and
routine.
Keep the
patient’s
legs
elevated
while he sits
in a chair to
improve
venous
return in the
heart.
7. Place the
patient in an
upright
position to
relieve
dyspnea.
8. Administer
oxygen as
needed to
prevent
tissue
hypoxia.
9. Keep the
patient in a
low sodium
diet.
Consult with
a dietitian to
ensure that
the patient
receives
foods that
he likes
while
adhering to
the diet
restrictions.
10. Allow the
patient to
express his
fears and
concerns
about the
disorder, it’s
impact on
his life, and
any
impending
surgery.
11. Monitor the
patient’s
vital signs,
weight, and
intake and
output for
signs of
fluid
overload.
12. Evaluate
patient’s
activity
tolerance
and degree
of fatigue.
13. Monitor the
patient for
chest pain
that may
indicate
cardiac
ischemia.
14. Regularly
assess the
patient’s
cardiopulmo
nary
function.
15. Observe the
patient for
complicatio
ns and
adverse
reactions to
drug
therapy.
Aortic
Regurgit
ation
Incompetent closure of the
aortic valve can result from
intrinsic disease of the
leaflets, cusp, diseases of
the aorta, or trauma.
Diastolic reflux through the
aortic valve can lead to left
ventricular volume overload.
An increase in systolic
stroke volume and low
diastolic aortic pressure
produces an increased
Mild aortic
regurgitation may
produce few
symptoms.
People with more
severe aortic
regurgitation may
notice heart
palpitations, chest
pain, fatigue, or
shortness of breath.
Other symptoms
include difficulty
breathing when lying
down, weakness,
fainting, or swollen
ankles and feet.
1. Electrocardiogram
ECG is rarely normal in
chronic aortic
regurgitation and often
exhibit significant
changes in
repolarization. On acute
aortic regurgitation ECG
may be normal. Visible
image of left ventricular
hypertrophy, increased
amplitude QRS, ST-Tshaped type of diastolic
overload, meaning that
the average vector
showed that ST is great,
and and T wave vector
parallel to the average of
pulse pressure. The clinical
signs of AR are caused by
the forward and backward
flow of blood across the
aortic valve, leading to
increased stroke volume. [5]
The severity of AR is
dependent on the diastolic
regurgitant valve area, the
diastolic pressure gradient
between the aorta and LV,
and the duration of diastole.
The pathophysiology of AR
depends on whether the AR
is acute or chronic. In acute
AR, the LV does not have
time to dilate in response to
the volume load, whereas in
chronic AR, the LV may
undergo a series of
adaptive (and maladaptive)
changes.
Acute aortic regurgitation
Acute AR of significant
severity leads to increased
blood volume in the LV
during diastole. The LV
does not have sufficient
time to dilate in response to
the sudden increase in
volume. As a result, LV enddiastolic pressure increases
rapidly, causing an increase
in pulmonary venous
pressure and altering
coronary flow dynamics. As
pressure increases
throughout the pulmonary
circuit, the patient develops
dyspnea and pulmonary
the QRS complex. Figure
shows the P-R interval
lengthening.
2. Thorax Radiography
Shows a progressive
enlargement of the heart.
Namely an enlarged left
ventricle, left atrium, and
aortic dilatation. The
shape and size of the
heart was unchanged in
acute insufficiency but
looks pulmonary edema.
3. Transthoracic
Echocardiography
Exposing the base of the
proximal aorta on
imaging.
4. Aortography.
5. Increased cardiac
isoenzyme (CPK and ck
mb)
6. Cardiac
catheterization
7. Transesophageal
Echocardiography (TEE)
edema. In severe cases,
heart failure may develop
and potentially deteriorate
to cardiogenic shock.
Decreased myocardial
perfusion may lead to
myocardial ischemia.
Early surgical intervention
should be considered
(particularly if AR is due to
aortic dissection, in which
case surgery should be
performed immediately).
Chronic aortic regurgitation
Chronic AR causes gradual
left ventricular volume
overload that leads to a
series of compensatory
changes, including LV
enlargement and eccentric
hypertrophy. LV dilation
occurs through the addition
of sarcomeres in series
(resulting in longer
myocardial fibers), as well
as through the
rearrangement of
myocardial fibers. As a
result, the LV becomes
larger and more compliant,
with greater capacity to
deliver a large stroke
volume that can
compensate for the
regurgitant volume. The
resulting hypertrophy is
necessary to accommodate
the increased wall tension
and stress that result from
LV dilation (Laplace law).
During the early phases of
chronic AR, the LV ejection
fraction (EF) is normal or
even increased (due to the
increased preload and the
Frank-Starling mechanism).
Patients may remain
asymptomatic during this
period. As AR progresses,
LV enlargement surpasses
preload reserve on the
Frank-Starling curve, with
the EF falling to normal and
then subnormal levels. The
LV end-systolic volume
rises and is an indicator of
progressive myocardial
dysfunction.
Eventually, the LV reaches
its maximal diameter and
diastolic pressure begins to
rise, resulting in symptoms
(dyspnea) that may worsen
during exercise. Increasing
LV end-diastolic pressure
may also lower coronary
perfusion gradients, causing
subendocardial and
myocardial ischemia,
necrosis, and apoptosis.
Grossly, the LV gradually
transforms from an elliptical
to a spherical configuration.
Tricuspid
Stenosis
tricuspid stenosis results
from alterations in the
structure of the tricuspid
valve that precipitate
inadequate excursion of the
valve leaflets. The most
common etiology is
There are few
symptoms to report.
Many patients with
this condition at
times report feeling:

tired and
lethargic

fragility

a quivering
In the treatment of
tricuspid stenosis,
medical care
consists of
assessment and
treatment of the
underlying cause
of the valvular
rheumatic fever, and
tricuspid valve involvement
occurs universally with
mitral and aortic valve
involvement. With rheumatic
tricuspid stenosis, the valve
leaflets become thickened
and sclerotic as the chordae
tendineae become
shortened. The restricted
valve opening hampers
blood flow into the right
ventricle and, subsequently,
to the pulmonary
vasculature. Right atrial
enlargement is observed as
a consequence. The
obstructed venous return
results in hepatic
enlargement, decreased
pulmonary blood flow, and
peripheral edema. Other
rare causes of tricuspid
stenosis include carcinoid
syndrome, endocarditis, end
omyocardial
fibrosis, systemic lupus
erythematosus, and
congenital tricuspid atresia
Tricuspid
Regurgit
ation
The pathophysiology of
tricuspid regurgitation focuses
on the structural incompetence
of the valve. The incompetence
can result from primary
structural abnormalities of the
leaflets and chordae or, more
often, be secondary to
myocardial dysfunction and
dilatation. [1]
Tricuspid valve insufficiency
feeling in the
neck

a rapid,
irregular
heartbeat called
a palpitation, or
both.

pain in the
upper right part
of their abdomen
which may be
caused by an
enlarged,
congested liver.
Symptoms are
rarely dramatic
enough to require
surgery to replace
the tricuspid valve.





Dyspnea
on
exertion
Orthopn
ea
Paroxys
mal
nocturnal
dyspnea
Ascites
Peripher
pathology, as
follows:

Treat
bacterial
endocarditis
with the
appropriate
antibiotics as
determined
by the
sensitivity of
the
organisms
cultured.

Medically
address
cardiac
arrhythmias
depending on
their
characterizati
on.

Decreasing
right atrial
volume
overload with
diuresis and
salt restriction
helps
decrease
symptoms
and improve
hepatic
function.
1.
Assess
mental status
(Restlessness
,
severe
anxiety and
confusion).
2. Check vital
signs (heart
rate
and
blood
due to leaflet abnormalities may
be secondary to endocarditis or
rheumatic heart disease. When
due to the latter, it generally
occurs in combination
with tricuspid stenosis. Ebstein
anomaly is the most common
congenital form of tricuspid
regurgitation.
Inspiration increases the
severity of tricuspid
regurgitation. Inspiration
induces widening of the RV,
which enlarges the tricuspid
valve annulus and thus
increases the effective
regurgitant orifice area. [2]
Chronically, tricuspid
regurgitation leads to RV
volume overload, which results
in right-sided congestive heart
failure (CHF). This manifests as
hepatic congestion, peripheral
edema, and ascites
al edema
3.
4.
5.
6.
7.
pressure).
Assess
heart sounds,
noting
gallops, S3,
S4.
Assess
manually
peripheral
pulses (with
weak rate,
rhythm
indicated
low cardiac
output).
Assess lung
sounds and
determine
any
occurrence
of
Paroxysmal
Nocturnal
Dyspnea
(PND)
or
orthopnea.
Monitor
central
venous, right
arterial
pressure
[RAP],
pulmonary
arterial
pressure(PA
P)
Routinely
Assess skin
colour and
temperature
(Cold,
clammy skin
is secondary
to
compensator
y increase in
sympathetic
nervous
system
stimulation
and
low
cardiac
output and
desaturation)
.
8. Carefully
maintain
intake output
and
daily
check
weight.
9. Administer
medication
as
prescribed,
noting
response and
watching for
side effects
and toxicity.
10. Administer
stool
softeners as
needed(s
training for a
bowel
movement
further
impairs
cardiac
output).
11. Explain
drug
regimen,
purpose,
dose,
and
side effects.
12. Maintain
adequate
ventilation
and
perfusion
(Place
patient
in
semito
highFowler’s
position or
supine
position).
13. Administer
O2 as
ordered.
14. Assess
response to
increased
activity and
help patient
in
daily
activities.
15. Maintain
physical and
emotional
rest (restrict
activity and
provide quiet
and relaxed
environment
).
16. Monitor
sleep
patterns;
administer
sedative.
17. If invasive
adjunct
therapies are
indicated
(e.g., intraaortic
balloon
pump,
pacemaker),
maintain
within
prescribed
protocol and
prepare
patient.
18. Explain diet
restrictions
(fluid,
sodium).
Pulmonic
Stenosis
Congenital pulmonary stenosis occurs 
due to improper development of the
pulmonary valve in the first 8 weeks of

fetal growth. It can be caused by a
number of factors, though most of the
time this heart defect occurs by chance,
with no clear reason evident for its

development.
Some congenital heart defects may have

a genetic link that causes heart
problems to occur more often in certain
families.
Heavy or 
rapid breathing
Shortness
of breath
Fatigue
Rapid heart
rate

Swelling in
the feet, ankles,
face, eyelids, and/or
abdomen

Chest Xray. A diagnostic
test that uses X-ray
beams to produce
images of internal
tissues, bones, and
organs onto film.
Electrocardio
gram (ECG or
EKG). A test that
records the electrical
activity of the heart,
shows abnormal
rhythms (arrhythmias),
and detects heart
muscle stress.
Echocardiogr
am (echo). A procedure
that evaluates the
structure and function
of the heart by using
sound waves recorded
on an electronic sensor
that produce a moving
picture of the heart and
heart valves.

Pulmonic
Regurgit
ation
Incompetence
of the
pulmonic valve occurs by 1
of 3 basic pathologic
processes: dilatation of the
pulmonic valve ring,
acquired alteration of
pulmonic valve leaflet
morphology, or congenital
Most patients
with mild to
moderate
pulmonary valve
regurgitation do
not experience
any symptoms.
They may lead a
normal life.
Patients with a
more severe
Cardiac
catheterization. A
cardiac catheterization
is an invasive procedure
that gives very detailed
information about the
structures inside the
heart. Under sedation, a
small, thin, flexible
tube (catheter) is
inserted into a blood
vessel in the groin, and
guided to the inside of
the heart. Blood
pressure and oxygen
measurements are taken
in the four chambers of
the heart, as well as the
pulmonary artery and
aorta. Contrast dye is
also injected to more
clearly visualize the
structures inside the
heart.
Pulmonic
regurgitation is
seldom severe
enough to warrant
special treatment
because the right
ventricle normally
adapts to lowpressure volume
overload without
absence or malformation of
the valve.
degree of PR
may experience
some of these
symptoms:
difficulty. Highpressure volume
overload leads to
right-sided heart
strain and,
Fatigue
ultimately, heart
Shortness of failure.
Underlying
breath,
especially
etiologies causing
during exertion
severe pulmonic
Chest pain
regurgitation,
whether congenital
Palpitations
or acquired, must
Enlarged liver
be treated to
Fainting with
prevent or reverse
exercise
right-sided heart
Exercise
strain and failure
intolerance
that may further
complicate the
clinical picture. A
discussion of
therapeutic
interventions in
pulmonary
hypertension by
etiology is beyond
the scope of this
article. Refer to the
articles for each
entity under
Differentials for a
detailed discussion
of treatment
options.
If pulmonary
hypertension is
identified with
pulmonic
regurgitation,
determining the
etiology is
essential to
institute
appropriate
therapy as
expeditiously as
possible. For
instance, primary
pulmonary
hypertension,
secondary
pulmonary
hypertension due
to
thromboembolism,
severe mitral
stenosis, and
pulmonary
carcinomatosis
can all manifest as
severe pulmonary
hypertension with
pulmonic
regurgitation.
No aspect of
medical
management of
heart failure is
uniquely
applicable to
pulmonic
regurgitation, and
the discussion of
management of
right-sided heart
failure is beyond
the scope of this
article. In general,
similar approaches
to those used in
the treatment of
patients with leftsided congestive
heart failure can
be useful. In some
circumstances,
such as in patients
with pulmonary
hypertension,
vasodilator
therapies must be
very carefully
considered and
monitored. In
addition, therapies
aimed toward the
underlying etiology
may also reduce
pulmonic
regurgitation
Cardiomyopathy
Dilated
cardiomyopathy is
characterized by
ventricular
chamber
enlargement and
systolic
dysfunction with
greater left
ventricular (LV)
cavity size with
little or no wall
hypertrophy.
Hypertrophy can
be judged as the
ratio of LV mass
to cavity size; this
ratio is decreased
in persons with
dilated
cardiomyopathies.
The enlargement
of the remaining
heart chambers is
primarily due to
LV failure, but it
may be
secondary to the
primary
cardiomyopathic
process. Dilated
cardiomyopathies
are associated
with both systolic
and diastolic
dysfunction. The
Symptoms are a
good indicator of the
severity of dilated
cardiomyopathy and
may include the
following:

Fatigue

Dyspnea on
exertion,
shortness of
breath, cough

Orthopnea,
paroxysmal
nocturnal
dyspnea

Increasing
edema, weight,
or abdominal
girth
On physical
examination, look for
signs of heart failure
and volume overload.
Assess vital signs
with specific attention
to the following:

Tachypnea

Tachycardia

Hypertension
or hypotension
1.
2.
3.
4.
5.
6.
Provide
oxygen at 2 to
4 L/min to
maintain or
improve
oxygenation.
Minimize
oxygen demand
by maintaining
the patient at
bed rest.
Provide
liquid diet on
acute phase,
Administer
diuretic as
prescribed to
reduce preload
and afterload.
Monitor
serum
potassium
before and after
administration
of loop
diuretics.
Prophylactic
heparin may be
ordered to
prevent
thromboembolu
s formation
decrease in
systolic function is
by far the primary
abnormality due
to adverse
myocardial
remodeling that
eventually leads
to an increase in
the end-diastolic
and end-systolic
volumes.
Progressive
dilation can lead
to significant
mitral and
tricuspid
regurgitation,
which may further
diminish the
cardiac output
and increase endsystolic volumes
and ventricular
wall stress. In
turn, this leads to
further dilation
and myocardial
dysfunction.
Early
compensation for
systolic
dysfunction and
decreased
cardiac output is
accomplished by
increasing the
stroke volume,
the heart rate, or
both (cardiac
output = stroke
volume × heart
rate), which is
also accompanied
by an increase in
peripheral
secondary to
venous
poisoning.
7.
Institute
pressure ulcer
prevention
strategies
secondary to
hypoperfusion
or
vasoconstrictio
n agents.
vascular tone.
The increase in
peripheral tone
helps maintain
appropriate blood
pressure. Also
observed is an
increased tissue
oxygen extraction
rate with a shift in
the hemoglobin
dissociation
curve.