lOMoARcPSD|11919074
Cardiac study guide
Nursing Fundamentals (Herzing University)
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lOMoARcPSD|11919074
3-1
Cardiovascular system : Anatomy & Physiology
Function of circulation:
Delivers 02, nutrients, hormones and
antibodies to organs, tissues and cells.
Removes the end product of cellular
metabolism.
1.
Function of the heart
Pumps oxygenated blood into the
arterial system to supply capillaries
and tissue.
Pumps oxygen poor blood from the
venous system through the lungs
to be reoxygenated.
2.
3.
Anatomy of the heart
4.
Cone shaped organ located in the
mediastinal space.
The pericardial sac encases the
heart and protects it, lubricates and
holds 5-20 ml of pericardial fluid.
This has two layers.
❖
the parietal pericardium
which is the outer
membrane.
❖
the visceral pericardium is
the inner membrane
attached to the heart.
Consists of 3 layers
❖
❖
❖
Epicardium : outermost
layer of the heart.
Myocardium: middle layer
of the heart, the
contracting muscle.
Endocardium: innermost
layer of the heart, lines the
inner chambers and the
valves.
4 chambers
❖
❖
❖
❖
4 valves
Two atrioventricular valves that close
at the beginning of ventricular
contraction. They prevent blood from
flowing back into the atria.
❖
❖
5.
6.
Tricuspid valve : on the
right side of the heart.
Bicuspid valve: on the left
side of the heart.
Two semilunar valves that prevent
blood from flowing back into the
ventricles during relaxation.
❖
Pulmonic semilunar valve:
between the right ventricle
and pulmonary artery.
❖
Aortic semilunar valve:
between the ventricle and
the aorta.
Right atrium: carries
deoxygenated blood from
the body via superior and
inferior vena cava.
Right ventricle: carries
blood from the right atrium
and pumps it into the lungs
through the pulmonary
artery.
Left atrium: carries
oxygenated blood from the
pulmonary veins.
Left ventricle: carries
oxygenated blood from the
left atrium and pumps it
into the systemic circuit
through the aorta.
❖
Right main coronary artery:
supplies the right atrium and
ventricle, the inferior left
ventricle, posterior septal
wall, SA and AV nodes.
Left main coronary artery:
consists of two main
branches left anterior
descending which supplies
blood to the left ventricle
and the ventricular septum
and circumflex arteries
which supply blood to the
left atrium and the
lateral/posterior aspects of
the left ventricle.
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From the superior and
inferior vena cava, oxygen
poor blood goes to the
right atria through the
tricuspid valve.
Right ventricle to the
pulmonary valve.
To the pulmonary trunk
and arteries into the lungs
CO2 is lost and 02 is gained
in the pulmonary
capillaries.
O2 rich blood enters the
pulmonary veins to the left
atrium.
Blood travels through the
bicuspid valve and enters
the left ventricle.
Blood moves through the
aortic valve and travels
through the aorta to the
systemic circuit.
Electrical conduction:
❖
SA node: pacemaker of
the heart and initiates
contraction at 60- 100
BPM.
❖
AV : receives impulses
from the SA node initiates
and sustains impulses at
40-60 BPM.
❖
Bundle of His:
continuation of the AV
node and branches into the
the bundle branches which
terminate in the purkinje
fibers.
❖
Purkinje fibers: network of
conducting strands
beneath the ventricular
endocardium. They can act
as a pacemaker when the
SA and AV fail as pace
makers. They can sustain
at 20-40 BPM.
Coronary arteries
❖
Blood flow of the heart
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3-1
lOMoARcPSD|11919074
Hypertension
3-2
What am I?
An elevation in blood pressure
above normal range.
❖
Prehypertension:
120-139/80-90 mmhg
❖
Stage1: 140-159/ 90-99
mmhg
❖
Stage 2: > 160/99 mmhg
Major risk factor for diseases
such as:
❖
Coronary,
❖
Cerebral,
❖
Renal, and
❖
PVD.
Assessment:
CNS: Visual changes, dizziness,
tinnitus,headache.
HEART : Increased HR, flushed
face.
RESP : Chest pain.
MISC.: Epistaxis.
❖
❖
❖
❖
Teaching:
H: Headaches
E: Epistaxis
A: Asymptomatic
R: Really bad chest pain
T : Tinnitus
❖
❖
❖
❖
❖
cardiac diet:
Low in sodium, and
Low saturated fat, trans fat
and cholesterol.
The client should read labels to
identify heart-healthy foods.
❖
❖
Physiology:
Hypertension is a chronic elevation
of blood pressure that, in the
long-term, causes end-organ
damage and results in increased
morbidity and mortality. Blood
pressure is the product of cardiac
output and systemic vascular
resistance.
Causes:
Primary HTN (no known cause):
aging, family history, African
American race, obesity, smoking,
stress, alcohol, hyperlipidemia,
excess salt intake, low potassium
intake.
Secondary HTN: caused by
precipitating disorders such as:
❖
Cardiovascular disorders
❖
Renal disorders
❖
Endocrine disorders
❖
Pregnancy
❖
Meds ( glucocorticoids,
mineralocorticoids,
estrogens)
Nursing interventions:
❖
❖
❖
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❖
❖
❖
❖
Provide a restful environment.
Explain all procedures in
detail.
Listen to the client.
Explain in detail diet
restrictions.
Document BP in the standing
and lying positions.
Encourage weight loss if the
client is obese.
Provide moderate salt
restricted diet.
Plan exercise regularly
Encourage stress reduction
measures.
Labs/ Diagnosis:
❖
❖
❖
❖
❖
❖
❖
❖
Urinalysis :Will detect
protein, RBC, pus, and
casts.
Blood count/ESR
Serum potassium,
chloride and C02.
Urinary catecholamine
metabolites: To dx
pheochromocytoma.
Urine ketosteroids.
IV pyelogram, urine
cultures, radioisotope.
Renal angiography : Test
for renal disease.
BUN and Creatinine.
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❖
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❖
Treatments:
❖
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3-2
Initially lifestyle changes
Beta blockers
Alpha Blockers
Alpha 2 agonist
Diuretics
Vasodilators
Calcium channel blockers
ACE inhibitors
ARBS
Medical treatment:
❖
❖
❖
❖
❖
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Lie down immediately if
feeling faint, rise slowly.
Avoid hot baths.
Avoid alcohol.
Avoid standing motionless.
Avoid constipation, it
interferes with drug
metabolism and can cause
hypotensive crisis.
Always take meds on time
and never skip.
Never take a larger dose.
Never suddenly d/c the
drug this can cause
rebound hypertension.
Should hypotensive crisis
occur wrap legs to
promote venous return.
Consult the HCP for use of
OTC meds.
Low sodium diet or cardiac
diet.
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Take clients BP and HR
right before administration.
Evaluate clients BP 30
mins post admin.
Monitor for dizziness and
hypotension.
Monitor labs, especially
potassium.
Note interactions between
NSAIDS and
antihypertensive
medication.
lOMoARcPSD|11919074
Heart failure : Right sided
3-3
Teaching:
What am I?
Inability of the heart to maintain
adequate cardiac output due to
impaired pumping ability.
Right sided heart failure develops
from a diseased right ventricle that
causes backflow to the right
atrium. Almost always follows left
side HF.
Types
❖
❖
Left sided :Backs up in the
pulmonary circuit.
Right sided: Backs up in
the systemic circuit.
Physiology:
Heart failure is the inability of the
heart to maintain adequate cardiac
output due to impaired pumping
ability. Diminished cardiac output
results in inadequate tissue
perfusion.
❖
❖
Acute: occurs suddenly
Chronic: develops
overtime, can be
accompanied by acute
episodes
Causes:
❖
❖
❖
❖
❖
❖
❖
❖
❖
Coronary artery disease
and heart attack
High blood pressure
(hypertension)
Faulty heart valves.
Damage to the heart
muscle (cardiomyopathy)
Myocarditis
Heart defects you're born
with (congenital heart
defects)
Abnormal heart rhythms
(heart arrhythmias)
Chronic diseases — such
as diabetes, HIV,
hyperthyroidism,
hypothyroidism, or a
buildup of iron
(hemochromatosis) or
protein (amyloidosis)
Acute infections
❖
❖
❖
Assessment:
CNS; anxiety and fear.
HEART : JVD, increased BP from
fluid excess or decreased BP from
pump, tachycardia, failure.
Dependent edema.
GI/GU : anorexia, abdominal
distention, weight gain.
MISC.: hepatomegaly,
splenomegaly, swelling of fingers
and hands.
S: Swelling of fingers and hands
W: Weight gain
O: Organ enlargement
L: Low hunger
L: Large abdomen
E: Edema in the periphery
N: Nocturnal diuresis
Nursing interventions:
❖
❖
❖
❖
❖
❖
❖
❖
❖
Administer cardiac
glycoside
Monitor vitals
Record intake and output
Daily weights
Meticulous skin care
02 therapy
Teach about disease
process
Provide a low sodium low
calorie diet
Bland foods and small
frequent meals
Labs/ Diagnosis:
❖
❖
❖
❖
❖
❖
❖
❖
Blood tests
Chest X-ray
Electrocardiogram (ECG)
Echocardiogram
Stress test
Cardiac computerized
tomography (CT) scan or
magnetic resonance
imaging (MRI)
Coronary angiogram
Myocardial biopsy
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
Educate the client on signs
of dig toxicity.
Have the client identify
risks of acute episodes.
Educate the client on
medications.
Notify HCP if side effects
occur.
Call HCP if unable to take
meds due to illness.
Avoid caffeine, alcohol,
tea, cocoa, soda.
Educate the client on a low
sodium, low fat, low
cholesterol diet.
Provide a list of potassium
rich foods.
Educate on fluid restriction.
Balance rest and activity.
Have them monitor daily
weight.
Monitor for signs of fluid
retention.
No isometric exercise, it
can overwork the heart.
Treatments:
❖
❖
❖
❖
❖
❖
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Digoxin
Diuretics
ACE
ARB
Low dose beta blockers
Vasodilators: nitrates,
milrinone
Morphine sulfate
Human B natriuretic
peptide: acute episodes
Medical treatment:
❖
❖
❖
❖
❖
❖
www.SimpleNursing.com
Downloaded by CHRISTIAN
LOLO (Christian96lolo@gmail.com)
Take clients BP and HR
right before administration.
Evaluate clients BP 30
mins post admin.
Monitor for dizziness and
hypotension.
Monitor labs, especially
potassium.
Note interactions between
NSAIDS and
antihypertensive,
medications.
Monitor labs and look for
signs of digoxin toxicity.
lOMoARcPSD|11919074
Heart failure : Left sided
3-4
What am I?
Inability of the heart to maintain
adequate cardiac output due to
impaired pumping ability.
Left sided HF: a result of left
ventricular dysfunction which
causes blood to backup into the
left atrium and into the pulmonary
veins.
❖
Left = Lung
Types
❖
❖
Left sided : backs up in
the pulmonary circuit.
Right sided : backs up in
the systemic circuit.
Physiology:
Inability of the heart to maintain
adequate cardiac output due to
impaired pumping ability.
Diminished cardiac output results
in inadequate tissue perfusion.
Acute: occurs suddenly.
Chronic: develops overtime, can be
accompanied by acute episodes.
Causes:
❖
❖
❖
❖
❖
❖
❖
❖
Coronary artery disease
and heart attack.
High blood pressure
(hypertension)
Faulty heart valves
Damage to the heart
muscle (cardiomyopathy)
Myocarditis
Heart defects you're born
with (congenital heart
defects)
Abnormal heart rhythms
(heart arrhythmias)
Chronic diseases — such
as diabetes, HIV,
hyperthyroidism,
hypothyroidism, or a
buildup of iron
(hemochromatosis) or
protein (amyloidosis)
Assessment:
CNS: Anxiety and fear, cerebral
anoxia, fatigue.
HEART: Decreased cardiac output,
s3 gallop, increased BNP.
RESP: Dyspnea, orthopnea,
cheyne stokes, pleural effusion ,
pulmonary edema cough, cardiac
asthma.
MISC.: Decreased renal function,
muscular weakness,
microalbuminuria.
❖
E: Edema (pleural)
P: Pleural effusion
I: Increased BNP
C: Cardiac asthma
❖
F: Fatigue
A: Anxiety
I: Inability to breath (dyspnea,
orthopnea)
L: Listen for S3 gallop
Nursing interventions:
❖
❖
❖
❖
❖
❖
❖
❖
❖
Administer cardiac
glycoside
Monitor vitals
Record intake and output
Daily weights
Meticulous skin care
02 therapy
Teach about disease
process
Provide a low sodium low
calorie diet
Bland foods and small
frequent meals
Teaching:
❖
❖
❖
❖
❖
❖
Treatments:
❖
❖
❖
❖
❖
❖
❖
❖
Labs/ Diagnosis:
❖
❖
❖
❖
❖
❖
❖
❖
❖
Blood tests
BNP
Chest X-ray
Electrocardiogram (ECG)
Echocardiogram
Stress test
Cardiac computerized
tomography (CT) scan or
magnetic resonance
imaging (MRI)
Coronary angiogram
Myocardial biopsy
www.SimpleNursing.com
Downloaded by CHRISTIAN
LOLO (Christian96lolo@gmail.com)
Educate the client to
maintain aseptic technique.
Instruct the client on how
to administer IV antibiotics.
Have the client record
temp daily for six weeks.
Encourage oral hygeine for
six weeks with a soft bristle
toothbrush 2x daily.
Have the client clean any
skin lacerations and apply
antibiotic ointment.
Client should inform all
HCP’s of hx of
endocarditis.
Client should use
prophylactic antibiotics for
oral procedures.
Tech the client the signs
and symptoms of emoli
and HF.
Digoxin
Diuretics
ACE
ARB
Low dose beta blockers
Vasodilators: nitrates,
milrinone
Morphine sulfate
Human B natriuretic
peptide: acute episodes
Medical treatment:
❖
❖
❖
❖
❖
❖
Take clients BP and HR
right before administration.
Evaluate clients BP 30
mins post admin.
Monitor for dizziness and
hypotension.
Monitor labs, especially
potassium.
Note interactions between
NSAIDS and
antihypertensive,
medications.
Monitor dig labs and look
for signs sx of dig toxicity.
lOMoARcPSD|11919074
3-5
Coronary Artery Disease
What AM I ?
Surgical Procedures
Narrowing or obstruction of one or
more coronary arteries as a result
of atherosclerosis.
❖
Physiology:
Atherosclerotic buildup will
cause decreased perfusion to
the myocardial tissue leading to
inadequate myocardial
oxygenation thus causing
hypertension, angina,
dysrhythmias, MI, HF or death.
Symptoms occur when the
coronary artery is occluded
50-75%.
Goal of treatment to decrease
atheroscleroic progression.
Causes:
Modifiable risks
❖
F: family history
❖
A: age
❖
T: thrombus
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
Assessment:
HEART: Chest pain, palpitations
RESP: Dyspnea
MISC.: Fatigue
RESP: Cough, hemoptysis
CNS: Syncope
L: Low energy
I: Irritating cough, hemoptysis
P: Palpitations
I: Intense chest pain
D: Dyspnea
S: Syncope
H: high cholesterol
E: ethnicity
A: alcohol abuse
R: release of stress
hormones
T: tobacco use
Labs/ Diagnosis:
❖
❖
PTCA: Compresses the
plaque against the walls
of the arteries and
dilates vessels.
Laser angioplasty:
Vaporizes the plaque.
Atherectomy : Removes
plaque from the artery.
Vascular stent: Prevent
the artery from closing
and restenosis.
Coronary artery bypass
graft: Improves blood
flow to the myocardium
decreasing the risk for
ischemia and infarction.
Treatments:
Nursing interventions:
❖
❖
ECG: to monitor for ST
elevation indicative of MI.
Cardiac Cath: to look for
extent of atherosclerotic
buildup.
Blood lipids: monitors
cholesterol levels such as
HDL. LDL and triglycerides.
❖
❖
❖
❖
Educate on the risk factors
of CAD.
Assist in goal setting for
smoking, alcohol and
substance abuse
cessation.
Educate the client on
proper diet, low sodium,
low calorie, low fat,
increased fiber.
Lifestyle changes are not
temporary.
Provide resources for
cessation of smoking and
substance abuse.
Explain the importance of
exercise.
❖
❖
❖
❖
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Nitrates: dilate the
coronary arteries and
decrease preload and
afterload.
Calcium channel
blockers: dilate
coronary arteries and
reduce vasospasm.
Cholesterol lowering
meds : HMG-COA
reductase inhibitors,
reduce the development
of plaques.
Beta Blockers: reduce
BP for clients who are
hypertensive.
lOMoARcPSD|11919074
3-6
Coronary Artery Disease: Angina
What am I?
Teaching:
Chest pain resulting from
myocardial ischemia resulting from
inadequate blood and 02 supply.
❖
❖
Stable angina : occurs during
active periods and subsides when
resting or after taking Nitroglycerin.
Unstable angina : occurs with
unpredictable amounts of exertion
and does not subside with rest or
nitroglycerin, lasts longer than 15
minutes.
Variant angina : results from
coronary artery spasm, can happen
during rest.
Physiology:
Angina pectoris is the result of
myocardial ischemia caused by an
imbalance between myocardial
blood supply and oxygen demand.
It is a common presenting
symptom (typically, chest pain)
among patients with coronary
artery disease (CAD).
❖
❖
❖
❖
Assessment:
HEART: Chest pain can be
crushing, substernal, squeezing,
and radiate to shoulders arms and
jaw pain palpitations, tachycardia,
HTN.
RESP: Dyspnea
MISC.: Fatigue, pallor, sweating.
GI: Dgestive disturbances.
CNS: Syncope, dizziness.
C: chest pain
H: hypertension
E: elevated HR
S: substernal pain
T: tiredness
Causes:
Modifiable risks
❖
Smoking
❖
High fat intake
❖
Sedentary lifestyle
❖
Diabetes
❖
Obesity
❖
Chronic stress
❖
Depression
❖
Birth control
❖
Substance abuse
❖
Non modifiable risks
❖
Age
❖
Family history
❖
Gender ( males)
❖
Race ( african american)
P: pallor
A: lot of sweating
I: intense squeezing pain
N: non normal respirations
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❖
❖
❖
Treatments:
❖
❖
❖
Nursing interventions:
❖
❖
❖
❖
Labs/ Diagnosis:
❖
ECG: ST depression or t wave
inversion during pain.
Stress Test: changes in EKG
or vitals could indicate
ischemia.
Cardiac enzyme levels:
findings are normal in angina.
Cardiac catheterization:
provides a definite dx by
monitoring patency of
coronary arteries.
Identify precipitating
events.
If chest pain occurs take
nitroglycerine as ordered
no more than 3x 5 min.
Apart. If chest pain is not
relieved call 911.
Provide diet restrictions.
Identify modifiable risk
factors.
Assist in goal setting.
Provide community
resources.
❖
❖
Assess pain and institute
relief measures.
Administer 02.
Assess vitals provide
continuous cardiac
monitoring.
Administer nitroglycerine
as prescribed.
Ensure bed rest is
maintained in semi-fowlers.
Obtain 12 lead EKG.
Establish IV access.
❖
❖
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Nitrates : Dilate the
coronary arteries and
decrease preload and
afterload.
Calcium channel
blockers: Dilate
coronary arteries and
reduce vasospasm.
Cholesterol lowering
meds : HMG- COA
reductase inhibitors,
reduce the development
of plaques.
Beta Blockers: Reduce
BP for clients who are
hypertensive.
Antiplatelet meds: To
inhibit platelet
aggregation and
decrease the risk of MI.
lOMoARcPSD|11919074
3-7
Peripheral vascular disease: Venous
Assessment:
What am I?
Refers to diseases of blood vessels
outside the heart and brain. A
narrowing of vessels that carry
blood to the legs, arms, stomach or
kidneys.
There are two types of PVD:
• Functional PVDs don’t involve
defects in blood vessels’ structure.
(The blood vessels aren’t physically
damaged.) These diseases often
have symptoms related to “spasm”
that may come and go.
• Organic PVDs are caused by
structural changes in the blood
vessels. Examples could include
inflammation and tissue damage.
There is a decrease in efficiency of
returning blood to the heart related
to incompetent valves and
inadequate pumping action of the
muscles surrounding the veins.
Thrombophlebitis
Venous stasis
Hypercoagulability
Injury to the venous wall
Advanced age causes
decreased competence of
the valves and greater
incidence of varicose veins
and slower wound healing
Labs/ Diagnosis:
Phelogram
Venous pressure
measurements: venous
Nursing interventions:
❖
❖
❖
❖
❖
❖
❖
❖
●
●
●
●
●
Assess pain and institute
relief measures.
Purple limb indicates
advanced progression.
Compare limb temp.
Ambulation should be
encouraged.
Elevate legs above the
heart, raise foot of bed.
Apply intermittent warm
moist packs to promote
circulation.
Support hose to promote
venous return.
Avoid standing or sitting.
Avoid temp extremes.
Monitor peripheral pulses.
Anticoagulant and
thrombolytic therapy.
●
●
Venous doppler
evaluation
Lung scan
D -dimer: global
coagulation test
❖
❖
❖
❖
❖
❖
❖
Educate the client to
maintain aseptic technique.
Instruct the client on how
to administer IV antibiotics.
Have the client record
temp daily for six weeks.
Encourage oral hygiene for
six weeks with a soft bristle
toothbrush 2x daily.
Have the client clean any
skin lacerations and apply
antibiotic ointment.
Client should inform all
HCP’s of hx of
endocarditis.
Client should use
prophylactic antibiotics for
oral procedures.
Tech the client the signs
and symptoms of emoli
and HF.
Treatments:
❖
Antiplatelet meds: to
inhibit platelet aggregation
and decrease the risk of
MI.
❖
DVT: pain redness and
decreased pulse in lower limb.
Look for Homan’s sign.
PE: embolism in the lungs,
tachycardia, SOB, feeling of
impending doom.
Embolism : stagnant
collection of blood in the
venous system.
Passive and active ROM.
Early ambulation
postoperative.
Elastic support hose.
Deep breathing exercises.
Avoid tight clothing.
Prevention:
Passive and active ROM
Early ambulation post op
Elastic support hose
Deep breathing exercises
Avoid tight clothing
COmplications:
❖
❖
occlusion in one limb
causes the pressure in the
other limb to be higher
●
Teaching:
❖
❖
Causes:
●
●
P: pain in the affected limb.
A: alteration in limb temp.
I: induration and redness.
N : normal or decreased pulse.
❖
❖
Physiology:
❖
❖
❖
❖
❖
HEART : Normal or decreased
pulses.
DERM: cool brown skin,
edema, ulcers, pain redness
and induration along the vein,
limb may be warmer.
MISC.: deep muscle
tenderness, risk for PE.
❖
❖
❖
❖
❖
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Valve Disorder
lOMoARcPSD|11919074
Assessment:
Aortic Stenosis
HEART: angina, systolic murmur
CNS: syncope, fatigue
Resp: orthopnea, nocturnal
dyspnea
Mitral
HEART: activity intolerance,
fluttering sensations, cyanosis,
signs of RIGHT ventricular failure,
decreased cardiac ,output,
diastolic murmur
CNS: fatigued
RESP: clear lung sounds
What am I?
With valve disorders you can have
stenosis or regurgitation. Prevents
efficent blood flow through the
heart.
Mitral Valve
Aortic valve
Mitral
Heart: signs of right ventricular
failure, edema, systolic murmur
Resp: pleural effusion
Misc: enlarged organs, ascites
Stenosis: hardening of the valve.
Regurgitation: valve is
incompetent and does not fully
close on systole.
Treatment:
Physiology:
Stenosis: the obstruction of blood
flow across the aortic or mitral
valve.
Regurgitation: due to
incompetence of the aortic or mitral
valve or any disturbance of the
valvular apparatus (eg, leaflets,
annulus of the aorta) resulting in the
diastolic flow of blood into the left
ventricular chamber.
Causes:
❖
❖
❖
❖
❖
❖
Assessment regurgitation Aortic
Heart: tachycardia,
fatigue,diastolic murmur
Resp: dyspnea, orthopnea,
nocturnal dyspnea
Born with an abnormal
valve or valves (congenital
heart disease)
History of rheumatic fever
Cardiomyopathy - a
disease of the heart muscle
Damage to the heart
muscle from a heart attack
Getting older
A previous infection with
endocarditis
❖
❖
❖
Anticoagulants
Platelet aggregation
inhibitors: aspirin,
clopidogrel breaking out in
a cold sweat, nausea or
lightheadedness
Chest pain that persists
after taking nitroglycerin 3x
5 mins apart
Interventions:
❖
❖
❖
❖
Call hcp about discontinuing
anticoagulants 72 hrs prior to
surgery.
Monitor for bleeding post op.
Monitor cardiac output and
signs of HF.
Administer digoxin as ordered
to maintain cardiac output.
Teaching:
❖
Maintain adequate rest.
Anticoagulant therapy for valve
replacement.
Do not eat green leafy veggies.
Practice good oral hygiene to
prevent endocarditis.
Avoid electric toothbrush.
Monitor incision and report
signs of infection.
Avoid dental procedures for six
months.
Educate the client on the
importance of prophylactic
antibiotics before dental
procedures.
Avoid heavy lifting.
❖
❖
❖
Balloon valvuloplasty
Commissurotomy
Valve replacement
❖
❖
❖
❖
❖
❖
❖
❖
Surgeries:
Labs / Diagnostics:
Echocardiography
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3-8
lOMoARcPSD|11919074
Endocarditis
3-9
Assessment:
What am I?
Inflammation of the inner lining of
the heart valves.
Occurs primarily with IV drug
abuse, valve replacement patients.
Points of entry include the mouth
( 3-6 months after oral procedure),
infections, surgery, and IV line
placement.
Physiology:
Infective endocarditis comprises at
least three critical elements:
preparation of the cardiac valve for
bacterial adherence, adhesion of
circulating bacteria to the prepared
valvular surface, and survival of the
adherent bacteria on the surface,
with propagation of the infected
vegetation.
IV drug abuse
Infection
Valve replacement
Oral surgery ( 3-6 mos)
Surgery
IV line placement
Labs/ Diagnosis:
❖
❖
❖
❖
❖
C: complication, risk for embolism
L: large spleen
O: overheated ( fever)
T: too many drugs ( substance
abuse)
Nursing interventions:
❖
❖
❖
Complete blood count
Electrolytes
Creatinine
Blood urea nitrogen (BUN),
glucose
Coagulation panel
Anemia is common in subacute
endocarditis. Leukocytosis is
observed in acute endocarditis.
M: murmur
A: anorexia
Y: yes they have cyanotic
symptoms ( clubbing)
❖
❖
Causes:
❖
❖
❖
❖
❖
❖
HEART: murmurs, HF
CNS: fatigue
GI/GU: anorexia
DERM: splinter hemorrhage in the
nail bed, clubbing, osler's nodes,
janeway lesions
HEME: embolic complications,
petechiae
MISC: fever, splenomegaly
❖
❖
❖
❖
❖
❖
❖
Provide adequate rest and
balanced activity, this
prevents thrombus
formation.
Anti Embolism stocking.
Monitor cardiovascular
status.
Monitor of signs of HF.
Monitor for signs of emboli,
splenic emboli will be
evidenced by abdominal
pain radiating to the left
shoulder and rebound
abdominal tenderness.
Monitor mental status.
Assess for petechiae on
skin oral mucosa and
conjunctiva.
Assess for osler's nodes
and janeway lesions.
Assess for clubbing.
Evaluate blood culture.
Administer antibiotics as
ordered.
Prepare to dc client with IV
line.
Teaching:
❖
❖
❖
❖
❖
❖
❖
❖
Educate the client to
maintain aseptic technique.
Instruct the client on how
to administer IV antibiotics
Have the client record.
temp daily for six weeks.
Encourage oral hygeine for
six weeks with a soft bristle
toothbrush 2x daily.
Have the client clean any
skin lacerations and apply
antibiotic ointment.
Client should inform all
HCP’s of hx of endocarditis
Client should use
prophylactic antibiotics for
oral procedures.
Tech the client the signs
and symptoms of emboli
and HF.
Treatments:
❖
❖
❖
❖
❖
NSAIDS
Corticosteroids
Analgesia
Diuretics
Digoxin
Medical treatment:
❖
❖
❖
❖
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Penicillin G at 12-18 million
U/d IV by continuous pump
or in six equally divided
doses for four weeks.
Ceftriaxone at 2 g/d IV for
four weeks.
Penicillin G and gentamicin
at 1 mg/kg (based on ideal
body weight) every 8 hours
for 2 weeks
Patients who are allergic to
penicillin, use vancomycin
at 30 mg/kg/d IV in two
equally divided doses for
four weeks.
lOMoARcPSD|11919074
Peripheral vascular disease:Arterial
3-10
Assessment:
HEART: decreased peripheral
pulses
DERM: cool shiny skin, hair loss,
ulcers, gangrene, impaired
sensation
MISC.: intermittent claudication
S: shiney skin
H: hair loss to the extremity
I: intermittent claudication
N: nasty ulcers
E: extremities will be cool
What am I?
Peripheral arterial disease is a set
of chronic or acute syndromes.
Derived from the presence of
occlusive arterial disease, which
causes inadequate blood flow and
perfusion to the limbs. The
underlying disease process is
usually arteriosclerotic disease and
it mainly affects the vascularization
to the lower limbs.
Physiology:
Arteries are incapable of dilating
and constricting normally due to
occlusion or disease process.
Causes:
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
●
●
●
●
Nursing interventions:
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
Percutaneous transluminal
angioplasty.
Laser assisted angioplasty.
Atherectomy catheters.
Intravascular stents.
Labs/ Diagnosis:
Angiography
Doppler ultrasound
Duplex imaging
Ankle brachial index; divide
ankle BP by brachial BP
normal is > /= to 0.9
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Educate the client to
maintain aseptic technique.
Instruct the client on how
to administer IV antibiotics.
Have the client record
temp daily for six weeks.
Encourage oral hygeine for
six weeks with a soft bristle
toothbrush 2x daily.
Have the client clean any
skin lacerations and apply
antibiotic ointment.
Client should inform all
HCP’s of hx of
endocarditis.
Client should use
prophylactic antibiotics for
oral procedures.
Tech the client the signs
and symptoms of emboli
and HF.
Treatments:
❖
❖
❖
Interventional radiology
❖
❖
❖
Arteriosclerosis
Raynauds
Buerger’s
Smoking
Diabetes
Hyperlipidemia
Hypertension
Obesity
Sedentary lifestyle
Age
Check extremities for
paleness, coolness or
necrosis
Meticulous foot care: warm
water, gently dry
thoroughly, use lubricants,
wear clean cotton socks
Do not cross legs
Regular exercise
No smoking
Weight loss
Teaching:
❖
Vasodilators
Anticoagulants
Platelet aggregation
inhibitors: aspirin,
clopidogrel
Medical treatment:
❖
❖
❖
❖
Arterial bypass with
autogenous vein or
synthetic graft.
Endarterectomy.
Patch graft angioplasty.
Amputation.
lOMoARcPSD|11919074
Pericarditis
3-11
Assessment:
What am I?
Acute inflammation of the
pericardium, it can be a chronic
disease that causes thickening of
the pericardium.
Physiology:
Chronic pericarditis constricts the
heart causing compression. Due to
inflammation loss of pericardial
elasticity can result or an
accumulation of fluid within the
sac, heart failure or cardiac
tamponade may result.
Causes:
❖
❖
❖
❖
❖
❖
Autoimmune disorders
Lupus
Scleroderma
Rheumatoid arthritis
Heart attack
Heart surgery
Heart: precordial pain that radiates
to the left side of the neck,
shoulder or back, pain aggravated
by breathing, pain is worse when
supine, pericardial friction rub,
signs of right of ventricular failure
CNS: fever and chills, fatigue and
malaise
HEME: elevated WBC
P: precordial pain
A: a-fib
I: inflamed pericardial sac
N: neck pain radiating from chest
E: elevated WBC
D: dysphagia, pain when
swallowing
H: has fluid in the pericardium.
E: elevated st segment
A: auscultate friction rub
R: right ventricular failure
symptoms
T: tiredness
Nursing interventions:
❖
❖
❖
❖
❖
❖
❖
❖
Teaching:
❖
❖
❖
❖
❖
Treatments:
❖
❖
❖
❖
❖
❖
❖
❖
❖
NSAIDS
Corticosteroids
Analgesia
Diuretics
Digoxin
Medical treatment:
❖
❖
Assess nature of pain.
Place client in High
fowler's position , upright
or leaning forward.
Administer analgesic,
NSAIDS and
corticosteroids.
Auscultate for pericardial
friction rub.
Administer antibiotics.
Administer digoxin and
diuretics.
Monitor for cardiac
tamponade.
Notify HCP if signs of
cardiac tamponade occur.
Labs/ Diagnosis:
❖
Educate the client on
compliance with
medications.
Have the client take HR
prior to administration of
digoxin.
Have the client keep
appointments for lab work.
Educate the client on signs
and symptoms of
exacerbation.
Educate the client to rest.
Electrocardiogram: A-fib,
ST elevation
Complete blood cell (CBC)
Coagulations studies
Serum electrolyte
Blood urea nitrogen (BUN)
and creatinine levels.
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Pericardiocentesis
Pericardiectomy
lOMoARcPSD|11919074
3-12
Cardiac Tamponade
What am i?
Cardiac tamponade puts pressure
on the heart and keeps it from filling
properly. The result is a dramatic
drop in blood pressure that can be
fatal.
Pysiology
❖
❖
❖
❖
Gun shot wounds
Blunt trauma
Accidental perforation
Punctures
Cancer
Pericarditis
Lupus
Radiation
Hypothyroid
Heart attack
Kidney failure
Cardiac infections
❖
❖
❖
❖
❖
Chest CT or MRI of chest
❖
Chest x-ray
❖
Coronary angiography
❖
ECG
❖
Right heart catheterization
Hemodynamic support
Fluid therapy
Pulmonary artery catheterization
Venous thromboembolism (VTE)
prophylaxis
Cardiopulmonary resuscitation
Client education / discharge
❖
Nursing Diagnoses
❖
❖
❖
❖
❖
❖
❖
❖
Labs & diagnostics
Treatments
Causes
❖
❖
❖
❖
❖
❖
Heart: pulsus paradoxus, increased CVP,
JVD, muffled heart sounds, decreased
cardiac output narrow pulse pressure.
RESP: clear lungs.
D: distended jugular veins.
R: respiratory tract and lungs clear.
O: outrageous pulse pattern ( pulsus
paradoxus.
W: wet inside the pericardial space.
N: no pulse ( death is a complication.)
E: pulmonary edema.
D: decreased cardiac output.
Cardiac tamponade is a clinical
syndrome caused by the
accumulation of fluid in the
pericardial space, resulting in
reduced ventricular filling and
subsequent hemodynamic
compromise. The condition is a
medical emergency, the
complications of which include
pulmonary edema, shock, and
death.
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
Assessment Pericarditis
❖
Activity intolerance
Acute pain
Anxiety
Decreased cardiac output
Deficient fluid volume
Deficient knowledge: Disease
process
Deficient knowledge: Treatment.
Fear
Impaired comfort
Impaired gas exchange
Impaired spontaneous ventilation
Ineffective breathing pattern
Risk for bleeding
Risk for decreased cardiac tissue
perfusion
Risk for impaired cardiovascular
function
Risk for impaired skin integrity
Risk for infection
❖
❖
❖
❖
Disorder, diagnostic testing, and
treatment, including medication
therapy, the need for possible
pericardiocentesis, equipment,
and monitoring.
Prescribed medications, including
drugs, dosages, routes, frequency
of administration, rationale for
use, expected results, and
potential adverse reactions.
Signs and symptoms of
increasing or recurrent
tamponade and the need to notify
the practitioner immediately if any
occur.
Pre pericardiocentesis and post
pericardiocentesis care, as
indicated.
Emergency procedures.
Importance of follow-up care,
including echocardiogram and
chest radiography within a month
to evaluate resolution of the
condition.
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Nursing interventions
❖
❖
❖
❖
❖
Hemodynamic
monitoring
Administer fluids IV
Chest x ray /
echocardiogram
Prepare the client for
pericardiocentesis
Monitor for tamponade
cardiomyopathy
lOMoARcPSD|11919074
What am I?
A subacute or chronic disorder of the
heart muscle. Treatment is palliative
not curative. The client will have many
changes to lifestyle and lifespan.
Physiology:
Dilated cardiomyopathy: Fibrosis of
the myocardium and endocardium,
dilated chambers, mural wall thrombi
prevalent.
Non-obstructive cardiomyopathy:
Hypertrophy of the walls,
hypertrophied septum, small chamber
size .
Obstructive cardiomyopathy: Same
as non obstructed except for
obstruction in the left ventricular wall.
Restrictive cardiomyopathy: Mimics
pericarditis, fibrosed walls can
expand or contract, emboli is
common.
Causes:
❖
❖
❖
❖
❖
❖
Genetic conditions.
Long-term high blood
pressure.
Heart tissue damage from a
previous heart attack.
Chronic rapid heart rate.
Heart valve problems.
Metabolic disorders, such as
obesity, thyroid disease or
diabetes.
Dilated cardiomyopathy
❖
Non obstructive cardiomyopathy
❖
CNS: Fatigue and weakness
Heart: HF, dysrhythmias and heart
block, systemic or pulmonary emboli,
s3, s4 gallop, cardiomegaly
RESP: Dyspnea
Heart: Angina , mild cardiomegaly, s4
gallop, ventricular dysrhythmias,
sudden death, HF Fatigue, syncope
obstructive cardiomyopathy
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
❖
RESP: Dyspnea
Heart: Angina , mild cardiomegaly, s4
gallop, ventricular dysrhythmias,
sudden death, HF Fatigue, syncope, ❖
mitral regurgitation, A- FIB
obstructive cardiomyopathy
RESP: Dyspnea
Heart: Mild cardiomegaly, s4 / s3
gallop, Fatigue, heart block, emboli
❖
❖
❖
❖
Treatments
❖
Medications:
❖
❖
❖
Labs & Diagnostics
Assessment:
Cardiac glycoside
Diuretic
Angiotensin-converting
enzyme inhibitor, such as
Oxygen
Antiarrhythmics
Beta-adrenergic blockers,
Aldosterone antagonist,
Vasodilator
Angiotensin II receptor
blocker
Inotropic agent
Anticoagulant
❖
Interventions/Teaching:
❖
❖
Dilated cardiomyopathy:
Symptomatic treatment of
❖
HF, vasodilators, heart
transplant , control
❖
dysrhythmias.
Nonobstructed
cardiomyopathy:
Symptomatic treatment, beta
blockers, cardioversion,
❖
ventricular myotomy, valve
replacement, digoxin, nitrates,
vasodilators.
obstructive
cardiomyopathy:
Symptomatic treatment, beta ❖
blockers, cardioversion,
ventricular myotomy, valve
replacement, digoxin, nitrates,
vasodilators.
Restrictive cardiomyopathy:
Supportive treatment for
symptoms, treatment of
hypertension,conversion,
exercise restrictions
emergency treatment of acute
pulmonary edema.
Plasma brain natriuretic peptide
Levels may reveal heart failure and its
severity used as an ongoing tool to
help to monitor the response to
treatment.
Serum troponin, creatine kinase
(CK), and CK-MB levels may be
acutely elevated if the patient has
myocarditis or acute coronary
syndrome.
Liver function tests May be
elevated.
B-type natriuretic peptide Levels
identify the presence and severity of
fluid overload.
Urine toxicology screening May
detect drugs leading to
cardiomyopathy.
Elevated creatinine May be related
to hypovolemia or ACE inhibitors as
etiology.
Angiography Results rule out
ischemic heart disease.
Chest radiography Demonstrates
moderate to marked cardiomegaly
and possible pulmonary edema.
Echocardiography May reveal
ventricular thrombi, global
hypokinesis, and the degrees of left
ventricular dilation and systolic
dysfunction.
Gallium scanning May identify
patients with dilated cardiomyopathy
and myocarditis.
Cardiac catheterization Can show
left ventricular dilation and
dysfunction, elevated left ventricular,
right ventricular filling pressures, and
diminished cardiac output.
Transvenous endomyocardial
biopsy May be used in determining
the underlying cause in some
patients (cardiac transplant patients)
including myocarditis, connective
disorders and amyloidosis.
Electrocardiography Identifies
arrhythmias and intraventricular
conduction defects, and may reveal
nonspecific ST-T wave changes and
Q waves.
Low-sodium, low fat
Fluid restriction
Avoid alcohol
Rest periods
Moderate exercise to prevent
deconditioning
Cardiac rehabilitation
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3-13
Myocardial Infarction
lOMoARcPSD|11919074
Assessment:
Lungs: Chest pain, severe or
crushing, apprehension. Acute
pulmonary edema, dyspnea,
gurgling or bubbling respirations.
What am I?
A myocardial infarction is localized
ischemia to the myocardium as a
result of an occluded coronary
artery.
Physiology:
Following the sudden occlusion of a
coronary artery, usually from plaque
build up, a localized part of the
heart becomes ischemic and goes
without oxygen or proper blood
supply. Oxygen is the money of the
body, without money you go broke.
Parts of the myocardium begin die.
Heart: Referred Pain in neck arm
or jaw.
Shock , systolic bp< 80
mmhg . Low grade fever
from leukocytosis from
destruction of myocardial
tissue. Indigestion/
heartburn. Left ventricle
may become severely
crippled in pumping action
from the infarction.
Gu: Oliguria , less than 30 ml / hr.
GI: Women may feel abdominal
pain.
Neuro : Altered mental status from
pain and hypoxia.
Causes:
❖
❖
❖
❖
❖
❖
❖
An MI can occur from a
complete or near complete
blockage of a coronary
artery.
Decreased 02 and blood
supply.
Hypertrophy of the heart,
CHF or HTN.
Coronary artery Embolism.
Smoking and drug abuse.
Poor diet.
Sedentary life style.
Warning signs:
❖
❖
❖
❖
Labs / Diagnostics:
EKG: ST elevation, T wave
inversion, Q wave formation
WBC: leukocytosis within 2 days,
leaves after a week
ESR: elevated
CPK: peaks in 18 hrs, normalizes
48-72 H
LDH: elevated for 5-7 days, peaks
48-72 H not cardiac specific
Myoglobin: rises in 1 h, peaks
4-6H normalizes <24 H
Troponin: peaks 4-6H remains
elevated for 2 weeks
❖
Uncomfortable pressure,
squeezing, fullness or pain
in the center of your chest.
Pain or discomfort in one
or both arms, the back,
neck, jaw or stomach.
Shortness of breath with or
without chest discomfort.
Other signs such as
breaking out in a cold
sweat, nausea or
lightheadedness.
Chest pain that persists
after taking nitroglycerin 3x
5 mins apart.
Medications:
Propranolol: Beta blocker, Blocks
sympathetic nerve impulse of the
heart.
Adverse Effect: Weakness,
Hypotension, bradycardia,
depression, bronchospasm do not
give to clients with hx of asthma.
Nifedipine: Calcium channel
blocker, reduces work load of left
ventricle, coronary vasodilation.
Adverse Effects: hypotension,
dizziness, GI distress, liver
dysfunction.
Morphine Sulfate: Opioid
analgesic, reduces cardiac
workload, preload, and afterload
pressures, relieves pain and
reduces anxiety.
Adverse Effects: Hypotension,
respiratory depression decreased
mental activity have naloxone on
hand in case of overdose.
Warfarin: Anticoagulant thins the
blood and decreases platelet
aggregation.
Adverse effects: Bleeding
Heparin: Low molecular weight
anticoagulant the decreases
platelet aggregation.
Adverse Effects: Bleeding.
Interventions:
Administer morphine sulfate.
Give oxygen to help with dyspnea
and chest pain.
Provide thrombolytic therapy.
Place client in semi fowler's
position to promote better
ventilation, monitor vitals, monitor
I&O too much fluid can can
exacerbate CHF, monitor IV access.
Teaching:
❖
❖
❖
❖
❖
Bed rest, it can take up to
six weeks to heal.
Lifestyle changes and heart
healthy diet. Low sodium.
Stop smoking, reduce
stress, decrease caffeine.
Exercise regularly.
Do not eat green leafy
veggies because of
anticoagulant therapy.
Surgeries:
❖
❖
Profound HTN and shock will be
noted.
❖
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”Cath Lab”Angioplasty and
stents to open the coronary
vessels.
Coronary artery bypass
graft: to bypass the
clogged vessels.
Cardiac catheterization: to
look for plaque in vessel
walls.
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3-14