Download Acute severe MR results in congestive heart failure

Cardiovascular Disorders
Inflammatory
Heart Disease
Pathophysiology
Rheumatic fever develops in some
children and adolescents following
pharyngitis with group A beta-hemolytic
Streptococcus
(ie,Streptococcus pyogenes). The
organisms attach to the epithelial cells
of the upper respiratory tract and
produce a battery of enzymes allowing
them to damage and invade human
Rheumatic
tissues. After an incubation period of 2-4
Fever/Rheumatic days, the invading organisms elicit an
Heart Disease
acute inflammatory response with 3-5
days of sore throat, fever, malaise,
headache, and an elevated leukocyte
count.
Sign and Symptoms
Common symptoms
Common symptoms of rheumatic
fever are described below.
Arthritis
Pain and swelling of the joints
(arthritis) is the most common
symptom of rheumatic fever,
affecting three out of four people.
Heart inflammation (carditis)
 Shortness of breath,
particularly when you're
physically active or when
sleeping (it can often wake
you up, gasping for breath).
 Persistent coughrapid
heartbeat (tachycardia).
 Feeling tired all the time.
 Chest pain.
Creditis can persist for several
months, but itshould improve over
Nursing Care
1) Decreased Cardiac
Output
Related to: a disturbance
in the closure of the
mitral valve (valve
stenosis).
2) Ineffective
Peripheral Tissue
Perfusion
Related to: decreased
metabolism primarily due
to vasoconstriction of
peripheral blood vessels.
3) Acute Pain
Related to: inflammation
of the synovial
membrane.
time.
Sydenham's chorea
Sydenham's chorea is a term that
describes a collection of symptoms
related to inflammation of the
nerves. These symptoms are:




4) Hyperthermia
Related to: inflammation
of the synovial
membrane, and
inflammation of the heart
valves.
5) Imbalanced
Nutrition, Less Than
Involuntary and
Body Requirements
uncontrollable jerking and
twitching of the body – most Related to: an increase in
stomach acid caused by
often, the hands and feet.
difficulty with tasks requiring the sympathetic nervous
fine hand movements, such as system compensation.
writing.
6) Activity intolerance
problems with balance.
unusual emotional outbursts, Related to: muscle
such as crying or laughing for weakness, prolonged bed
rest or immobilization.
no apparent reason.
Skin rash
The rash is usually painless, nonitchy and spreads slowly over the
child's body. It may only be
noticeable in children with fair skin.
The rash usually comes and goes
over the course of a few weeks or
months,
7) Self-Care Deficit
Related to:
Musculoskeletal
Disorders: polyarthritis /
arthralgia and therapy
bed rest.
before disappearing altogether.
It's rare for adults with rheumatic
fever to develop a skin rash.
Less common symptoms
Less common symptoms of
rheumatic fever include:
 Subcutaneous skin nodules –
small painless bumps or
lumps under the skin, usually
found on the wrists, elbows
and knees.
 a high temperature (fever)
of 39C (102F) or above
 abdominal pain
 nosebleeds
Endocarditis
Endocarditis infection occurs along the
edges of the heart valves. The lesions,
called vegetations, are masses composed
of fibrin, platelets, and infecting
organisms, held together by
agglutinating antibodies produced by
the bacteria. As inflammation continues,
ulceration may result in erosion or
perforation of the valve cusps, leading to
valvular incompetence, damage to the
conduction pathway (if in the septal
Endocarditis is rarely an obvious
diagnosis for a generalist. It may
present with a wide variety of
clinical signs, some subtle; the
diagnosis may be difficult or the
signs misleading, and there is a
wide differential diagnosis to
consider. However, there is a
wealth of clinical signs to look for.
8) Impaired Skin
Integrity
Related to: inflammation
of the skin and tissue
subcutaneous.
9) Risk for Impaired
Gas Exchange
Related to: the
accumulation of blood in
the lungs due to increased
atrial filling.
10) Risk for Injury
1) Obtain a history of
allergies prior to the
administration of
antibiotics.
2) Ensure patency of IV
and prevent the
complications of longterm IV therapy.
area), or rupture of a sinus of Valsalva
(if in the aortic area).
Although endocarditis can affect native
and prosthetic valves, infection seldom
affects a previously normal heart – the
majority (60%) of IE patients have a
predisposing cardiac condition.
Vegetations usually affect the left side of
the heart, with the most common
underlying lesions being mitral valve
prolapse and degenerative mitral and
aortic regurgitation.
Constitutional symptoms
Endocarditis should be considered
in patients with vague or
generalized constitutional
symptoms such as fever, rigors,
night sweats, anorexia, weight loss,
or arthralgia.
Cardiac signs
The presence of a new murmur is
very significant, as is a change in
the nature of an existing murmur
(a regurgitant murmur may
disappear on worsening).
Rheumatic disease is a risk factor for the Myocardial involvement or valvular
development of endocarditis. Other
dysfunction may both contribute to
predisposing cardiac lesions include
left ventricular failure.
hypertrophic cardiomyopathy with
associated mitral reflux, subaortic
Skin lesions
stenosis, and ventricular aneurysm.
Endocarditis is indicated by:
There are also congenital lesions that
predispose adults to endocarditis: these
 Osler's nodes – tender
include ventricular septal defect (VSD),
lesions found on finger pulps
bicuspid aortic valve, and coarctation of
and thenar/hypothenar
the aorta.
eminences Janeway lesions
– transient, nontender
Vegetations occur when a high-pressure
macular papules on palms or
jet enters a low-pressure cavity through
soles
3) Observe for signs and
symptoms of
complications such as
CHF, renal failure, or
emboli.
4) Educate the patient
about his condition and
the need for continued
treatment and
prophylactic antibiotics.
5) Teach the patient to
recognize the symptoms
of endocarditis and to
seek medical assistance
should symptoms recur.
a narrow orifice. This explains why
endocarditis complicates a small VSD,
but is not associated with a large VSD,
mitral stenosis, or an atrial septal defect.
In the presence of a VSD, vegetations can
be found on the right ventricular side of
the VSD, on the tricuspid valve, or where
the jet impinges on the right ventricular
wall. Vegetations found in coarctation
usually occur distal to the obstruction.
Finally, in children, cyanotic heart
disease is still the most common cause of
endocarditis, and the risk does not
diminish after surgical repair as
prostheses carry their own risk.
 splinter hemorrhages
 petechiae (embolic or
vasculitic)
 Clubbing– in long-standing
disease.
Eyes
Roth spots (boat-shaped
hemorrhages with pale centers, in
retina) and conjunctival splinter
hemorrhages may be found.
Splenomegaly
Splenic infarction may occur as a
result of emboli. In this case, splenic
palpation may be painful and
tender, and a rub may be heard.
Neurological
An acute confusional state is
common in patients with infective
endocarditis (IE). Cerebral emboli,
which usually affect the middle
cerebral artery, result in
hemiplegia and sensory
dysfunction. Mycotic aneurysms
also affect the middle cerebral
artery, where rupture may cause a
subarachnoid hematoma. Mycotic
aneurysms can occur several years
after endocarditis has been treated.
Renal
Infarction causes loin pain and
hematuria. Immune complex
deposition may result in
glomerulonephritis.
The pathogenesis of myocarditis is not
entirely clear. However, in viralmediated myocarditis, animal models
have implicated 3 significant
mechanisms:
An infectious organism directly invades
the myocardium
Myocarditis
Local and systemic immunological
activation quickly ensues
Cellular (CD4+) and humoral (B-cell
clonal multiplication) activation occurs,
causing worsening local inflammation,
anti-heart antibody production and
further myonecrosis.
Common myocarditis symptoms
include:
 Chest pain
 Rapid or abnormal heart
rhythms (arrhythmias)
 Shortness of breath, at rest
or during physical activity
 Fluid retention with
swelling of your legs, ankles
and feet
 Fatigue
Other signs and symptoms you'd
have with a viral infection, such as
a headache, body aches, joint pain,
fever, a sore throat or diarrhea.
Myocarditis in children
When children develop
myocarditis, they might have
1. Give a comfortable
position (semifowler position).
2. Monitor pain
characteristics and
administer
analgesics as
needed and use
salicylates around
the clock.
3. Give O2
supplement and
ensure saturation
˃90%.
4. Give drugs as
indicated (Aspirin,
Steroids).
5. Give anti pyretic
drug if fever
present.
signs and symptoms including:
 Fever
 Fainting
 Breathing difficulties
 Rapid breathing
 Rapid or abnormal heart
rhythms (arrhythmias)
6. Provide a calm and
quite environment
and give emotional
support while
patient is confined
to hospital or
home with
restrictive
intravenous
therapy.
7. Check vital sign
and record it
carefully.
8. Carefully monitor
intake output.
9. Closely monitor
sign for cardiac
tamponade.
10.
Ensure bed
rest to reduce
myocardial oxygen
requirements and
reduce heart rate.
11.
Ensure rest
and activity
according to
degree of
tolerance.
12.
Ensure high
protein, high
carbohydrate, and
low sodium diet to
meet adequate
nutrition.
13.
Explain all
procedures to
patient that
improve patient
confidence.
14.
Prepare
patient for surgery
if needed
15.
If patient
received surgical
treatment, provide
postsurgical care
and instruction.
16.
After
surgery, monitor
patient’s
temperature, fever
may be present for
weeks.
17.
Provide 4
hourly mouth
cares and serve
attractive meals
that stimulate
appetite.
18.
Instruct to
avoid people who
have an upper
respiratory tract
infection.
19.
Monitor for
signs and
symptoms of organ
damage such as
stroke (CVA, brain
attack), meningitis,
heart failure,
myocardial
infarction,
glomerulonephritis
, and
splenomegaly.
20.
Instruct
patient and family
about activity
restrictions,
medications, and
signs and
symptoms of
infection.
Pericarditis
The pericardium consists of a 2-layered The symptoms of pericarditis
pliable, fibroserous sac that covers the
can include the following:
surface of the heart. The inner layer, the
visceral pericardium, is adherent to the
 Sharp pain in the chest,
myocardium. It has a microvillous
sometimes central, other
surface that secretes pericardial fluid.
times to the left; may
The outer layer, or parietal pericardium,
decrease in intensity when
is contiguous with the inner layer. It is
sitting up and leaning
composed of collagen layers with
forward.
interspersed elastin fibrils. Both layers
 Palpitations
are normally only 1 to 2 mm thick and a
 Shortness of breath,
space containing 15 to 35 mL of
especially when reclining.
pericardial fluid separates them. The
 Minor fever.
pericardium is perfused by the internal
 General weakness.
mammary arteries and innervated by
 Swelling of the abdomen or
the phrenic nerve. The pericardium
legs.
protects and restrains the heart. In
 Cough.
addition, it determines cardiac filling
 Pain in the shoulder.
patterns, limits chamber dilatation, and
equilibrates compliance between the 2
ventricles.
1. Pain r/t pericardial
inflammation.
2. Potential for
decreased CO r/t
cardiac tamponade
(heart cannot fill
up and pump out).
3. Knowledge deficit
r/t procedures &
4. medications& f/u
care.
Valvular Heart
Disease
Mitral Stenosis
Pathophysiology
Sign and symptoms
Mitral valve stenosis commonly
The normal mitral valve has an orifice
leads to shortness of breath,
area of about 4 cm that permits free
especially during exercise or when
flow of blood from the left atrium into
lying down.
the left ventricle during diastole. As the Other common symptoms
valve orifice becomes reduced in mitral include:
stenosis, flow between left atrium and
 cough, with or without blood
left ventricle is progressively impeded
 chest pain, or chest
and pressure in the left atrium remains
discomfort
higher than that of the left ventricle.
 fatigue
By restricting flow, mitral stenosis
 swelling in ankles and/or feet
results in 2 primary pathophysiological
 respiratory infections
consequences:
 plum-colored cheeks
Increased left atrial pressure is
 If mitral valve stenosis is
referred to the lungs, where it leads to
severe, you may feel your
congestion and the symptoms
heart fluttering or beating
associated with it
rapidly.
The restricted orifice limits filling of
Rarely, you may feel discomfort in
the left ventricle, thereby limiting
your chest. Your chest might feel
cardiac output.
tight or constricted, or you may feel
Thus, although left ventricular
pain that radiates outward from
contractility is usually normal, the
your chest.
pathophysiological effects of mitral
stenosis produce a syndrome
In some cases, mitral valve stenosis
mimicking left heart failure.
may not cause any symptoms, or
the symptoms may appear only
during exercise. You might develop
Nursing Care
Activity intolerance
related to pulmonary
congestion and decreased
blood supply to meet the
demands of the body.
symptoms when your body
undergoes stress such as during an
infection or pregnancy.
In addition to the common
symptoms, children with this issue
might experience slower growth.
Mitral
Regurgitation
MR can be caused by organic disease
(e.g., rheumatic fever, ruptured chordae
tendineae, myxomatous degeneration,
leaflet perforation) or a functional
abnormality (i.e., a normal valve may
regurgitate [leak] because of mitral
annular dilatation, focal myocardial
dysfunction, or both). Congenital MR is
rare but is commonly associated with
myxomatous mitral valve disease.
Alternatively, it can be associated with
cleft of the mitral valve, as occurs in
persons with Down syndrome, or an
ostium primum atrial septal defect.
Acute mitral regurgitation
Acute MR is characterized by an
increase in preload and a decrease in
afterload causing an increase in enddiastolic volume (EDV) and a decrease
in end-systolic volume (ESV). This leads
to an increase in total stroke volume
When associated with coronary
artery disease (CAD) and acute
myocardial infarction (MI),
significant acute MR is
accompanied by the following
symptoms:
 Dyspnea
 Fatigue
 Orthopnea
 Pulmonary edema (often the
initial manifestation)
The following may be noted with
chronic MR:
 Some patients may remain
asymptomatic for years.
 Patients may have normal
exercise tolerance until
systolic LV dysfunction
develops, at which point
they may experience
Nursing Care Plans for
Mitral insufficiency, or
mitral regurgitation,
Primary nursing care
plans diagnosis:
Activity intolerance
related to diminished
cardiac output
(TSV) to supernormal levels. However,
forward stroke volume (FSV) is
diminished because much of the TSV
regurgitates as the regurgitate stroke
volume (RSV). This, in turn, results in an
increase in left atrial pressure (LAP).
According to the Laplace principle,
which states that ventricular wall stress
is proportional to both ventricular
pressure and radius, LV wall stress in the
acute phase is markedly decreased since
both of these parameters are reduced.
Chronic compensated mitral
regurgitation
In chronic compensated MR, the left
atrium (LA) and ventricle have sufficient
time to dilate and accommodate the
regurgitant volume. Thus LA pressure is
often normal or only minimally elevated.
Because of the left ventricular dilatation
via the process of eccentric hypertrophy,
TSV and FSV are maintained. Wall stress
may be normal to slightly increased as
the radius of the LV cavity increases but
the end-diastolic LV pressure remains
normal. As the LV progressively
enlarges, the mitral annulus may stretch
and prevent the mitral valve leaflets
symptoms of a reduced
forward cardiac output.
 Patients may feel chest
palpitations if AF develops
as a result of chronic atrial
dilatation.
 Patients with LV
enlargement and more
severe disease eventually
progress to symptomatic
congestive heart failure
(CHF) with pulmonary
congestion and edema.
Palpation may reveal the
following:
 Brisk carotid upstroke and
hyperdynamic cardiac
impulse.
 Prominent LV filling wave.
Auscultation may reveal the
following:
 Diminished S 1 in acute MR
and chronic severe MR with
defective valve leaflets.
 Wide splitting of S 2 as a
from coapting properly during systole,
thus worsening the MR and LV
dilatation.
Chronic decompensated mitral
regurgitation
In the chronic decompensated phase,
muscle dysfunction has developed,
impairing both TSV and FSV (although
ejection fraction still may be normal).
This results in a higher ESV and EDV,
which in turn causes an elevation of LV
and LA pressure, ultimately leading to
pulmonary edema and, if left untreated,
cardiogenic shock.
Mitral Valve
Prolapse
Mitral valve prolapse (MVP) is
characterized primarily by myxomatous
degeneration of the mitral valve leaflets.
In younger populations, there is gross
redundancy of both the anterior and
posterior leaflets and chordal
apparatus. This is the extreme form of
myoxomatous degeneration, known as
Barlow’s syndrome. In older populations,
however, MVP is characterized by
fibroelastic deficiency, sometimes with
superimposed chordal rupture due to a
result of early closure of the
aortic valve.
 S 3 as a result of LV
dysfunction or increased
blood flow across the MV.
 Accentuated P 2 if
pulmonary hypertension is
present.
 Characteristic murmur.
Most people with mitral valve
prolapse have no symptoms. They
also never experience any health
problems due to mitral valve
prolapse.
Consult with and refer to
cardiologist for continued
monitoringand follow-up.
• Teach about MVP,
including heart valve
anatomy, physiology,and
 Chest pain is the most
frequent symptom in people function, common
manifestations of MVP,
who have symptoms with
and treatment
mitral valve prolapse. The
rationale.
chest pain may be very
bothersome and frightening, • Discuss symptoms of
lack of connective tissue support. These
anatomic abnormalities result in
malcoaptation of mitral valve leaflets
during systole, resulting in
regurgitation. Mitral annular dilatation
may also develop over time, resulting in
further progression of mitral
regurgitation (MR). Acute severe MR
results in congestive heart failure
symptoms without left ventricular
dilatation. Conversely, chronic or
progressively severe MR can lead to
ventricular dilatation and dysfunction,
neurohormonal activation, and heart
failure. Elevation in left atrial pressures
can result in left atrial enlargement,
atrial fibrillation, pulmonary congestion,
and pulmonary hypertension.
Myxomatous proliferation is the most
common pathologic basis for MVP, and
it can lead to myxomatous degeneration
of the loose spongiosa and
fragmentation of the collagen fibrils.
Disruption of the endothelium may
predispose patients to infectious
endocarditis and thromboembolic
complications. However, the vast
majority of patients with MVP have only







but it does not increase the
progressive mitral
risk of heart attack, death, or regurgitation, and
other heart problems.
theneed to report these to
the cardiologist.
• Discuss recommended
Mitral valve prolapse is the
follow-up care and its
most common cause
rationale.
of mitral regurgitation.
• Allow to verbalize
That's a condition in which
some blood flows backward feelings and share
concerns about MVP.
through the mitral valve
Encourage to attend an
with each heartbeat.
MVP support group
meeting.
Over years, moderate or
• Discuss the prognosis
severe mitral regurgitation
for MVP, emphasizing
can cause weakness of the
that most clientslive
heart muscle, known
normal lives using diet
as congestive heart failure.
and lifestyle
Symptoms of congestive
management.
heart failure include:
• Instruct to keep a
Shortness of breath with
weekly record of
exertion
Swelling in the legs and feet symptoms and their
frequencyfor 1 month.
• Discuss lifestyle changes
Mitral valve prolapse has
to manage symptoms:
also been associated with
aerobic exercisewith
other symptoms:
Fluttering or rapid heartbeat warmup and cooldown
periods; maintaining
called palpitations
adequatefluid intake,
Shortness of breath,
a minor derangement of the mitral valve
structure that is usually clinically
insignificant.




especially with exercise
Dizziness
Passing out or fainting ,
known as syncope
Panic and anxiety
Numbness or tingling in the
hands and feet
especially during hot
weather or exercise;
relaxation techniques
(e.g., meditation, deepbreathing exercises,music
therapy, yoga, guided
imagery, heat therapy,
orprogressive muscle
relaxation) to perform
daily; avoiding
caffeineand crash diets;
forming healthy eating
habits.
• Teach about infective
endocarditis risk and
prevention
withprophylactic
antibiotics. Encourage
notifying dentist and
otherhealth care
providers of MVP before
dental or any invasive
procedure.
Aortic Stenosis
The human aortic valve normally
consists of three cusps or leaflets and
has an opening of 3.0-4.0 square
centimeters. When the left ventricle
contracts, it forces blood through the
valve into the aorta and subsequently to
the rest of the body. When the left
ventricle expands again, the aortic valve
closes and prevents the blood in the
aorta from flowing backward
(regurgitation) into the left ventricle. In
aortic stenosis, the opening of the aortic
valve becomes narrowed or constricted
(stenotic) (i.e., due to calcification).
Degenerative aortic stenosis, the most
common variety, and bicuspid aortic
stenosis both begin with damage to
endothelial cells from increased
mechanical stress. Inflammation is
thought to be involved in the earlier
stages of the pathogenesis of AS and its
associated risk factors are known to
promote the deposition of LDL
cholesterol and a highly damaging
substance known as Lipoprotein(a) into
the aortic valve resulting in significant
damage and stenosis over time.
Symptoms related to aortic stenosis Assist the patient in
depend on the degree of stenosis.
bathing, if necessary.
Most people with mild to moderate
1. Provide a bedside
aortic stenosis do not have
commode because
symptoms. Symptoms usually
using a commode
present in individuals with severe
puts less stress on
aortic stenosis, though they may
the heart than
occur in those with mild to
using a bedpan.
moderate aortic stenosis as well.
2. Offer diversional
activities that are
Angina
physically
Angina in setting of heart failure
undemanding.
also increases the risk of death. In
3. Alternate periods of
people with angina, the 5-year
rest to prevent
mortality rate is 50% if the aortic
extreme fatigue
valve is not replaced.
and dyspnea.
4. To reduce anxiety,
Syncope
allow the patient to
Syncope(fainting spells) from
express his
aortic valve stenosis is usually
concerns about the
exertional. In the setting of heart
effects of activity
failure it increases the risk of death.
restrictions on his
In people with syncope, the 3 year
resposibilities and
mortality rate is 50%, if the aortic
routine.
valve is not replaced.
5. Keep the patient’s
legs elevated while
Congestive heart failure
he sits in a chair to
Congestive heart failure (CHF)
improve venous
As a consequence of this stenosis, the left carries a grave prognosis in people
return in the heart.
ventricle must generate a higher
pressure with each contraction to
effectively move blood forward into the
aorta. Initially, the LV generates this
increased pressure by thickening its
muscular walls (myocardial
hypertrophy). The type of hypertrophy
most commonly seen in AS is known as
concentric hypertrophy, in which the
walls of the LV are (approximately)
equally thickened.
In the later stages, the left ventricle
dilates, the wall thins, and the systolic
function deteriorates (resulting in
impaired ability to pump blood
forward). Morris and Innasimuthu et al.
showed that different coronary anatomy
is associated with different valve
diseases. Research is ongoing to see if
different coronary anatomy might lead
to turbulent flow at the level of valves
leading to inflammation and
degeneration.
with AS. People with CHF
attributable to AS have a 2-year
mortality rate of 50% if the aortic
valve is not replaced.[citation
needed] CHF in the setting of AS is
due to a combination of left
ventricular hypertrophy with
fibrosis, systolic dysfunction (a
decrease in the ejection fraction)
and diastolic dysfunction (elevated
filling pressure of the LV).
Associated symptoms
In Heyde's syndrome, aortic
stenosis is associated with
gastrointestinal bleeding due
toangiodysplasia of the colon.
Recent research has shown that the
stenosis causes a form of von
Willebrand disease by breaking
down its associated coagulation
factor (factor VIII-associated
antigen, also called von Willebrand
factor), due to increased turbulence
around the stenotic valve.
6. Place the patient in
an upright position
to relieve dyspnea.
7. Administer oxygen
as needed to
prevent tissue
hypoxia.
8. 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.
9. Allow the patient to
express his fears
and concerns about
the disorder, it’s
impact on his life,
and any impending
surgery.
10.
Monitor the
patient’s vital signs,
weight, and intake
and output for
signs of fluid
overload.
11.
Evaluate
patient’s activity
tolerance and
degree of fatigue.
12.
Monitor the
patient for chest
pain that may
indicate cardiac
ischemia.
13.
Regularly
assess the patient’s
cardiopulmonary
function.
14.
Observe the
patient for
complications and
adverse reactions
to drug therapy.
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
Aortic
Regurgitation
Symptoms of aortic insufficiency Assess mental status
are similar to those of heart
(Restlessness, severe
failure and include the following: anxiety and confusion).
1. Check vital signs
(heart rate and
 Dyspnea on exertion
blood pressure).
 Orthopnea
2. Assess heart
 Paroxysmal nocturnal
sounds, noting
dyspnea
gallops, S3, S4.
 Palpitations
Acute AR of significant severity leads to
3. Assess manually
 Angina pectoris
increased blood volume in the LV during
peripheral pulses
 Cyanosis (in acute cases)
diastole. The LV does not have sufficient
(with weak rate,
time to dilate in response to the sudden
rhythm indicated
increase in volume.
low cardiac
output).
Chronic aortic regurgitation
4. Assess lung sounds
and determine any
Chronic AR causes gradual left
occurrence of
ventricular volume overload that leads
Paroxysmal
to a series of compensatory changes,
Nocturnal Dyspnea
including LV enlargement and eccentric
(PND) or
hypertrophy. LV dilation occurs through
orthopnea.
the addition of sarcomeres in series
5. Monitor central
(resulting in longer myocardial fibers),
venous, right
as well as through the rearrangement of
arterial pressure
myocardial fibers.
[RAP], pulmonary
arterial
pressure(PAP)
6. Routinely Assess
skin colour and
temperature (Cold,
clammy skin is
secondary to
compensatory
increase in
sympathetic
nervous system
stimulation and
low cardiac output
and desaturation).
7. Carefully maintain
intake output and
daily check weight.
8. Administer
medication as
prescribed, noting
response and
watching for side
effects and toxicity.
9. Administer stool
softeners as
needed(s training
for a bowel
movement further
impairs cardiac
output).
10.
Explain drug
regimen, purpose,
dose, and side
effects.
11.
Maintain
adequate
ventilation and
perfusion (Place
patient in semi- to
high-Fowler’s
position or supine
position).
12.
Administer
O2 as ordered.
13.
Assess
response to
increased activity
and help patient in
daily activities.
14.
Maintain
physical and
emotional rest
(restrict activity
and provide quiet
and relaxed
environment).
15.
Monitor sleep
patterns;
administer
sedative.
16.
If invasive
adjunct therapies
are indicated (e.g.,
intra-aortic balloon
pump, pacemaker),
maintain within
prescribed protocol
and prepare
patient.
17.
Explain diet
restrictions (fluid,
sodium).
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
Tricuspid stenosis 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
There are few symptoms to
report. Many patients with this
condition at times report feeling:
 tired and lethargic
 fragility
 a quivering feeling in the
neck
 A rapid, irregular heartbeat
called a palpitation, or both.
 Pain in the upper right part
of their abdomen which may
Assessment and
treatment of the
underlying aetiology
for the valvular
pathology (e.g.,
antibiotics for bacterial
endocarditis or
somatostatin analogues
for carcinoid syndrome)
1. Fluid and sodium
become shortened. The restricted valve
be caused by an enlarged,
opening hampers blood flow into the
congested liver.
right ventricle and, subsequently, to the Symptoms are rarely dramatic
pulmonary vasculature. Right atrial
enough to require surgery to
enlargement is observed as a
replace the tricuspid valve.
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, endomyocardial
fibrosis, systemic lupus erythematosus,
and congenital tricuspid atresia.
In the rare instances of congenital
tricuspid stenosis, the valve leaflets may
manifest various forms of deformity,
which can include deformed leaflets,
deformed chordae, and displacement of
the entire valve apparatus. Other
cardiac anomalies are usually present.
Tricuspid
Regurgitation
Normal tricuspid valves develop
dysfunction with elevation of right
ventricular systolic and/or diastolic
pressure, right ventricular cavity
enlargement, or tricuspid annular
dilation with leaflet tethering. View
image The pathological consequences of
restriction
2. Medicines to treat
cardiac
arrhythmias
secondary to right
atrial distension
(usually atrial
fibrillation and/or
flutter)
3. Pharmacotherapy
with diuretics to
reduce morbidity
associated with
systemic venous
congestion.
Activity is usually selflimited by the patient due
to easy tiring and
diminished pulmonary
blood flow.
Mild tricuspid regurgitation may
1. For patients in
not cause any symptoms.
whom tricuspid
Symptoms of heart failure may
regurgitation is
occur, and can include:
secondary to leftsided heart failure,
Active pulsing in the neck veins
treatment centers
Decreased urine output
on adequate
advanced tricuspid regurgitation (TR)
are related to a reduced cardiac output
and elevated right atrial pressure,
which, if long-standing, leads to atrial
distension with reduced contractile
reserve and atrial fibrillation. Often,
patients with chronic severe TR will
present with ascites from advanced liver
disease from chronic congestion or
fibrosis (cardiac cirrhosis), gut
congestion with symptoms of dyspepsia
or indigestion, and fluid retention with
leg oedema.
Fatigue, tiredness
General swelling
Swelling of the abdomen
Swelling of the feet and ankles
Weakness
control of fluid
overload and
failure symptoms
(eg, diuretic
therapy). Patients
should be
instructed to
reduce their intake
of salt. Elevation of
the head of the bed
may improve
symptoms of
shortness of breath.
2. Digitalis, diuretics
(including
potassium-sparing
agents),
angiotensinconverting enzyme
(ACE) inhibitors,
and anticoagulants
are all indicated in
the care of these
patients.
Antiarrhythmics
are added as
needed to control
atrial fibrillation.
PS can be due to isolated valvular
(90%), subvalvular, or peripheral
(supravalvular) obstruction, or it may
be found in association with more
complicated congenital heart disorders.
The characteristics of the various types
of PS are described in this section.
Valvular pulmonic stenosis
Isolated valvular PS comprises
approximately 10% of all congenital
heart disease. Typically, the valve
commissures are partially fused and the
Pulmonic Stenosis 3 leaflets are thin and pliant, resulting in
a conical or dome-shaped structure with
a narrowed central orifice. Poststenotic
pulmonary artery dilatation may occur
owing to "jet-effect" hemodynamics.
Subvalvular pulmonic stenosis
Subvalvular PS occurs as a narrowing of
the infundibular or subinfundibular
region, often with a normal pulmonic
valve. This condition is present in
individuals with tetralogy of Fallot and
can also be associated with a ventricular
septal defect (VSD).
Pulmonary valve stenosis affects
the body’s ability to get oxygenated
blood. Many children do not show
symptoms until adulthood.
Examples of pulmonary valve
stenosis symptoms include:
Sometimes, treatment
may not be needed if the
disorder is mild.
When there are also
other heart defects,
medications may be
used to:
heart murmur
 Help blood flow
prominent and enlarged jugular
through the heart
vein
(prostaglandins)
bluish tint to the skin
 Help the heart beat
chest pain
stronger
fainting
 Prevent clots (blood
heart palpitations
thinners)
unexplained fatigue
 Remove excess fluid
failure to thrive
(water pills)
difficulty breathing
 Treat abnormal
Pulmonary valve stenosis can cause
heartbeats and
sudden death in severe instances.
rhythms
This is why diagnosis and
treatment is vital to your health.
Percutaneous balloon
pulmonary dilation
(valvuloplasty) may be
performed when no
other heart defects are
present.
 This procedure is
done through an
artery in the groin.
 The doctor sends a
flexible tube
(catheter) with a
balloon attached to
the end up to the
heart. Special xrays are used to
help guide the
catheter.
 The balloon
stretches the
opening of the
valve.
Some patients may need
heart surgery to repair or
replace the pulmonary
valve. The new valve can
be made from different
materials. If the valve
cannot be repaired or
replaced, other
procedures may be
needed.
Double-chambered right ventricle is a
rare condition associated with
fibromuscular narrowing of the right
ventricular outflow tract with right
ventricular outflow obstruction at the
subvalvular level.
Pulmonic
Regurgitation
Incompetence of the pulmonic valve
occurs by 1 of 3 basic pathologic
Because pulmonic regurgitation is
the result of other factors in the
Pulmonic regurgitation is
seldom severe enough to
processes: dilatation of the pulmonic
valve ring, acquired alteration of
pulmonic valve leaflet morphology, or
congenital absence or malformation of
the valve.
body, any noticeable symptoms are
ultimately caused by an underlying
medical condition rather than the
regurgitation itself.
warrant special
treatment because the
right ventricle normally
adapts to low-pressure
volume overload without
However, more severe
difficulty. High-pressure
regurgitation may contribute to
volume overload leads to
right ventricular enlargement by
right-sided heart strain
dilation, and in later stages, right
and, ultimately, heart
heart failure.
failure.
1. Underlying
A diastolic decrescendo murmur
etiologies causing
can sometimes be identified,( heard
severe pulmonic
best) over the left lower sternal
regurgitation,
border
whether congenital
or acquired, must
be treated to
prevent or reverse
right-sided heart
strain and failure
that may further
complicate the
clinical picture.
2. 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.
3. 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.
4. 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 (see
Heart Failure).
5. The American
Heart Association
and the American
College of
Cardiology have
published
guidelines on the
management of
patients with
valvular heart
disease.
The pathophysiology of
cardiomyopathies is better understood
at the cellular level with advances in
molecular techniques. Mutant proteins
can disturb cardiac function in the
contractile apparatus (or
mechanosensitive complexes).
Cardiomyocyte alterations and their
persistent responses at the cellular level
cause changes that are correlated with
sudden cardiac death and other cardiac
problems.
Cardiomyopathy
Symptoms may appear at any age
and usually include signs of
pulmonary congestion and/or low
cardiac output. There is often a
history of fatigue and exertional
symptoms for months or even years
prior to diagnosis (Elliott, 2000).
Symptoms are often progressive
and can necessitate cardiac
transplantation. Arrhythmias,
thromboembolism and sudden
death are common and may occur
at any stage. Symptoms include
dyspnoea, palpitations, reduced
exercise capacity, fatigue,
orthopnoea, paroxysmal nocturnal
dyspnoea, oedema and syncope.
The presentation within a
family may range from
the asymptomatic
patient, who requires no
treatment, to heart
failure and in some cases,
sudden cardiac death.
Cardiomyopathy is a
chronic condition with
extensive emotional and
social ramifications.
Anxiety levels are high,
especially in symptomatic
patients (Cox et al, 1997).
Cardiomyopathy is
genetically inherited in
many cases, giving rise to
fear of transmission and
issues surrounding
genetic counselling.
Parents may feel guilty
for passing on the
condition and it can
change family dynamics.
The nurse is in an ideal
position to help guide the
family through the
difficult stages of
diagnosis and treatment
and support the family
through the screening
process.