Download Cardiovascular Disorders

Cardiovascular Disorders
Inflammatory
Heart Disease
Rheumatic
Fever/Rheumat
ic 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 tissues. After an
incubation period of 2-4 days, the invading
organisms elicit an 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.
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
Heart inflammation (carditis)
 Shortness of breath, particularly when of peripheral blood vessels.
you're physically active or when
3) Acute Pain
sleeping (it can often wake you up,
Related to: inflammation of the
gasping for breath).
synovial membrane.
 Persistent cough rapid heartbeat
(tachycardia).
4) Hyperthermia
 Feeling tired all the time.
Related to: inflammation of the
 Chest pain.
synovial membrane, and
Creditis can persist for several months, but it inflammation of the heart valves.
should improve over time.
5) Imbalanced Nutrition, Less
Cardiovascular Disorders
Sydenham's chorea
Sydenham's chorea is a term that describes a
collection of symptoms related to
inflammation of the nerves. These symptoms
are:
 Involuntary and uncontrollable
jerking and twitching of the body –
most often, the hands and feet.
 difficulty with tasks requiring fine
hand movements, such as writing.
 problems with balance.
 unusual emotional outbursts, such as
crying or laughing for no apparent
reason.
Skin rash
The rash is usually painless, non-itchy 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,
before disappearing altogether.
It's rare for adults with rheumatic fever to
Than Body Requirements
Related to: an increase in
stomach acid caused by the
sympathetic nervous system
compensation.
6) Activity intolerance
Related to: muscle weakness,
prolonged bed rest or
immobilization.
7) Self-Care Deficit
Related to: Musculoskeletal
Disorders: polyarthritis /
arthralgia and therapy bed rest.
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.
Cardiovascular Disorders
develop a skin rash.
10) Risk for Injury
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 area), or rupture of a sinus of
Valsalva (if in the aortic area).
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.
Constitutional symptoms
1) Obtain a history of allergies
prior to the administration of
antibiotics.
2) Ensure patency of IV and
prevent the complications of
long- term IV therapy.
3) Observe for signs and
symptoms of complications such
Cardiovascular Disorders
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.
Rheumatic disease is a risk factor for the
development of endocarditis. Other predisposing
cardiac lesions include hypertrophic
cardiomyopathy with associated mitral reflux,
subaortic stenosis, and ventricular aneurysm. There
are also congenital lesions that predispose adults to
endocarditis: these include ventricular septal defect
(VSD), bicuspid aortic valve, and coarctation of the
aorta.
Vegetations occur when a high-pressure jet enters a
low-pressure cavity through 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
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). Myocardial
involvement or valvular dysfunction may
both contribute to left ventricular failure.
Skin lesions
Endocarditis is indicated by:
 Osler's nodes – tender lesions found
on finger pulps and thenar/hypothenar
eminences Janeway lesions –
transient, nontender macular papules
on palms or soles
 splinter hemorrhages
 petechiae (embolic or vasculitic)
 Clubbing – in long-standing disease.
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.
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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.
Eyes
Roth spots (boat-shaped hemorrhages with
pale centers, in retina) and conjunctival
splinter hemorrhages may be found.
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.
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.
Cardiovascular Disorders
The pathogenesis of myocarditis is not entirely
clear. However, in viral-mediated myocarditis,
animal models have implicated 3 significant
mechanisms:
An infectious organism directly invades the
myocardium
Local and systemic immunological activation
quickly ensues
Myocarditis
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 signs and symptoms including:
 Fever
 Fainting
 Breathing difficulties
 Rapid breathing
 Rapid or abnormal heart rhythms
(arrhythmias)
1. Give a comfortable
position (semi-fowler
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.
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
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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
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(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 pliable,
fibroserous sac that covers the surface of the heart.
The inner layer, the visceral pericardium, is
adherent to the myocardium. It has a microvillous
surface that secretes pericardial fluid. The outer
layer, or parietal pericardium, is contiguous with the
inner layer. It is composed of collagen layers with
interspersed elastin fibrils. Both layers are normally
only 1 to 2 mm thick and a space containing 15 to
35 mL of pericardial fluid separates them. The
pericardium is perfused by the internal mammary
The symptoms of pericarditis can include the
following:
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Sharp pain in the chest, sometimes
central, other times to the left; may
decrease in intensity when sitting up
and leaning forward.
Palpitations
Shortness of breath, especially when
reclining.
Minor fever.
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General weakness.
Swelling of the abdomen or legs.
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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.
Cardiovascular Disorders
arteries and innervated by the phrenic nerve. The
pericardium protects and restrains the heart. In
addition, it determines cardiac filling patterns, limits
chamber dilatation, and equilibrates compliance
between the 2 ventricles.
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Cough.
Pain in the shoulder.
Cardiovascular Disorders
Valvular Heart
Pathophysiology
Disease
Mitral Stenosis
The normal mitral valve has an orifice area of about
4 cm that permits free flow of blood from the left
atrium into the left ventricle during diastole. As the
valve orifice becomes reduced in mitral stenosis,
flow between left atrium and left ventricle is
progressively impeded and pressure in the left
atrium remains higher than that of the left ventricle.
By restricting flow, mitral stenosis results in 2
primary pathophysiological consequences:
Increased left atrial pressure is referred to the lungs,
where it leads to congestion and the symptoms
associated with it
The restricted orifice limits filling of the left
ventricle, thereby limiting cardiac output.
Thus, although left ventricular contractility is usually
normal, the pathophysiological effects of mitral
stenosis produce a syndrome mimicking left heart
failure.
Sign and symptoms
Mitral valve stenosis commonly leads to
shortness of breath, especially during exercise
or when lying down.
Other common symptoms include:
 cough, with or without blood
 chest pain, or chest discomfort
 fatigue
 swelling in ankles and/or feet
 respiratory infections
 plum-colored cheeks
 If mitral valve stenosis is severe, you
may feel your heart fluttering or
beating rapidly.
Rarely, you may feel discomfort in your chest.
Your chest might feel tight or constricted, or
you may feel pain that radiates outward from
your chest.
In some cases, mitral valve stenosis may not
cause any symptoms, or the symptoms may
appear only during exercise. You might
develop 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.
Nursing Care
Activity intolerance related to
pulmonary congestion and
decreased blood supply to meet
the demands of the body.
Cardiovascular Disorders
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.
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)
Acute mitral regurgitation
Acute MR is characterized by an increase in preload
and a decrease in afterload causing an increase in
end-diastolic volume (EDV) and a decrease in endsystolic volume (ESV). This leads to an increase in
total stroke volume (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.
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 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.
Chronic compensated mitral regurgitation
Palpation may reveal the following:
In chronic compensated MR, the left atrium (LA) and
 Brisk carotid upstroke and
ventricle have sufficient time to dilate and
hyperdynamic cardiac impulse.
accommodate the regurgitant volume. Thus LA
 Prominent LV filling wave.
Nursing Care Plans for Mitral
insufficiency, or mitral
regurgitation,
Primary nursing care plans
diagnosis:
Activity intolerance related to
diminished cardiac output
Cardiovascular Disorders
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 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 lack of connective tissue support. These
anatomic abnormalities result in malcoaptation of
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 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.

Chest pain is the most frequent
symptom in people who have
symptoms with mitral valve prolapse.
The chest pain may be very
bothersome and frightening, but it
does not increase the risk of heart
attack, death, or other heart
Consult with and refer to
cardiologist for continued
monitoring and follow-up.
• Teach about MVP, including
heart valve anatomy,
physiology,and function, common
manifestations of MVP, and
treatment
rationale.
• Discuss symptoms of
Cardiovascular Disorders
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 a minor derangement
of the mitral valve structure that is usually clinically
insignificant.
problems.

Mitral valve prolapse is the most
common cause of mitral regurgitation.
That's a condition in which
some blood flows backward through
the mitral valve with each heartbeat.

Over years, moderate or severe mitral
regurgitation can cause weakness of
the heart muscle, known
as congestive heart failure. Symptoms
of congestive heart failure include:
Shortness of breath with exertion
Swelling in the legs and feet
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Mitral valve prolapse has also been
associated with other symptoms:
Fluttering or rapid heartbeat called
palpitations
Shortness of breath, especially
with exercise
Dizziness
Passing out or fainting , known as
syncope
Panic and anxiety
Numbness or tingling in the hands and
feet
progressive mitral regurgitation,
and the need to report these to
the cardiologist.
• Discuss recommended followup care and its rationale.
• Allow to verbalize feelings and
share concerns about MVP.
Encourage to attend an MVP
support group meeting.
• Discuss the prognosis for MVP,
emphasizing that most clients live
normal lives using diet and
lifestyle management.
• Instruct to keep a weekly record
of symptoms and their frequency
for 1 month.
• Discuss lifestyle changes to
manage symptoms: aerobic
exercise with warmup and
cooldown periods; maintaining
adequate fluid intake, especially
during hot weather or exercise;
relaxation techniques (e.g.,
meditation, deep-breathing
exercises, music therapy, yoga,
guided imagery, heat therapy, or
progressive muscle relaxation) to
perform daily; avoiding caffeine
and crash diets; forming healthy
eating habits.
• Teach about infective
endocarditis risk and prevention
Cardiovascular Disorders
with prophylactic antibiotics.
Encourage notifying dentist and
other health 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 depend
on the degree of stenosis. Most people with
mild to moderate aortic stenosis do not have
symptoms. Symptoms usually present in
individuals with severe aortic stenosis, though
they may occur in those with mild to
moderate aortic stenosis as well.
Angina
Angina in setting of heart failure also
increases the risk of death. In people with
angina, the 5-year mortality rate is 50% if the
aortic valve is not replaced.
Syncope
Syncope (fainting spells) from aortic valve
stenosis is usually exertional. In the setting of
heart failure it increases the risk of death. In
people with syncope, the 3 year mortality rate
is 50%, if the aortic valve is not replaced.
Assist the patient in bathing, if
necessary.
1. Provide a bedside
commode because using
a commode puts less
stress on the heart than
using a bedpan.
2. Offer diversional
activities that are
physically undemanding.
3. Alternate periods of rest
to prevent extreme
fatigue and dyspnea.
4. To reduce anxiety, allow
the patient to express his
concerns about the
effects of activity
restrictions on his
resposibilities and
routine.
5. Keep the patient’s legs
Cardiovascular Disorders
As a consequence of this stenosis, the left 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.
Congestive heart failure
Congestive heart failure (CHF) carries a grave
prognosis in people 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
to angiodysplasia 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.
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elevated while he sits in a
chair to improve venous
return in the heart.
Place the patient in an
upright position to relieve
dyspnea.
Administer oxygen as
needed to prevent tissue
hypoxia.
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.
Allow the patient to
express his fears and
concerns about the
disorder, it’s impact on
his life, and any
impending surgery.
Monitor the patient’s
vital signs, weight, and
intake and output for
signs of fluid overload.
Evaluate patient’s activity
tolerance and degree of
fatigue.
Monitor the patient for
chest pain that may
indicate cardiac ischemia.
Cardiovascular Disorders
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
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.
Chronic aortic regurgitation
Chronic AR causes gradual left ventricular volume
overload that leads to a series of compensatory
Symptoms of aortic insufficiency are similar
to those of heart failure and include the
following:
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Dyspnea on exertion
Orthopnea
Paroxysmal nocturnal dyspnea
Palpitations
Angina pectoris
Cyanosis (in acute cases)
Assess mental status
(Restlessness, severe anxiety and
confusion).
1. Check vital signs (heart
rate and blood pressure).
2. Assess heart sounds,
noting gallops, S3, S4.
3. Assess manually
peripheral pulses (with
weak rate, rhythm
indicated low cardiac
output).
4. Assess lung sounds and
determine any
occurrence of Paroxysmal
Nocturnal Dyspnea (PND)
Cardiovascular Disorders
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.
or orthopnea.
5. Monitor central venous,
right arterial pressure
[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
Cardiovascular Disorders
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(Place patient in semi- to
high-Fowler’s position or
supine position).
Administer O2 as
ordered.
Assess response to
increased activity and
help patient in daily
activities.
Maintain physical and
emotional rest (restrict
activity and provide quiet
and relaxed
environment).
Monitor sleep patterns;
administer sedative.
If invasive adjunct
therapies are indicated
(e.g., intra-aortic balloon
pump, pacemaker),
maintain within
prescribed protocol and
prepare patient.
Explain diet restrictions
(fluid, sodium).
Cardiovascular Disorders
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 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,
endomyocardial fibrosis, systemic lupus
erythematosus, and congenital tricuspid atresia.
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 be caused by an
enlarged, congested liver.
Symptoms are rarely dramatic enough to
require surgery to replace the tricuspid valve.
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
advanced tricuspid regurgitation (TR) are related to a
Mild tricuspid regurgitation may not cause
any symptoms. Symptoms of heart failure
may occur, and can include:
Active pulsing in the neck veins
Decreased urine output
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
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 self-limited by
the patient due to easy tiring and
diminished pulmonary blood
flow.
1. For patients in whom
tricuspid regurgitation is
secondary to left-sided
heart failure, treatment
centers on adequate
control of fluid overload
Cardiovascular Disorders
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
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 potassiumsparing agents),
angiotensin-converting
enzyme (ACE) inhibitors,
and anticoagulants are all
indicated in the care of
these patients.
Antiarrhythmics are
added as needed to
control atrial fibrillation.
Pulmonic
Stenosis
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.
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:
Valvular pulmonic stenosis
Isolated valvular PS comprises approximately 10% of
all congenital heart disease. Typically, the valve
commissures are partially fused and the 3 leaflets
heart murmur
prominent and enlarged jugular vein
bluish tint to the skin
chest pain
Sometimes, treatment may not
be needed if the disorder is mild.
When there are also other heart
defects, medications may be
used to:
 Help blood flow through
the heart
(prostaglandins)
 Help the heart beat
stronger
Cardiovascular Disorders
are thin and pliant, resulting in a conical or domeshaped 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).
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.
fainting
heart palpitations
unexplained fatigue
failure to thrive
difficulty breathing
Pulmonary valve stenosis can cause sudden
death in severe instances. This is why
diagnosis and treatment is vital to your health.



Prevent clots (blood
thinners)
Remove excess fluid
(water pills)
Treat abnormal
heartbeats and rhythms
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 x-rays 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.
Cardiovascular Disorders
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 absence or
malformation of the valve.
Because pulmonic regurgitation is the result of
other factors in the body, any noticeable
symptoms are ultimately caused by an
underlying medical condition rather than the
regurgitation itself.
However, more severe regurgitation may
contribute to right ventricular enlargement by
dilation, and in later stages, right heart failure.
Pulmonic
Regurgitation
A diastolic decrescendo murmur can
sometimes be identified,( heard best) over the
left lower sternal border
Pulmonic regurgitation is seldom
severe enough to warrant special
treatment because the right
ventricle normally adapts to lowpressure volume overload
without difficulty. High-pressure
volume overload leads to rightsided heart strain and, ultimately,
heart failure.
1. Underlying etiologies
causing severe pulmonic
regurgitation, whether
congenital or acquired,
must be treated to
prevent or reverse rightsided 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
Cardiovascular Disorders
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 rightsided heart failure is
beyond the scope of this
article. In general, similar
approaches to those used
in the treatment of
patients with left-sided
congestive heart failure
Cardiovascular Disorders
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.
Cardiomyopathy
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.
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).
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.
Symptoms are often progressive and can
necessitate cardiac transplantation.
Arrhythmias, thromboembolism and sudden
death are common and may occur at any
Cardiomyopathy is a chronic
condition with extensive
emotional and social
ramifications. Anxiety levels are
Cardiovascular Disorders
stage. Symptoms include dyspnoea,
palpitations, reduced exercise capacity,
fatigue, orthopnoea, paroxysmal nocturnal
dyspnoea, oedema and syncope.
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.
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