Ayoko na

Perpetual Help College of Manila
1240 V Conception St., Sampaloc Manila, Philippines, 1008
PROJECT
IN
CARE OF OLDER ADULT
Submitted by:
Andrea O. Manabat
BSN III - N22A
Submitted to:
Mr. Darwin Tan, RN

Tables of Elements
Atrial fibrillation
Case Study
You are the nurse practitioner in cardiology at the local medical center. Mr.
E is a 69-year-old male with HTN, COPD, and type 2 diabetes mellitus who
was referred to your clinic for evaluation and to discuss options for elective
cardioversion for new-onset atrial fibrillation (AF). He has a past medical
history of CAD with one prior infarct, which was treated with a PCI and
placement of a drug-eluting stent (DES) to his LAD coronary artery. He has
preserved ventricular function (ejection fraction, or EF) of 50% on a
Transthoracic echocardiogram last year. His recent echocardiogram has
also demonstrated mild to moderate aortic stenosis (AS). He also has a
long-standing history of COPD with a 40 pack-year smoking history.
During his review of systems, he relates several recent episodes of not

"feeling right" for the past week, excessive fatigue, and more dyspnea than
usual on exertion. He notices when he has palpitations he gets exhausted
more quickly.
His medications include furosemide 20 mg daily, atenolol 50 mg daily, and

aspirin 81 mg daily. He is allergic to calcium channel blocking drugs.
His physical examination reveals the following: temperature, 98.6 °F; heart
rate, 108 and irregular; respiratory rate, 16; and blood pressure, 130/85.
His jugular venous pressure (JVP) is 9 cm with the head of the bed at 45°.
On pulmonary examination, he has a prolonged expiratory phase and no
crackles. His cardiac examination reveals a lateral PMI, variable S1 and
single S2, and a II/VI holosystolic murmur heard best at the upper sternal
border which radiates to his neck. He has 1+ peripheral edema and no
clubbing or cyanosis. His ECG reveals AF with ventricular response of 124
and ST depression in I, AVL, and V2-V6.
I. Specific and General Objectives
Specific Objectives:
o To detect and classify atrial fibrillation using diagnostic tools like

ECG and wearable monitors.
o To evaluate the effectiveness of pharmacological
(anticoagulants, antiarrhythmics) and non-pharmacological
(cardioversion, ablation) interventions.
o To prevent stroke and other thromboembolic events using risk

assessment tools like CHA₂DS₂-VASc.
o To improve patients’ quality of life and treatment adherence.
o To identify key risk factors and the prevalence of atrial

fibrillation in specific populations.
General Objective:
The overarching goal of atrial fibrillation (AFib) treatment is to

improve the quality of life for patients by managing symptoms,
preventing complications, and reducing the risk of future
cardiovascular events.
II. Introduction
Atrial fibrillation (AFib) is an irregular and often very rapid heart rhythm.
An irregular heart rhythm is called an arrhythmia. AFib can lead to blood
clots in the heart. The condition also increases the risk of stroke, heart
failure and other heart-related complications.
III. Signs and Symptoms
Heart palpitations - A feeling of a rapid, fluttering, or pounding

heartbeat.
Fatigue - Feeling tired or weak.
Shortness of breath - Difficulty breathing, especially during physical

activity.
Dizziness or lightheadedness - A sensation of spinning or

unsteadiness.
Chest pain - Discomfort or pressure in the chest.

Fainting - Loss of consciousness.
ConfusionDifficulty thinking clearly.
Anxiety - Feeling nervous or uneasy.
IV. Anatomy
Atrial Fibrillation (AFib) is a heart rhythm disorder characterized by rapid

and irregular electrical impulses in the heart's upper chambers (atria).
Normal Heart Rhythm
Sinus Rhythm -The heart's electrical impulses originate from the

sinoatrial (SA) node, located in the right atrium.
Regular P-wave - The P-wave on an electrocardiogram (ECG)

represents the electrical activity that causes the atria to contract.
Regular QRS complex - The QRS complex represents the electrical

activity that causes the ventricles to contract.
Atrial Fibrillation
Rapid and Irregular Atrial Activity - The atria contract rapidly and
irregularly, without a coordinated pattern.
Loss of P-Wave - The ECG shows a baseline of irregular, wavy
lines called "fibrillatory waves" instead of distinct P-waves.
Irregular Ventricular Response - The ventricles receive a rapid and

irregular stream of electrical signals from the atria, leading to an
irregular ventricular rhythm.
Pulmonary Veins - These veins return oxygenated blood from the

lungs to the left atrium. They are often involved in the initiation and
maintenance of AFib.
Atrial Fibrosis - Over time, AFib can lead to scarring (fibrosis) in the
atria, which can further disrupt electrical signals and contribute to the
persistence of the arrhythmia.
V. Pathophysiology and Concept Map
Pathophysiology
Atrial Fibrillation
Shortening of the refactory period, ionic channels,

connexins, genetic influence.
Increase in intra-atrial pressure
Atrial and ventricular extrasystoles, atrial

tachycardias
Alterations in autonomic tone
Atrial fibrosis and inflammation

Concept Map
Atrial Fibrillation
Risk Factors:
Irregular, rapid ventricular
Previous stroke response rate
Age > 65
Diatolic filling time
Hypertension
Diabetes
Preload (LVEDV)
Decompensated Frank Starling

response
Stroke Volume
Cardiac output
Pre-existing coronary , myocardial

or valvular disease
Myocardial ischemia
Heart Failure
Myocardial infration
VI. Diagnostic Test
 Electrocardiogram (ECG or EKG)
o Standard 12-Lead ECG: This is the most common test used to

diagnose AFib. It records the electrical activity of the heart and can
show an irregular, rapid heartbeat characteristic of AFib.
o Holter Monitor: This portable device records the heart's electrical

activity continuously over 24-48 hours. It can detect intermittent
episodes of AFib that may not be captured during a standard ECG.
o Event Recorder: This device records the heart's rhythm only when
activated by the patient, usually when they experience symptoms. It's
useful for diagnosing infrequent episodes of AFib.
 Echocardiogram: This test uses sound waves to create images of the

heart. It can help assess the heart's structure and function, as well
as identify any underlying heart conditions that may contribute to
AFib.
 Electrophysiology Study (EPS): This invasive procedure involves

inserting thin tubes (catheters) into the heart to map the electrical
activity and identify the source of the arrhythmia. It's often used to
plan and guide catheter ablation procedures.
Laboratory Test
 Complete Blood Count (CBC): To check for anemia or infection.
 Basic Metabolic Panel: To assess kidney function, electrolyte

balance, and blood glucose levels.
 Thyroid Function Tests: To evaluate thyroid hormone levels, as
thyroid disorders can contribute to heart rhythm disturbances.
 Lipid Panel: To assess cholesterol levels and identify risk factors

for heart disease.
 Cardiac Enzymes: To rule out heart damage, especially in cases

of chest pain or other concerning symptoms.
 Coagulation Tests: To assess blood clotting factors, particularly if

anticoagulation therapy is being considered.
VII. Drugs Study
Drug Mechanis Indicatio Adverse Action Nursing

order m of ns effects responsibiliti
action es
Furosemi Acts on Edema on headache, Increas Observe 10

de 20mg the CHF vertigo, e the rights in giving
q8 descendin dizziness, patient' medication
g loop of orthostatic s urine
Test if the
Henle in hypotensio output
patient is
the kidney: n.
allergic to the
inhibiting abdominal
drug
reabsorpti discomfort
on of and pain, To prevent
electrolyte diarrhea, nocturia, give
s sodium PO and IM
and preparations
chloride, in the morning
causing Give second
excretion dose in early
of sodium, afternoon
calcium, Monitor
magnesiu weight, blood
m, pressure, and
chloride
water and pulse rate
some routinely with
potassium long term use
and during
rapid dieresis
Use can lead

to profound
water and
electrolyte
depletion
If oliguria or
azotemia
develops or
increases, the
drug
may need to
be stopped
Monitor fluid
intake and
output and
electrolyte,
BUN, and
carbon
dioxide levels
Watch for
signs of
hypokalemia,
such as
muscle
weakness and
cramps.
Drug Mechanis Indication Adverse Action Nursing
order m of s effects responsibiliti
action es
Atenol Atenolol is Hypertensi Bradycardi Reduces Monitor heart

ol a beta- on (high a (slow blood rate and blood
blocker blood heart rate) pressure pressure
50 mg
that pressure) regularly,
Hypotensi Controls
selectively especially
Angina on (low heart
inhibits before
(chest blood rate and
beta-1 administering
pain) pressure) arrhythmi
receptors
a Assess for
in the Post- Fatigue,
signs of
heart, myocardial dizziness
bradycardia
reducing infarction Prevents
Cold (e.g.,
heart rate, (to improve angina
extremities dizziness,
cardiac survival) and
Depressio weakness)
output, improves
Arrhythmia
n (rare) survival Monitor for
and blood s (to
pressure. after signs of
manage Shortness
It also heart depression or
abnormal of breath
reduces attacks mood
heart (especially
myocardia rhythms) in patients changes
l oxygen with Caution when

demand. asthma or administering
COPD) to patients
with
respiratory
issues (e.g.,
asthma)
Educate the
patient to
avoid sudden
discontinuatio
n of the drug,
as this can
cause
rebound
hypertension
Drug Mechanism Indications Adverse Action Nursing

order of action effects Responsibili
ties
Aspirin 81 Aspirin Cardiovascul Gastrointes Reduces Monitor for

mg irreversibly ar disease tinal the risk signs of
inhibits prevention irritation of blood gastrointestin
cyclooxygen (e.g., (nausea, clots by al bleeding
ase (COX-1 prevention of ulcer inhibiting (e.g., black
and COX-2 heart attack, formation) platelet stools,
enzymes), stroke, and aggregat hematemesis
which leads other ion, )
Gastrointes
to reduced thrombotic thereby
tinal Advise the
production events) decreasi
bleeding patient to
of ng the
Secondary (risk take with
thromboxan likelihoo
prevention of increases food to
e A2, a d of
cardiovascul with high reduce
substance thrombot
ar events in doses or in gastrointestin
that ic events
patients with combinatio al irritation
promotes such as
a history of n with other
platelet heart Monitor for
myocardial anticoagula
aggregation attacks signs of
infarction, nts)
(clotting). or tinnitus
stroke, or
This Tinnitus strokes. (ringing in
peripheral
decreases (ringing in the ears),
artery
the disease the ears, especially at
formation of especially higher doses
Pain relief
blood clots. at high
(mild to Assess for
doses)
moderate any bleeding
pain) and Allergic disorders or
anti- reactions a history of
inflammatory (rare) ulcers
for conditions
Educate the
like arthritis
patient on
the
importance
of regular
blood tests if
on long-term
aspirin
therapy
Caution
when taking
with other
anticoagulant
s (increases
the risk of
bleeding)
VIII. Nursing Care Plan
Assessm Nursing Planning Implementa Rationale Evaluatio

ent Diagno tion n
sis
Subjectiv Decreas After 8 Regularly Monitoring After 8

e: ed hours assess the vital signs hours
cardiac patient patient’s helps to patient
“I’m
having a output is will vitals, paying track reports
short related demonstr special changes in decreased
breath as to ate attention to the shortness
verbalized failure improved heart rate, patient’s of breath
by pt” of the oxygenati respiratory condition and
heart to on and rate, and and guide increased
Objective
pump cardiac oxygen clinical comfort.
:
adequat output, saturation to decisions
Vital signs
Pale e blood as track any regarding
stabilize
looking to the evidence improvement medication
within
V/S: T rest of d by s or adjustment
normal
98.6 °F; the stable deterioration. s, oxygen
limits, and
HR, 108 body as vital therapy, or
Provide the patient
and evidenc signs, further
supplementa demonstrat
irregular; ed by normal interventio
l oxygen to es
RR 16; chest skin ns.
improve improved
BP130/85 pain. color,
oxygenation Oxygen skin color
and relief
and reduce therapy (e.g., no
from
the workload assists in longer
shortness
on the heart. improving pale).
of breath
oxygen
Elevate the No further
saturation,
head of the complaints
which can
bed to of chest
relieve
reduce the pain or
symptoms
work of dizziness.
of
breathing
shortness The patient
and promote
of breath, verbalizes
better lung
reduce understand
expansion.
cardiac ing of
Ensure workload, signs to
medications and report in
are given as improve case of
per the overall worsening
healthcare comfort. symptoms.
provider’s Positioning
orders to in semi-
improve Fowler’s
cardiac promotes
function and better lung
reduce expansion,
symptoms reduces
like the effects
shortness of of gravity
breath and on lung
irregular function,
heart rate. and aids in
breathing.
Use active
listening to Administeri
assess the ng
level of prescribed
distress and medication
tailor s helps
interventions manage
accordingly. underlying
conditions
Monitor for
such as
signs of
heart
electrolyte
failure and
imbalances
arrhythmia
or heart
s, thereby
failure
improving
biomarkers,
cardiac
which may
output and
require
alleviating
adjustment
symptoms.
of
medication Encouragi
or further ng
intervention. verbalizati
on allows
Teach the the patient
patient to to express
report signs any
such as worsening
increased symptoms
shortness of and helps
breath, to identify
dizziness, potential
chest pain, complicati
or swelling, ons early.
which could
Monitoring
indicate
lab results
worsening
is essential
heart failure.
to detect
early signs
of
electrolyte
imbalance
or
worsening
heart
failure,
guiding
timely
adjustment
s to
treatment.
Patient
education
empowers
the patient
to actively
participate
in
managing
their
symptoms,
improving
early
detection
and
preventing
complicati
ons.
IX. Nursing Responsibilities
Assessment and Monitoring:
Vital Signs: Monitor blood pressure, heart rate, respiratory rate, and
temperature.
Cardiac Rhythm: Assess heart rhythm through ECG monitoring or pulse

checks.
Symptom Assessment: Evaluate symptoms such as palpitations,

shortness of breath, chest pain, and fatigue.
Neurological Assessment: Check for signs of stroke, including changes

in mental status, speech, vision, or motor function.
Medication Administration and Monitoring:
Anticoagulants: Administer anticoagulants as prescribed to prevent

blood clots.
Antiarrhythmic Medications: Administer medications to control heart rate

or convert the heart rhythm to sinus rhythm.
Monitor for Adverse Effects: Observe for side effects of medications,

such as bleeding, dizziness, or nausea.
Patient Education:
Disease Process: Explain the nature of AFib, its causes, and potential
complications.
Medication Adherence: Educate patients on the importance of taking

medications as prescribed and recognizing side effects.
Lifestyle Modifications: Advise patients on lifestyle changes, such as

regular exercise, a healthy diet, stress management, and smoking
cessation.
Symptom Management: Teach patients how to recognize and respond

to symptoms, such as palpitations or shortness of breath.
Emergency Procedures: Instruct patients on how to respond to

emergencies, such as chest pain or severe shortness of breath.
Procedural Care:
Cardioversion: Assist with cardioversion procedures, either

pharmacologic or electrical, to restore normal heart rhythm.
Catheter Ablation: Prepare patients for and assist with catheter ablation
procedures, a minimally invasive procedure to correct abnormal heart
rhythms.
Collaboration with Healthcare Team:
Communicate with Physicians: Report any changes in the patient's

condition, including changes in heart rhythm, symptoms, or laboratory
values.
Coordinate Care: Work with other healthcare providers, such as

cardiologists and pharmacists, to ensure optimal care.
Heart Failure
Case Study:
Mr. E is admitted to the intermediate unit after his cardioversion for post-
procedure recovery. His EF on the TTE is down from his previous
findings and is now found to be 20%-25%. There is no significant wall
motion abnormality. He also is found to have moderate AS.
You are concerned that Mr. E's reduction in EF may be related to

prolonged tachycardia-mediated stress and hope that restoring a regular
rhythm will improve his EF. While he is hospitalized, you choose to be
more aggressive with his diuresis due to his DOE and edema. Mr. E
takes 20 mg of furosemide at home, and you increase this to 40 mg for
the time being and chose to deliver it intravenously. You order daily
weights and strict intake and output. His renal function is normal and
electrolytes also WNL.
You initiate ACE-I on Mr. E along with resumption of his BB and

diuretics. Since his EF is <35%, you discuss possible ICD/CRT but
agree to defer with outpatient follow-up. The differential for his HF
includes potential worsening from prolonged tachycardia, which is
currently controlled after cardioversion. For the AF, he will continue on
the beta-blockage and apixaban. For his CAD, you will continue a high-
intensity statin and aspirin. He receives dietary teaching for a low-
sodium, heart-healthy diet. He will monitor his weight daily and notify
you if he gains more than 2 lbs in 1 day or 5 lbs in a week. You provide
him with the Medicare discharge planning checklist, He will follow up in 1
week with you in the GDMT clinic with plans for close monitoring of
symptoms and up-titration of his mediations as tolerated over the next
several weeks. Considerations of care will include initiation of ARNI as
well as an outpatient echocardiogram to evaluate for any improvement
in EF, progression of AS, and further discussion of consideration for
ICD/CRT
Specific Objectives
 To accurately identify heart failure using clinical evaluation and

diagnostic tools.
 To classify heart failure into HFrEF, HFpEF, and HFmrEF based

on ejection fraction.
 To evaluate the effectiveness of pharmacological (e.g., ACE

inhibitors, beta-blockers) and advanced interventions (e.g., CRT,
ICD).
 To prevent complications such as arrhythmias and reduce

hospitalizations and mortality.
 To improve quality of life and promote adherence to treatments

through education.
General Objectives
To enhance the understanding, prevention, diagnosis, and

management of heart failure to improve patient outcomes and
reduce its impact on public health.
II. Introduction
Heart failure is a term used to describe a heart that cannot keep up

with its workload. The body may not get the oxygen it needs. Heart
failure is a serious condition, and usually, there’s no cure. However
many people with heart failure lead a full, enjoyable life when the
condition is managed with heart failure medications and a healthy
lifestyle. It’s also helpful to have the support of family and friends who
understand your condition.

Shortness of breath (also called dyspnea) - blood "backs up" in
the pulmonary veins (the vessels that return blood from the lungs
to the heart) because the heart can't keep up with the supply. This
causes fluid to leak into the lungs.
Persistent coughing or wheezing - fluid builds up in the lungs.
Buildup of excess fluid in body tissues (edema) - swelling in

the feet, ankles, legs, fingers, abdomen, and in other tissues and
organs. As a result, weight gain is common.
Tiredness and fatigue - a tired feeling all the time and difficulty
with everyday activities, such as shopping, climbing stairs, carrying
groceries or walking. You may also feel sleepy after eating, feel
weak in the legs when walking and get short of breath while being
active.
Lack of appetite and nausea - a feeling of being full or sick to

your stomach.
Confusion or impaired thinking - changing levels of certain

substances in the blood, such as sodium, can result in reduced
blood flow to the brain, which can confuse.
Increased heart rate - heart palpitations, which feel as if your

heart is racing or throbbing.
Weight changes - reduced blood flow to your stomach can make

it harder to absorb nutrients from your food and may cause weight
loss. Extra fluid retention may cause your weight to increase.
IV. Anatomy
The anatomy of heart failure refers to the structural and functional changes
in the heart that contribute to its inability to pump blood effectively. Here’s a
breakdown:
Atria
 Left Atrium - Enlargement may occur due to increased pressure

from poor left ventricular filling.
 Right Atrium - Enlargement can happen in right-sided heart failure or

from secondary pulmonary hypertension.
Ventricles
Left Ventricle (LV)
 HFrEF (Heart Failure with Reduced Ejection Fraction) - The LV

becomes dilated and weak, reducing its ability to pump blood
effectively.
 HFpEF (Heart Failure with Preserved Ejection Fraction) - The LV

becomes stiff and cannot relax properly, impairing blood filling.
Right Ventricle (RV)
 Fails due to increased pressure in the pulmonary arteries or

conditions like cor pulmonale.
Valves
 Mitral and Tricuspid Valves - Regurgitation may occur due to
chamber dilation, and worsening heart failure.
 Aortic and Pulmonary Valves - Stenosis or insufficiency can

increase cardiac workload.
Blood Vessels
 Pulmonary Vessels - Congestion occurs in left-sided heart failure,

leading to pulmonary edema.
 Systemic Veins - Congestion occurs in right-sided heart failure,

causing peripheral edema and ascites.
Coronary Arteries
 Blockages or reduced blood flow due to coronary artery disease can

weaken the myocardium and lead to heart failure.
Myocardium (Heart Muscle)
 Hypertrophy: Thickened myocardium in response to increased

workload. Common in HFpEF.
 Dilation: Thinned and stretched myocardium in HFrEF, reducing

contractile strength.
Pericardium
 Pericardial Effusion or Constriction: Can exacerbate heart failure by

restricting the heart's ability to fill or pump effectively.

Pathophysiology
Heart Failure
Risk factors for people in this stage include

hypertension, coronary vascular disease,
diabetes, obesity, exposure to cardiotoxic
agents, genetic variants for cardiomyopathy
and family history of cardiomyopathy.
Previous symptoms of heart failure but

with either structural heart disease, or
increased filling pressures in the heart.
People with current or previous

symptoms of heart failure
People with heart failure symptoms that

interfere with daily life functions or lead to
repeated hospitalizations
Concept Map
Atrial Fibrillation
Risk Factors:
Irregular, rapid ventricular
Previous stroke response rate
Age > 65
Diatolic filling time
Hypertension
Diabetes
Preload (LVEDV)
Decompensated Frank Starling

response
Stroke Volume
Cardiac output
Pre-existing coronary , myocardial

or valvular disease
Heart Failure Myocardial ischemia
Myocardial infration
VI. Diagnostic Test
Clinical Evaluation
o History and Physical Examination: Assessment of symptoms
(e.g., dyspnea, fatigue, edema) and signs (e.g., jugular venous
distension, pulmonary crackles, peripheral edema).
Imaging Studies
Echocardiography (ECHO)
o Ejection Fraction (EF): Differentiates HFrEF, HFpEF, and

HFmrEF.
o Structural abnormalities (e.g., valve dysfunction, chamber size).
o Diastolic dysfunction in HFpEF.
Chest X-Ray
o Pulmonary congestion or edema.
o Cardiomegaly (enlarged heart).
Cardiac MRI
o Provides detailed images of myocardial structure and function.

Useful for detecting fibrosis or infiltrative diseases.
Coronary Angiography
o Detects ischemic causes of heart failure, such as coronary

artery disease.
Laboratory Tests
Blood Tests
B-type Natriuretic Peptide (BNP) or NT-proBNP: Elevated in heart

failure due to increased ventricular wall stress.
Complete Blood Count (CBC): Identifies anemia or infection.
Electrolytes and Kidney Function: Assesses fluid balance and organ

perfusion.
Thyroid Function Tests: Evaluates thyroid disorders that may

contribute to heart failure.
Liver Function Tests: Detects hepatic congestion due to right-sided
heart failure.
Biomarkers
Troponins: Rule out concurrent myocardial infarction.
Electrocardiogram (ECG)
o Identifies arrhythmias, ischemic changes, or signs of left

ventricular hypertrophy.
Stress Testing
o Assesses the functional capacity of the heart and detects

ischemia or coronary artery disease.
VII. Drugs Study
Drug Mechani Indicatio Adverse Action Nursing

order sm of ns effects responsibili
action ties
Furosemi Inhibits Edema Hypotensio Adjust Monitor

de 40 mg reabsorpti (ex, CHF, n, electrolyt blood
IV on of renal dehydration e pressure,
sodium dysfunctio , electrolyte imbalanc heart rate,
and n, or liver imbalances es as and
chloride cirrhosis), (e.g., needed; electrolyte
in the hypertensi hypokalemi ensure levels.
loop of on a, proper
Assess urine
Henle, hyponatrem hydratio
output and
promoting ia), n;
fluid status.
diuresis. ototoxicity administ
(at high er IV Administer
doses), slowly to IV dose
dizziness, reduce slowly (over
nausea risk of 1-2 minutes).
ototoxicit Educate
patient about
y. potential side
effects and
safety.
Assessm Nursing Plannin Implementat Rationale Evaluati

ent Diagnos g ion on
is
Subjective Activity After 8 Monitor vital Monitoring After 8

: Intoleran hours pt. signs vital signs hours pt.
ce will frequently helps - reports
“I’m
related experien (e.g., blood assess the improved
having
to ce a pressure, patient’s tolerance
chest pain
imbalanc reductio heart rate, cardiovascu to
and short
e n in oxygen lar and activities
breath as
between fatigue saturation respiratory can walk
verbalized
oxygen and levels). status, longer
by pt.”
supply improvin identifying distance
Administer
Objective: and g any signs of s without
oxygen as
(+) demand toleranc worsening excessiv
prescribed
Fatigue as by e to condition. e fatigue
to improve
fatigue activity or
(+) Pale oxygenation. Administeri
by the shortnes
looking ng oxygen
end of Provide rest s of
helps
the shift periods breath.
improve
and between
oxygenatio
decreas activities to
n, reducing
e in reduce
the
chest exertion.
symptoms
pain and Educate of
shortnes patient on shortness
s of the of breath
breath. importance and fatigue.
of energy
conservation Rest
techniques periods and
and pacing energy
during daily conservatio
activities. n prevent
further
If
exacerbatio
prescribed,
n of fatigue
administer
and
medications
decrease
for chest
the risk of
pain (e.g.,
injury.
nitroglycerin
or pain Medication
relief). s, if
prescribed,
can
alleviate
chest pain
and
improve
comfort,
making it
easier to
tolerate
activity.
 Monitor vital signs: heart rate, blood pressure, respiratory rate, and
oxygen saturation.
 Assess for symptoms of heart failure: dyspnea, fatigue, peripheral

edema, weight gain, and jugular vein distension.
 Perform daily weight checks to monitor fluid retention.

 Evaluate laboratory and diagnostic results (e.g., BNP levels,
electrolyte balance, chest X-ray, echocardiography findings).
 Diuretics (e.g., furosemide): Monitor for fluid output and electrolyte

imbalances.
o ACE inhibitors/ARBs: Observe for hypotension and renal

function changes.
o Beta-blockers: Monitor for bradycardia or worsening symptoms.
o Anticoagulants: Educate on bleeding risks and monitor INR (if

on warfarin).Implement fluid restriction as prescribed to reduce
fluid overload.
 Educate patients about low-sodium diets to prevent fluid retention.
 Monitor for signs of dehydration or fluid overload.
 Teach patients and families about:
o Recognizing early signs of worsening heart failure (e.g., sudden

weight gain, increased shortness of breath).
o The importance of medication adherence.
o Lifestyle modifications such as smoking cessation, exercise,

and stress management.
 Provide guidance on how to self-monitor symptoms and when to seek

medical attention.
 Offer emotional support to reduce anxiety and depression associated

with chronic illness.
 Encourage participation in support groups or counseling if needed.
 Watch for signs of complications such as:
o Pulmonary edema: Increased shortness of breath, crackles in

lungs.
o Arrhythmias: Palpitations, dizziness, or fainting.

o Renal impairment: Reduced urine output or rising creatinine
levels.
 Collaborate with the healthcare team to ensure comprehensive care,

including timely diagnostic testing and follow-ups.
 Arrange for cardiac rehabilitation or home health services if required.
 Provide clear instructions on post-discharge care and follow-up

appointments.
 Ensure patients understand their medication regimen and lifestyle

recommendations.
 Reinforce emergency protocols for worsening symptoms.
Aortic Dissection
Case Study
Mrs. S is an 89-year-old white female who resides at home with

her daughter: who presents to the ED reporting 7/10 intermittent,
aching, generalized chest pain. radiating to mid back which started
about 3 hr ago. She notes that she has never felt this pain before
and it is different from her arthritis pain. About 2 hr later she
started to feel weak, faint, and nauseous. She laid down and
attempted to take a nap, but was unable to get to sleep due to the
aching pain. She decided to tell her daughter, who felt that it was
appropriate to seek medical attention Her past medical history
includes type 2 diabetes with peripheral neuropathy HTN,
hyperlipidemia, CAD, arthritis, sleep apnea, breast cancer treated
with chemotherapy and radiation, hypothyroidism, and depression
She is allergic to penicillins, which cause anaphylaxis Her
immunizations include pneumococcal pneumonia > 10 years ago
and the influenza vaccine in October 2019. Her current
medications are metoprolol 50 mg PO BID, lisinopril 40 mg PO
daily, gabapentin 300 mg TID, Lantus 12 units SC every morning.
Humalog per sliding scale TID before meals, Lipitor 40 mg every
evening, levothyroxine 150 µg at 0630 daily. St John's wort 150
mg daily, and Tylenol 650 mg every 6 hr PRN. Her father and
paternal grandfather were both deceased by age 65 years
secondary to myocardial infarction. Both also had diabetes and
CAD. Her mother died at age 92 and had COPD, HTN, diabetes,
breast cancer, arthritis, and GERD.
Her sister, who is 87, has diabetes, GERD, IBS, and depression.
Her brother, whos 80, has HTN, BPH, GERD, depression, and
hypothyroidism. Mrs SHIGEO worker who has two daugh to the
senior son and enjoy gardening, playing cards, and playing bingo.
She waltimes per week center, which is approximately a quarter of
a mile from home, four times per week and helps ve lunchgorses a
25 pack-year smoking history (cigaret per week didual 14 years
serve ago She dinks two glasses of red wine about two times per
week, usually with dinner. She has had the following surgeries and
procedures, right hip replaced in 2012, bilateral cataract surgery in
2009, a cholecystectomy in 1961, and bilateral mastectomy with
reconstructive surgery in 2005. You elicit the following information
with your review of systems General: denies fever, fatigue, or
unexpected weight changes Neuro denies dizziness or
lightheadedness, but feels faint and has a mild headache HEENT
endorses intermittent blurry vision; denies discharge from eyes,
ears, or nose, denies eye or ear pain, denies tinnitus, denies
congestion, denies trouble chewing/swallowing Cardiac endorses
7/10 intermittent, aching, generalized chest pain, sudden onset,
radiating to neck and upper back which started about 3 hr ago, it is
aggravated by movement and not relieved when resting, nothing
has helped improve it • Respiratory denies SOB, DOE, orthopnea,
cough, or hemoptysis, denies flu like symptoms Gl: denies
vomiting or changes in bowel habits, endorses persistent nausea
GU: denies dysuria, frequency, hesitancy, urgency, or foul-
smelling urine Musculoskeletal endorses intermittent joint pain,
denies tenderness Integumentary: fungal rash under abdominal
folds, otherwise no skin changes, denies appearance of lesions
Her physical examination revealed the following Height, 167.64 cm
(66 in), weight, 96 kg (211.2 lbs) Vital signs temperature, 99 "F,
HR, 120 bpm; RR, 26 breaths/min; BP, 189/105 mm Hg, Spo2,
93% on RA General. She is tachypneic but able to converse in full
sentences and appears well-developed and well-nourished for her
stated age. Neurological: Her eyes open spontaneously. She
tracks and focuses. Her visual acuity is intact and speech is clear
and appropriate. She reports generalized weakness and is alert
and oriented to person and time with disorganized thinking. Pupils,
equal, round and reactive to light results are 3 mm brisk. She has
a right facial droop. Her tongue is midline. She is moving all
extremities with equal strength, and sensation is intactHer sister,
who is 87, has diabetes, GERD, IBS, and depression. Her brother,
whos 80, has HTN, BPH, GERD, depression, and hypothyroidism.
Mrs SHIGEO worker who has two daugh to the senior son and
enjoy gardening, playing cards, and playing bingo. She waltimes
per week center, which is approximately a quarter of a mile from
home, four times per week and helps ve lunchgorses a 25 pack-
year smoking history (cigaret per week didual 14 years serve ago
She dinks two glasses of red wine about two times per week,
usually with dinner. She has had the following surgeries and
procedures, right hip replaced in 2012, bilateral cataract surgery in
2009, a cholecystectomy in 1961, and bilateral mastectomy with
reconstructive surgery in 2005. You elicit the following information
with your review of systems General: denies fever, fatigue, or
unexpected weight changes Neuro denies dizziness or
lightheadedness, but feels faint and has a mild headache HEENT
endorses intermittent blurry vision; denies discharge from eyes,
ears, or nose, denies eye or ear pain, denies tinnitus, denies
congestion, denies trouble chewing/swallowing Cardiac endorses
7/10 intermittent, aching, generalized chest pain, sudden onset,
radiating to neck and upper back which started about 3 hr ago, it is
aggravated by movement and not relieved when resting, nothing
has helped improve it • Respiratory denies SOB, DOE, orthopnea,
cough, or hemoptysis, denies flu like symptoms Gl: denies
vomiting or changes in bowel habits, endorses persistent nausea
GU: denies dysuria, frequency, hesitancy, urgency, or foul-
smelling urine Musculoskeletal endorses intermittent joint pain,
denies tenderness Integumentary: fungal rash under abdominal
folds, otherwise no skin changes, denies appearance of lesions
Her physical examination revealed the following Height, 167.64 cm
(66 in), weight, 96 kg (211.2 lbs) Vital signs temperature, 99 "F,
HR, 120 bpm; RR, 26 breaths/min; BP, 189/105 mm Hg, Spo2,
93% on RA General. She is tachypneic but able to converse in full
sentences and appears well-developed and well-nourished for her
stated age. Neurological: Her eyes open spontaneously. She
tracks and focuses. Her visual acuity is intact and speech is clear
and appropriate. She reports generalized weakness and is alert
and oriented to person and time with disorganized thinking. Pupils,
equal, round and reactive to light results are 3 mm brisk. She has
a right facial droop. Her tongue is midline. She is moving all
extremities with equal strength, and sensation is intact
Cardiac: She has sinus arrhythmia with frequent PVCs. You

appreciate a V IV diastolic murmur Pulses are 1+ to both upper
and lower extremities, and she has generalized nonpitting trace
edema. She has a right carotid bruit and abdominal aorta bruit. •
Respiratory: She is tachypneic, her lungs are clear bilaterally with
diminished sounds to both bases. Chest wall excursion is
symmetric, and respirations are nonlabored GI: She has normal
bowel sounds. Her abdomen is soft and mildly tender diffusely on
palpation. There are no visible pulsations and no masses felt GU:
She has clear amber urine with light sediment Musculoskeletal:
She has no inflammation, tenderness, or edema to joints. She is
hypermobile with loose joints and a ROM appropriate for her age
Integumentary Her skin is hyperelastic, dry, and fragile, with
scattered bruising. Based on the information you have received,
your must-not-miss diagnoses include STEMI, aortic dissection,
and PE. Other top differentials would include acute
infectious/inflammatory pulmonary process Your diagnostics
should include an ECG to rule out STEMUNSTEMI A CXR, which
may assist in your differential for aortic dissection and other
pulmonary or thoracic concerns, and computed tomography with
arterial contrast enhancement (CTA) of chest and abdomen for
evaluation for aortic disease, PE, and abdominal aortic aneurysm
(AAA). Laboratory tests would include CBC to evaluate for
infections/inflammation, anemia, a metabolic panel for electrolyte
abnormalities, renal dysfunction, cardiac enzymes, lactic acid, and
pro-BNP Pertinent results you obtain from Mrs. S's tests include
the following CBC: WBC, 9.7 10*3/ul, Hbg, 7.6 g/dl, Hct, 25.6%,
MCV, 85 II: PLT, 133 10-3/ul Chemistry: Na, 139 mmol/L, K, 5.1
mmol/L, chlor 92 mmol/L, HCO 27 mmol/L, BUN, 10 mg/dl,
creatine, 0.8 mg/dl, glucose, 189 mg/dl, Ca, 9.1 mg/dl, Mg, 2.4
mg/dl, Phos, 4.2 mg/dl, lactic, 3.1 Cardiac enzymes troponin, 1.7
ng/ml, CK, 1319 U/L, CKMB, 4.7, pro-BNP 350 pg/ml, d-dimer, 20
ng/ml UA. glucose, negative, ketones, negative, blood, negative,
pH, 57, specific gravity, 1010, protein, negative, leukocytes,
negative, nitrite, negative ECG. HR, 90 bmp, normal PR, QRS,
sinus rhythm, normal axis, no ST or T wave abnormalities You
order a CXR
Your interpretation is as follows:
 Widened mediastinum
 Diffuse enlargement of the aorta, with poor definition of the

aortic contour.
 Enlarged cardiac silhouette.
Specific Objectives
o To recognize clinical signs and confirm diagnosis through

imaging techniques (e.g., CT angiography, MRI, TEE).
o To identify and manage high-risk populations, including those

with hypertension, genetic disorders, or aortic aneurysms.
o To provide appropriate treatment based on the type of

dissection (medical management or surgery) and prevent
complications (e.g., rupture, stroke).
o To monitor for complications and ensure ongoing management
(blood pressure control, imaging) post-treatment to prevent
recurrence.
General Objectives
To understand, diagnose, and manage aortic dissection effectively

to improve patient outcomes, prevent complications, and reduce
mortality through early detection and appropriate intervention.
II. Introduction
An aortic dissection is a serious condition in which a tear occurs in the

inner layer of the body's main artery (aorta). Blood rushes through the
tear, causing the inner and middle layers of the aorta to split (dissect). If
the blood goes through the outside aortic wall, aortic dissection is often
deadly.
Severe, Sudden Chest or Back Pain
 Sharp, tearing, or ripping pain, often described as the worst pain the
patient has ever experienced.
 The pain typically starts suddenly and is located in the chest, but can
radiate to the back (between the shoulder blades) or abdomen.
Blood Pressure Differences
 Unequal blood pressure in the arms (e.g., systolic BP in one arm is

higher than in the other).
 Severe hypertension (elevated blood pressure) is often present, but

hypotension may occur if the dissection leads to rupture.
Pulse Deficits or Abnormal Pulses
 Weak or absent pulses in one or both arms or legs due to reduced

blood flow.
 Loss of pulses in the carotid or femoral arteries, depending on the

dissection site.
Syncope or Fainting
 Loss of consciousness may occur due to reduced blood flow to the

brain, especially with a rupture or severe dissection.
Shortness of Breath (Dyspnea)
 Difficulty breathing due to the disruption of blood flow or compression

of the lungs or heart.
Stroke Symptoms (Neurological Deficits)
 Symptoms such as sudden weakness, numbness, difficulty speaking,

or vision changes, indicating reduced blood flow to the brain
(especially if the dissection involves the aortic arch).
Abdominal Pain
 Severe abdominal pain, particularly if the dissection extends to the

abdominal aorta.
Cough or Hoarseness
 Hoarseness or difficulty swallowing may occur if the dissection

involves the aortic arch, which can compress the recurrent laryngeal
nerve.
Other Possible Symptoms
Nausea and vomiting - particularly if the dissection affects

abdominal organs or causes shock.
Cold extremities - due to poor blood circulation in the legs or arms.
IV. Anatomy
An aortic dissection is caused by a weakened area of the aorta's wall.Aortic
dissections are divided into two groups, depending on which part of the
aorta is affected:
 Type A - This more common and dangerous type involves a tear in

the part of the aorta where it exits the heart. The tear may also occur
in the upper aorta (ascending aorta), which may extend into the
abdomen.
 Type B - This type involves a tear in the lower aorta only (descending
aorta), which may also extend into the abdomen.
Aortic Dissection
Most common risk factor, for people in

this stage include, increasing shear stress
on the aortic wall, Chronic inflammation,
Conditions like Marfan syndrome, and
Pre-existing aneurysms increase the risk
of dissection.
A tear in the intima is the initiating

event, often in areas of high
hemodynamic stress
Blood under high pressure enters the
medial layer, separating it and creating
a false lumen
Blood leakage into the pericardial

sac (hemopericardium) leads to
tamponade, a fatal condition.
Concept Map
Aortic Dissection
Risk Factors:
Persistent high blood pressure exerts
Blunt Trauma shear stress on the aortic intima.
Age > 50-70 years

Intimal Tear
Hypertension
Poorly Controlled
Lipids
Media Separation
Expansion of the False

Lumen
True Lumen Compression
Malperfusion
syndrome
Propagation of Dissection
Recurrent dissection Chronic Dissection
Aneurysm formation
VI. Diagnostic Test
CT Angiography (CTA)
o Gold standard for diagnosing aortic dissection.
o Provides high-resolution images of the aorta, including the dissection

flap, false lumen, and true lumen.
o Can identify complications like rupture, aortic aneurysm, or organ

ischemia.
Magnetic Resonance Angiography (MRA)
o Non-invasive and provides detailed images of the aorta.
o Particularly useful in patients with contraindications to contrast

material or those with renal insufficiency.
o Can visualize the extent of the dissection and involvement of

branches of the aorta.
Transesophageal Echocardiography (TEE)
o A highly sensitive test for diagnosing aortic dissection, especially for

Type A dissections (involving the ascending aorta).
o Provides real-time imaging of the aorta and heart, allowing for

assessment of the dissection flap and blood flow.
o Often used in emergency settings when other imaging methods are

unavailable or contraindicated.
Chest X-Ray
o Initial test often performed to evaluate for signs of aortic dissection.
o May show a widened mediastinum, which is suggestive of aortic

dissection, though not diagnostic
Laboratory Tests
D-dimer
o Elevated levels of D-dimer may suggest the presence of thrombus or
clot formation, which can occur in aortic dissection.
o Although not specific to aortic dissection, D-dimer testing can help

rule out other conditions (e.g., deep vein thrombosis, pulmonary
embolism) in the differential diagnosis.
Complete Blood Count (CBC)
o To assess for anemia, which may indicate internal bleeding, or signs

of infection.
o A low hemoglobin level can suggest blood loss from rupture or other
complications.
Renal Function Tests (Creatinine, BUN)
o Important to monitor kidney function, as aortic dissection can cause

renal ischemia or failure due to decreased blood supply to the
kidneys.
o Elevated creatinine or BUN levels may indicate renal impairment.
Electrolytes (Potassium, Sodium, Calcium)
 To assess electrolyte imbalances that may arise from fluid shifts,

kidney dysfunction, or medication effects.
Troponin Levels
 May be elevated if the dissection causes myocardial ischemia or

damage to the heart muscle, particularly if the dissection affects
coronary arteries.
Arterial Blood Gases (ABG)
 To assess for hypoxia or acidosis, which may occur if there is

significant blood loss or organ ischemia.
Electrocardiogram (ECG)
 Not typically used to diagnose aortic dissection but can help rule out
myocardial infarction (MI), which presents with similar chest pain.
 ST-segment changes or elevated troponins could indicate concurrent
heart issues, especially if the dissection impacts the coronary
arteries.
Echocardiography (Transthoracic Echocardiogram - TTE)
 Can be used in some cases, though TEE is more accurate for

visualizing the aorta.
 Helpful for identifying valve involvement or pericardial effusion if the

dissection affects heart structures.
Ultrasound (In Special Cases)
 Carotid or femoral artery ultrasound may be used if there is suspicion

of dissection affecting branch vessels of the aorta (e.g., carotid artery
dissection).
 CT Angiography remains the most widely used and definitive

diagnostic tool for aortic dissection.
 TEE is critical in emergency settings, particularly for Type A

dissections.
VII. Drugs Study
Drug Mechanis Indications Adverse Action Nursing

order m of effects responsibiliti
action es
Metoprol Beta- Hypertensio Bradycardi Monitor Check blood

ol 50 mg blocker: n, angina, a, heart pressure and
PO BID reduces heart hypotensio rate, pulse before
heart rate failure, n, fatigue, blood administration
and blood arrhythmias dizziness, pressur . Educate
pressure depression e, and patient on
by ECG. signs of low
blocking heart rate
beta- (bradycardia).
adrenergic
receptors
in the
heart.

order m of s effects responsibiliti
action es
Lisinop ACE Hypertensi Hyperkalem Monitor Assess renal

ril 40 inhibitor: on, heart ia, blood function
mg PO inhibits failure, hypotension pressure, (creatinine,
daily angiotensi post-MI , dizziness, kidney BUN),
n- cough, function, monitor
converting renal and potassium
enzyme, impairment electrolyt levels, and
reducing es. educate
blood patient about
pressure potential
and cough.
improving
heart
function.

order m of s effects responsibilitie
action s
Lantus Long- Type 1 or Hypoglycemi Monito Instruct patient

12 acting Type 2 a, weight r blood on proper
units insulin: diabetes gain, glucos injection
SC regulates injection site e technique,
every blood reactions levels monitor for
mornin glucose by before signs of
g promoting meals. hypoglycemia,
glucose and adjust diet
uptake into or activity
cells. accordingly.

order m of action effects responsibilit
ies
Lipitor Statin: Hyperlipide Muscle pain, Monitor Assess liver

40 mg inhibits mia, liver lipid function
every HMG-CoA cardiovascul dysfunction, profile (AST/ALT),
eveni reductase ar disease gastrointesti and monitor for
ng to lower prevention nal upset liver signs of
cholesterol enzyme muscle pain
and prevent s. or weakness,
cardiovascu and educate
lar disease. on diet and
lifestyle
changes.
Drug Mechanism Indication Adverse Action Nursing

order of action s effects responsibiliti
es
Tylen Inhibits Pain relief, Hepatotoxicit Monitor Assess pain

ol 650 prostaglandi fever y (with liver level, monitor
mg n synthesis reduction overdose), functio for signs of
every in the CNS nausea, n. overdose
6 hr to reduce rash, (jaundice,
PRN pain and stomach confusion),
fever. upset and ensure the
patient does
not exceed the
daily dose
(4g).
Assessment Nursing Planning Implementa Rationale Evaluati

Diagnosis tion on
Subjective: Decreased After 8 Administer Medication After 8

Cardiac hours pt will medications s to control hours pt.
“ I’m having
Output have as heart rate will be
shortness of
related to improved prescribed and blood decrease
breath lately
altered oxygenation (e.g., pressure Vital
as
heart rate and cardiac antihyperten help signs are
verbalized
as output, as sives, improve within
by the
evidenced evidenced diuretics, or cardiac normal
patient”
by by stable medications output and limits (HR
Objective: shortness vital signs for heart rate reduce < 100
(+) Fatigue of breath. (e.g., HR < control). workload bpm, BP

100 bpm, on the < 140/90
(+) Pale skin Administer
BP < heart. mmHg,
supplementa
V/S 140/90 SpO2 >
l oxygen if Monitoring
mmHg, 95%).cre
T 99 "F, HR SpO2 vital signs
SpO2 > ase
120 bpm remains allows for
95%).
below 94% early
RR 26
(as per detection
BP 189/105 protocol).vita of
Spo2, 93% l signs worsening
frequently cardiac
(blood function
pressure, and
heart rate, adequate
respiratory response
rate, SpO2). to
interventio
Elevate the
ns.
head of the
bed to ease Oxygen
breathing if supplemen
the patient is tation
experiencing improves
dyspnea. tissue
oxygenatio
Provide rest
n,
periods and
addressing
limit physical
hypoxia
exertion to
and
reduce
preventing
cardiac
further
workload.
complicatio
Educate ns.
patient on
Rest
lifestyle
periods
changes,
and
including salt
limiting
and fluid
exertion
restrictions,
reduce
and the
strain on
importance
the heart
of
and help
medication
alleviate
adherence.
symptoms
of fatigue
and
shortness
of breath.
Patient
education
encourage
s
adherence
to lifestyle
modificatio
ns and
medication
s, which
are crucial
for
managing
decreased
cardiac
output.
Assessment and Monitoring
 Monitor vital signs closely, including blood pressure, heart rate,

respiratory rate, and oxygen saturation.
o Blood pressure should be controlled to prevent further

dissection or rupture.
o Regularly check for pulses (especially in the arms and legs) to

detect any changes in circulation.
 Assess pain: Frequently assess the patient's pain level using a pain
scale, as severe, sudden chest or back pain is a hallmark of aortic
dissection.
 Perform neurological checks to assess for signs of stroke, including

confusion, numbness, or weakness, which may indicate reduced
blood flow to the brain.
 Monitor for signs of organ ischemia, such as decreased urine output,

cold extremities, or changes in mental status, indicating poor
perfusion.
 Assess for complications: Monitor for signs of aortic rupture or

complications like hemothorax, stroke, or myocardial infarction.
Watch for sudden changes in vitals or consciousness.
Medication Administration and Management

 Administer antihypertensive medications as prescribed (e.g., beta-
blockers, calcium channel blockers) to reduce stress on the aorta and
control blood pressure.
 Pain management: Administer pain medications as prescribed,

ensuring comfort and reducing stress on the cardiovascular system.
 Monitor for medication side effects, such as bradycardia,

hypotension, or electrolyte imbalances, which can complicate aortic
dissection management.
 Assist in the management of sedation during diagnostic procedures

(e.g., CT, MRI, or TEE).
Support During Diagnostic Procedures
 Prepare the patient for diagnostic tests like CT angiography, MRA, or

TEE by explaining the procedure and addressing any concerns.
 Monitor the patient during and after diagnostic procedures for any
adverse reactions, such as allergic reactions to contrast material.
Educating the Patient and Family
 Explain the condition: Provide information about the nature of aortic

dissection, treatment options (medical vs. surgical), and the
importance of early detection.
 Discuss lifestyle modifications: Educate on controlling risk factors

such as blood pressure management, avoiding strenuous physical
activity, and smoking cessation.
 Instruct the patient and family on recognizing symptoms of

complications or recurrence (e.g., sudden chest pain, fainting,
neurological changes).
 Provide emotional support: Aortic dissection is often a life-threatening

condition, so offering emotional reassurance and guidance to reduce
anxiety is essential.
Postoperative and Post-Treatment Care

 After surgical intervention or repair of the aorta, monitor for signs of
infection, hemorrhage, or re-dissection.
 Assist with post-operative recovery: Help the patient regain mobility

and perform activities of daily living while closely monitoring for
complications such as infection, blood clots, or wound healing issues.
 Monitor fluid and electrolyte balance, especially if the patient is

receiving intravenous fluids or blood products post-surgery.
 Ensure adherence to follow-up appointments for imaging studies and

ongoing blood pressure management.
Collaboration and Communication
 Collaborate with the healthcare team (cardiologists, surgeons,

radiologists, and ICU staff) to ensure optimal care, especially in
emergency situations or post-surgery.
 Communicate any changes in the patient's condition promptly to the

medical team, particularly if signs of complications (e.g., rupture or
stroke) are detected.
Emergency Preparedness
 Be prepared to act quickly in the event of a rupture or other life-

threatening complication. This includes maintaining equipment for
resuscitation, blood products, and emergency medications at the
bedside.
 Manage life support: In the event of cardiac arrest or severe

hypotension, be ready to assist with CPR or advanced cardiac life
support (ACLS) as required.
Documentation
 Document all assessments and interventions accurately, including

vital signs, pain levels, medication administration, and any changes in
the patient’s condition.
 Chart diagnostic test results, nursing interventions, and patient/family
education to ensure continuity of care.
Delirium and Depression
Case Study
Mrs. J is a 78-year-old widowed female who lives in independent

senior living. Her daughter brings her to the emergency room and
reports, "My mother is not herself! For the past 2 weeks, she hasn't
answered her phone and her friends informed me she is not attending
lunches at the senior center. When she visited me last Sunday, she
was withdrawn and tearful, and slept all afternoon. Then in the past 2
days, she talked gibberish, was disoriented, and was awake all night.
She may have fallen, I'm afraid she may have had a stroke! When I
went to pick her up to bring to the hospital, I found a note on her desk
stating she wanted to die!" On mental status examination, the patient
is a frail, elderly female who is disoriented, inattentive, and irritable.
She complains of chest and hip pain. She recognizes her daughter
but does not understand where she is. Her speech varies from being
inaudible to excessively loud. She frequently falls asleep during the
interview but is easily aroused. She admits to feeling depressed and
starts to cry. She denies suicidal thoughts but states, "I would be
better off dead!" She is unable to describe her sleep patterns or
recent appetite. Her thoughts are disorganized. She denies auditory
or visual hallucinations. Her daughter reports that her mother's short-
term memory has been worsening over the past 6 months, although
her long-term memory is good. The patient lacks insight and
judgment. As the AGACNP caring for the patient, you complete the
history and physical. examination of the patient, documenting and
ordering the following: Medical comorbidities: HTN,
hypercholesteremia, hypothyroidism, depression. Medications:
Lisinopril 20 mg PO qd, Lipitor 40 mg PO qd, Synthroid 50 µg PO qd,
venlafaxine XR 37.5 mg po q am, nortriptyline (NTP) 100 mg PO qhs
Medical workup includes CBC w/diff, comprehensive metabolic panel,
LFTS, thyroid panel, RPR, UA, toxicology screen (alcohol,
acetaminophen, benzodiazepines, opioids), NTP level, vitamin B12,
folate, vitamin D, ECG, head CT, CXR, hip XR, screen for cognitive
impairment (Mini-Mental State Examination [MMSE] or Montreal
Cognitive Assessment ( MoCA), screen for depression.
Mrs. J complains that she has been more forgetful for months and her
daughter confirms this. She tells the APR she is frightened that she
may have. Alzheimer disease. When pressed for time, administration
of the mini-Cog is reasonable. For a more comprehensive screening,
the APRN informs the patient and her daughter that she will begin
cognitive screening using the MOCA Instrument. Also, the APRN
educates the patient and daughter that impaired concentration and
memory are symptoms of depression. Once depression is treated,
baseline cognitive status will be reevaluated and often is improved.
Specific Objectives
Delirium
To identify the underlying causes or triggers of delirium (e.g.,

infections, medications, or metabolic imbalances).
To assess the cognitive, behavioral, and motor changes

associated with delirium.
To differentiate between delirium and other neurocognitive

disorders, such as dementia.
To evaluate the effectiveness of treatment interventions, such

as pharmacological or non-pharmacological approaches.
To monitor the progression and resolution of delirium through

clinical observation and diagnostic tools.
Depression
To identify the symptoms of depression based on diagnostic
criteria.
To determine the potential risk factors and causes, such as

genetic, environmental, or psychological influences.
To assess the severity and impact of depression on daily

functioning and quality of life.
To evaluate the effectiveness of therapeutic interventions,

including psychotherapy, medication, or lifestyle modifications.
To explore the relationship between depression and comorbid

conditions, such as anxiety or chronic illnesses.
General Objectives
Delirium
To improve the understanding, diagnosis, and management of

delirium across clinical settings.
To prevent complications associated with untreated delirium,

such as long-term cognitive impairment or increased mortality.
To promote early detection and intervention to improve patient

outcomes.
Depression
To enhance awareness and recognition of depression in

various populations.
To reduce the prevalence and burden of depression through

effective prevention and treatment strategies.
To promote mental health and well-being by addressing social,

psychological, and medical factors contributing to depression.
II. Introduction
Delirium is a serious change in mental abilities. It results in
confused thinking and a lack of awareness of someone's
surroundings. The disorder usually comes on fast — within hours
or a few days.
Delirium can often be traced to one or more factors. Factors may

include a severe or long illness or an imbalance in the body, such
as low sodium. The disorder also may be caused by certain
medicines, infection, surgery, or alcohol or drug use or withdrawal.
Depression is a mood disorder that causes a persistent feeling of

sadness and loss of interest. Also called major depressive disorder
or clinical depression, it affects how you feel, think and behave
and can lead to a variety of emotional and physical problems. You
may have trouble doing normal day-to-day activities, and
sometimes you may feel as if life isn't worth living.
Delirium
Cognitive Changes:
o Sudden confusion or disorientation.
o Impaired memory, especially short-term memory.
o Difficulty focusing, sustaining, or shifting attention.
Behavioral Changes:
o Restlessness or agitation.
o Lethargy or reduced activity (hypoactive delirium).
o Sleep-wake cycle disturbances (e.g., reversal of day and night).
Emotional Changes:
o Irritability, anxiety, or fear.
o Hallucinations (seeing or hearing things that aren’t there).
o Paranoia or delusions.
Physical Signs:
o Tremors or other motor disturbances.
o Fluctuations in alertness (e.g., hypervigilance to stupor).
o Signs of an underlying cause (e.g., fever, dehydration, or

hypoxia).
Depression
Emotional Symptoms:
o Persistent sadness, emptiness, or hopelessness.
o Feelings of worthlessness, guilt, or helplessness.
o Loss of interest or pleasure in previously enjoyed activities

(anhedonia).
Cognitive Symptoms:
o Difficulty concentrating, making decisions, or remembering

things.
o Recurrent thoughts of death or suicide.
Behavioral Symptoms:
o Social withdrawal or isolation.
o Reduced engagement in routine activities.
o Changes in speech patterns (e.g., slowed or less frequent).
Physical Symptoms:
o Fatigue or low energy.
o Changes in appetite or weight (loss or gain).
o Sleep disturbances (insomnia or hypersomnia).
o Psychomotor agitation or retardation (restlessness or slowed

movements).
IV. Anatomy
Delirium is an acute disorder of attention and cognition, caused by
disturbances in the brain's neurochemical signaling and network
interactions.
Brain Regions Involved:
o Prefrontal Cortex - Impairments here affect attention, decision-

making, and executive function.
o Parietal Lobe - Dysfunction in this area contributes to

disorientation and spatial awareness issues.
o Thalamus - Acts as a sensory relay center; disruptions may

impair alertness and perception.
o Basal Ganglia - Involved in motor regulation; contributes to

agitation or lethargy in delirium.
o Hippocampus - Dysfunction leads to memory impairments

commonly observed in delirium.
Neurochemical Changes:
o Reduced levels of acetylcholine (linked to attentional deficits).
o Increased activity of dopamine (causing hallucinations or

agitation).
o Imbalances in serotonin and gamma-aminobutyric acid (GABA).
Pathophysiological Factors:
o Neuroinflammation from infections, trauma, or illness.
o Disruptions in cerebral blood flow or oxygenation (e.g.,

hypoxia).
o Metabolic abnormalities (e.g., electrolyte imbalances).
Anatomy of Depression
Depression is a chronic mood disorder with structural and functional

changes in key brain areas related to mood regulation, cognition, and
behavior.
Key Brain Regions Involved:
o Prefrontal Cortex - Hypoactivity in this area impairs decision-

making, emotional regulation, and executive function.
o Amygdala - Hyperactivity here heightens negative emotions

such as fear and sadness.
o Hippocampus - Reduced volume and activity contribute to

memory problems and emotional regulation deficits.
o Anterior Cingulate Cortex (ACC) - Dysfunction affects

processing of emotions and coping with stress.
o Basal Ganglia and Striatum: Altered function here can affect

motivation and reward systems.
Neurochemical Changes:
o Reduced levels of serotonin, norepinephrine, and dopamine

(affecting mood, energy, and pleasure).
o Dysregulation of GABA and glutamate systems (affecting

neural excitability and plasticity).
Structural and Functional Changes:
o Decreased connectivity between brain regions responsible for

mood and cognition.
o Reduced neurogenesis in the hippocampus, possibly linked to

prolonged stress and elevated cortisol levels.
Pathophysiology
Delirium
Depression
Older adults are at higher Common Triggers are

Infections, surgery,
risk due to decreased
medications, metabolic
brain resilience, chronic disturbances
illness, trauma
Neurotransmitter
Imbalance
Neurotransmitter
Dysregulation
Neural Network
Disruption
Cognitive slowing
Hallucinations,
Agitation, Disorganized
thinking, Acute onset
Structural and and fluctuating
Functional Brain attention
Changes
Concept Map
Depression Delirium
RISK FACTORS:
Old age, Infections,

surgery, medications,
metabolic disturbances,
Stress, genetics, chronic
illness, trauma
Neurotransmitter Neurotransmitter
Dysregulation Imbalance
Loss of interest, Hallucinations, Agitation,

Persistent sadness, Disorganized thinking,
Inflammation, Structural Acute onset and
and Functional Brain fluctuating attention
Changes
Supportive Care,
Hydration and Nutrition,
Antipsychotic
Medications,
Encouraging Sleep
VI. Diagnostic Test and Laboratory Test
Hygiene and Monitoring
Delirium
Diagnostic Tools:
Clinical Assessment:
o Confusion Assessment Method (CAM) - A widely used tool to

identify delirium, focusing on acute onset, inattention,
disorganized thinking, and altered level of consciousness.
o Delirium Rating Scale (DRS): Measures severity and

symptomatology.
Neurocognitive Testing:
o Mini-Mental State Examination (MMSE) or Montreal Cognitive

Assessment (MoCA) - Evaluate cognitive impairment and rule
out other causes such as dementia.
Laboratory Tests:
 Complete Blood Count (CBC) - Detects infections (e.g., sepsis).
 Electrolyte Panel - Assesses for imbalances like hypernatremia or

hyponatremia.
 Blood Glucose Levels - Identifies hypoglycemia or hyperglycemia.
 Liver Function Tests - Evaluates hepatic encephalopathy.
 Renal Function Tests - Checks for uremia or kidney dysfunction.
 Thyroid Function Tests - Detects thyroid imbalances like

hypothyroidism.
 Urinalysis - Screens for urinary tract infections (UTIs).
 Toxicology Screening - Identifies substance intoxication or

withdrawal.
 Arterial Blood Gas (ABG) - Determines oxygenation and acid-base

imbalances.
Imaging Studies
 Brain CT or MRI: Rules out structural abnormalities like stroke or

trauma.
 EEG (Electroencephalogram): Shows diffuse slowing, typical in
delirium.
Depression
Diagnostic Tests:
 Clinical Interviews:
o Use diagnostic criteria from DSM-5 or ICD-10.
o Structured tools such as the Hamilton Depression Rating Scale

(HDRS) or Beck Depression Inventory (BDI).
Psychological Screening Tools:
o PHQ-9 (Patient Health Questionnaire) - A self-reported

measure for severity.
o Geriatric Depression Scale (GDS) - Specific for older adults.
Laboratory Tests
 Thyroid Function Tests (T3, T4, TSH) - Hypothyroidism or

hyperthyroidism can mimic depression.
 Vitamin D and B12 Levels - Deficiencies are linked to mood

changes.
 Complete Blood Count (CBC) - Screens for anemia.
 Electrolyte Panel - Identifies imbalances affecting mood.
 Liver and Kidney Function Tests - Evaluate organ function for

potential impacts.
 Cortisol Levels - Elevated in cases of chronic stress or Cushing’s

syndrome.
Imaging and Specialized Tests
 Brain Imaging (MRI or CT) - Used in atypical cases to rule out

structural causes such as tumors or cerebrovascular disease.
 EEG - May be used if depression is suspected to have a neurological
origin.
VII. Drug Study
Drug Mechanism Indications Adverse Action Nursing

order of action effects responsibil
ities
Lisinop ACE Hypertensio Hyperkalemia Monitor Monitor BP

ril 20 inhibitor: n, heart , hypotension, blood regularly,
mg PO inhibits the failure, dizziness, pressure check renal
qd enzyme that post-MI, cough, renal , kidney function
converts diabetic impairment function, (creatinine,
angiotensin nephropath and BUN),
I to y electrolyt assess for
angiotensin es. signs of
II, resulting hyperkalem
in ia, educate
vasodilation patient
and lowered about
BP. possible
persistent
cough.

orde m of effects responsibiliti
r action es
Lipito Statin: Hyperlipidemi Hyperlipidemi Monitor Assess liver

r 40 inhibits a, prevention a, prevention lipid function
mg HMG-CoA of of profile (AST/ALT),
PO reductase cardiovascul cardiovascul and liver monitor for
qd to reduce ar disease ar disease enzyme muscle pain,
cholestero s. and educate
l on lifestyle
synthesis, changes for
leading to lipid control.
lower LDL
and total
cholestero
l levels.
Assessment Nursing Planning Implement Rational Evaluation

Diagnosis ation e
Subjective:’ Acute After 8 hours Conduct a Cognitive After 8 hours

Confusion pt. will comprehen assessm pt.
“my mom
related to demonstrate sive ents help improvement
has memory
cognitive improved cognitive identify in memory
loss
decline, as cognitive assessment the recall and
sometimes
evidenced function, as extent of cognitive
as Perform a
by memory evidenced by memory function
verbalized full physical
loss. better recall loss or
by SO” assessment
and confusion
to rule out
Objective: engagement ,
underlying
(+) Pale in activities. providing
conditions
looking data for
such as
diagnosis
anemia
.
Monitor
Physical
dietary
assessm
intake and
ents and
assess for
lab tests
any signs of
help
malnutrition
identify
or poor
possible
appetite.
causes of
Administer pallor,
any such as
prescribed anemia
medications or
for cognitive nutritional
enhanceme deficienci
nt es.
Provide a Monitorin
calm, g
structured nutrition
environmen helps
t to help ensure
reduce that
confusion physical
and anxiety. health,
including
Educate the
cognitive
significant
function,
other on
is
strategies
supporte
for
d by
managing
adequate
memory
intake.
loss,
including Medicatio
routine, ns, if
memory indicated,
aids, and can help
regular slow
check-ups. cognitive
decline or
address
any
underlyin
g
deficienci
es.
Structure
d
routines
and a
calm
environm
ent can
alleviate
confusion
and
reduce
the risk of
further
cognitive
decline.
Delirium
 Frequent Neurological Assessments: Monitor mental status using

tools like the Confusion Assessment Method (CAM).
 Vital Signs Monitoring: Check for signs of infection, hypoxia, or

metabolic imbalances.
 Pain Assessment: Evaluate and manage pain, as it can

exacerbate delirium.
Safety Measures
 Prevent Falls and Injuries: Use side rails, bed alarms, and
maintain a clutter-free environment.
 Supervision: Provide constant monitoring, especially for patients

with agitation or confusion.
 Medication Administration: Administer prescribed medications

(e.g., antipsychotics) carefully and observe for side effects.
Environmental Management
 Provide a Calm and Structured Environment: Minimize noise, use

soft lighting, and maintain a consistent daily routine.
 Orient the Patient Regularly: Use clocks, calendars, and familiar

objects to reduce disorientation.
 Promote Sleep Hygiene: Reduce nighttime disturbances and

provide comfort.
 Assist in the collection of specimens for lab tests and imaging.
 Monitor the effectiveness of treatments addressing the root cause,

such as antibiotics for infections or fluids for dehydration.
 Use simple, clear instructions.
 Speak calmly and avoid overwhelming the patient with too much
information.
Family Education and Support
 Inform family members about the condition, expected behaviors,

and progress.
 Encourage family participation in the patient's care to provide

comfort.
Depression
 Establish Trust and Rapport: Build a therapeutic relationship to

make the patient feel understood and supported.
 Active Listening: Encourage the patient to express feelings without

judgment.
 Encourage Positive Coping Mechanisms: Promote activities like

journaling, relaxation exercises, or mindfulness.
 Assess for Suicidal Ideation: Regularly evaluate for thoughts of

self-harm or suicide using validated tools and report immediately.
 Observe for Behavioral Changes: Watch for signs of worsening

depression or side effects of medications.
 Monitor Compliance: Ensure the patient adheres to prescribed
antidepressants or psychotherapy.
Motivate the patient to engage in daily routines, including

grooming and light physical activities, which can improve mood.
 Create a non-judgmental atmosphere where the patient feels safe.
 Encourage social interactions to reduce isolation.
 Administer antidepressants as prescribed, monitor for therapeutic

effects, and observe for adverse reactions like sedation or
agitation.
 Educate the patient about the importance of adherence and

potential delays in the onset of therapeutic effects (2–4 weeks).
 Teach About the Disorder: Help patients and families understand

depression and its management.
 Promote Therapy Participation: Encourage attendance at

psychotherapy sessions, such as cognitive-behavioral therapy
(CBT).
 Discuss Lifestyle Modifications: Highlight the importance of

balanced nutrition, regular exercise, and sleep hygiene.
Parkinson’s Disease
Case Study
Mr. A appeared to be a 72-year retired teacher and had progressive

tremors of right hands and stooped postural abnormality with initial
difficulty making movements during the last year. Occasionally, his
wife confirms that he experiences episodes of freezing during walking
along with increased difficulty with fine hand movements such as
buttoning his shirt. Neurological examination revealed the presence
of resting tremor of the right hand with bradykinesia, rigidity, and
postural instability which were in support of the diagnosis of
Parkinson's disease.
The diagnosis was made based on clinical criteria and the symptoms
were classified as Hoehn and Yahr Stage 2. Carbidopa-levodopa was
recommended to ameliorate motor symptoms and he was also
referred for physical therapy to enhance his gait and balance. This
case brings into light the significance of early diagnosis and
multimodal therapeutic management in the preservation of life quality.
Specific Objectives
o Control motor symptoms (e.g., tremors, rigidity, bradykinesia)

through appropriate pharmacological treatments like levodopa
and dopamine agonists.
o Address non-motor symptoms (e.g., depression, sleep

disturbances) with medication and supportive care.
o Improve mobility, daily functioning, and speech through

physical, occupational, and speech therapy.
o Educate caregivers on assisting while encouraging the patient’s

independence.
o Teach patients and caregivers about Parkinson’s disease,

treatment options, and lifestyle adjustments for better disease
management.
General Objectives
Improve of quality life to enhance the physical, emotional, and

social well-being of patients by managing both motor and non-
motor symptoms effectively early diagnosis and Treatment to
ensure early identification and timely initiation of treatment to slow
disease progression and prevent complications.
II. Signs and Symptoms
Motor Symptoms
Tremors (Resting Tremor):
o A characteristic shaking or trembling, most often starting in one

hand, that occurs when the muscles are at rest.
o The tremor is typically visible in the fingers, hands, or chin and

is often described as a "pill-rolling" tremor.
Bradykinesia (Slowness of Movement):
o A reduction in the ability to initiate and complete movements.
o This leads to slower, smaller steps while walking, difficulty

getting out of bed or a chair, and a general reduction in facial
expressions (masked face).
Rigidity (Muscle Stiffness):
o Stiffness or resistance to movement in the muscles, causing

discomfort or pain.
o This can affect any muscle group and can lead to a decrease in
the range of motion.
Postural Instability (Balance Problems):
o Impaired balance and coordination, which increases the risk of

falls.
o Patients may have difficulty maintaining an upright posture and

may lean forward or backward.
Shuffling Walk:
o A characteristic of Parkinson's disease where the patient’s gait

becomes slow with short steps, and the arms may not swing as
they normally would.
Non-Motor Symptoms
Cognitive Changes:
o In the later stages, patients may develop cognitive impairments

such as memory problems, attention difficulties, and issues with
executive function (planning, organizing, and decision-making).
o Some individuals may progress to Parkinson's disease

dementia (PDD).
Depression and Anxiety:
o Mood disorders, including depression and anxiety, are common

and can significantly impact the patient's quality of life.
Sleep Disturbances:
o Patients may experience difficulty falling asleep, frequent

waking, restless legs, or REM sleep behavior disorder (acting
out dreams).
Autonomic Dysfunction:
o Includes symptoms such as orthostatic hypotension (low blood

pressure when standing), excessive sweating, and urinary
urgency or incontinence.
Speech Changes (Dysarthria):
o Reduced volume or slurring of speech, making communication

more difficult.
Swallowing Problems (Dysphagia):
o Difficulty swallowing food or liquids, which can lead to choking

or aspiration pneumonia.
Other Symptoms
o Micrographia: Small, cramped handwriting.
o Fatigue: Extreme tiredness or lack of energy despite adequate rest.
o Constipation: Difficulty with bowel movements is common, often due

to the slowing of the digestive system.
III. Anatomy
Parkinson’s Disease is considered predominantly a disorder of

the basal ganglia. The basal ganglia are a group of nuclei situated
deep and centrally at the base of the forebrain. They have robust
connections with the cerebral cortex and thalamus in addition to other
areas of the brain. Their vast system of communication allows them
to involved with a variety of functions, including automatic and
voluntary motor control, procedural learning relating to routine
behaviors, and emotional functions. The association with other
cortical areas ensures smoothly orchestrated movement control and
motor behavior.
IV. Pathophysiology and Concept Map
Pathophysiology
Old age of 60 is the most significant
risk factor with the risk increasing with
age, Genetic Mutations, Rural Living,
Traumatic Brain Injury, Family History
and Neuroinflammation
Mitochondrial Dysfunction and

Oxidative Stress
Reduced ATP production and Excessive

production of reactive oxygen species
(ROS), causing neuronal damage.
Autonomic Dysfunction and

Cognitive Decline
Concept Map
Progressive neurodegenerative
disease and Widespread
degeneration of the substania
gravis leads to a decrease in
dopamine resulting in loss of
voluntary refined movement
Signs/Symptoms: Actual and Potential

Problems:
 Altered motor
control pathways  Risk for injury
 Speech Changes related to altered
(Dysarthria) gait
 Swallowing  Self-care deficit
Problems  Imbalanced
(Dysphagia) nutrition less than
 Constipation body requirements
related to difficulty
chewing and
swallowing as
Treatment:
 Physical therapy to help

them with ADLs
 Dopamine agonist
 Entacapone
 Deep Brain Stimulation
V. Diagnostic Test and Laboratory Test
Clinical Diagnosis
Medical History and Physical Examination:
o The first step in diagnosing Parkinson’s disease is a thorough

medical history and neurological examination.
o Doctors look for the characteristic symptoms of PD, such as
resting tremor, bradykinesia, rigidity, and postural instability. A
detailed assessment of motor and non-motor symptoms is
performed.
Parkinson’s Disease Rating Scales
Unified Parkinson’s Disease Rating Scale (UPDRS):
o A widely used tool to assess the severity of Parkinson’s disease

symptoms, including motor and non-motor functions.
o It helps evaluate the patient's disease progression over time.
Hoehn and Yahr Staging Scale
o A scale used to classify the severity of PD symptoms based on

physical impairment and disability.
Imaging Tests
Imaging can help support the diagnosis of Parkinson's disease,

although it is not typically used to confirm the disease.
Magnetic Resonance Imaging (MRI)
o MRI is used to rule out other conditions that could mimic PD,
such as brain tumors, strokes, or other neurodegenerative
diseases.
o In early Parkinson's, MRI may appear normal, but in later

stages, brain atrophy may be evident.
Single Photon Emission Computed Tomography (SPECT)
o A SPECT scan using DAT (Dopamine Transporter) imaging can

provide a visual representation of the dopaminergic system in
the brain.
o A reduced uptake of dopamine in the basal ganglia is indicative
of Parkinson’s disease, helping to differentiate it from other
movement disorders.
Positron Emission Tomography (PET):
o PET scans can also be used to visualize the function of

dopaminergic neurons and the brain’s metabolic activity, but
they are less commonly used due to high costs and availability
Laboratory Tests
Blood Tests:
o Thyroid function tests to rule out thyroid disorders that could

mimic PD symptoms.
o Complete blood count (CBC) to check for signs of infection or

anemia.
o Liver and kidney function tests to rule out other systemic

conditions.
o Vitamin B12 and folate levels: Low levels can contribute to

neurological symptoms.
o Serum ceruloplasmin: Can be measured to rule out Wilson’s

disease (copper accumulation disorder) which can present with
Parkinsonism.
Cerebrospinal Fluid (CSF) Analysis:
o In certain cases, CSF may be analyzed to rule out other

neurological disorders, though it is not routinely used for
diagnosing PD.
o A CSF 14-3-3 protein test can be used to rule out Creutzfeldt-

Jakob Disease (CJD), a rare prion disease that can mimic PD in
some cases.
Genetic Tests:
o In cases with early-onset Parkinson’s disease (before age 50)

or a strong family history of PD, genetic testing may be
conducted to detect mutations in genes such as LRRK2 or
Parkin. These tests are more commonly used in research
settings.
Olfactory Testing
Smell Identification Test:
o Loss of the sense of smell (anosmia) is an early non-motor

symptom of Parkinson’s disease. Although not diagnostic by
itself, anosmia can be an early indicator of PD, as it is often one
of the first symptoms to appear.
Electromyography (EMG) and Nerve Conduction Studies
 These tests are typically used to rule out other causes of motor
symptoms, such as neuropathies or myopathies, that may present
with symptoms similar to Parkinson’s.
VI. Drug Study
Drug Mechanism Indicatio Adverse Action Nursing

order of action ns effects responsibiliti
es
Carbido Levodopa is Restores Nausea Restores Monitor for

pa/ converted to dopamine and dopamin signs of
Levodop dopamine in levels to vomiting e activity dyskinesia
a the brain, reduce in the (uncontrolled,
Orthostatic
replacing the tremors, brain to involuntary
hypotensio
dopamine rigidity, help movements).
n
that is and control
Assess for
deficient in bradykine Dyskinesia moveme
orthostatic
Parkinson’s sia. (involuntary nt
hypotension,
disease. movements sympto
especially
Carbidopa ) ms in
when the
prevents Hallucinatio Parkinso
patient stands
levodopa ns, n’s
up.
from being confusion,
broken down or vivid disease. Administer
before it dreams with food to
reaches the reduce
Dry mouth
brain. nausea, but
Darkening avoid high-
of urine or protein meals
sweat that may
interfere with
absorption.
Monitor for
any changes
in mental
status, such
as confusion
or
hallucinations
.
Encourage
hydration to
prevent dry
mouth and
constipation.
Educate the
patient and
family about
potential side
effects and
the
importance of
adherence to
the
medication
schedule.
VII. Nursing Care Plan
Assess Nursing Plannin Implementatio Rationale Evaluatio

ment Diagnos g n n
is
Subjecti Impaired After 8 Monitor for Monitoring vital After 8

ve: Physical hours signs of signs ensures hours pt.
Mobility pt. will dyskinesia, early demonstr
“My
related experie such as identification of ates
husband
to nce involuntary any side improved
having a
tremors, improve movements, effects mobility
tremors
rigidity, d and assess the with less
and Assistance
and mobility frequency and difficulty
difficulty with mobility
bradykin and severity of performin
with and physical
esia as reductio tremors. g ADLs
moveme therapy helps
evidence n in
nt as Offer maintain
d by tremors
verbalize assistance with muscle
difficulty and
d by SO” mobility and strength and
moving rigidity,
encourage functional
Objectiv and allowing
physical independence.
e: performi them to
therapy to
ng particip Educating the
(+) Pale improve
activities ate in patient helps to
looking muscle
of daily ADLs ensure
strength and
living more medication
coordination.
(ADLs). effectiv adherence and
ely. Educate minimize

patient on adverse effects
taking the like nausea or
medication dyskinesia.
with food to
Carbidopa/
minimize
Levodopa
nausea and
helps manage
avoid large motor
protein meals. symptoms,
improving
Encourage
mobility and
regular follow-
quality of life.
up visits with
the healthcare
provider to
adjust
medication
doses as
needed.
Administer
Carbidopa/Lev
odopa as
prescribed.
o Regularly assess motor and non-motor symptoms (e.g.,

tremors, rigidity, cognitive changes).
o Monitor medication effectiveness and side effects, ensuring

timely adjustments as needed.
o Administer prescribed medications (e.g., levodopa) and ensure

adherence.
o Monitor for side effects and complications, adjusting treatment

plans accordingly.
o Educate patients and caregivers about Parkinson’s disease, its

progression, and symptom management.
o Teach safe practices for medication administration, symptom

monitoring, and daily activities.
o Encourage patients to maintain functional independence

through physical and occupational therapy.
o Provide strategies for mobility and safety, such as fall
prevention and adaptive devices.
o Offer emotional support to both patients and caregivers,

addressing concerns like depression, anxiety, and stress.
o Refer to mental health professionals when needed.
o Work closely with neurologists, therapists, and dietitians to

ensure comprehensive care.
o Participate in team discussions for coordinated management of

symptoms and quality of life.
Iron deficiency Anemia
Case Study
Mr. D, who is 64 years old and resides at Bgy 319, has a complicated
medical background involving anemia and cardiomegaly. His present
medication regimen consists of Losartan (50mg) and Clopidogrel (75mg),
showing attempts to care for his cardiovascular well-being. Yet, because of
his advanced age and resulting speech impairment, Buddy encounters
extra obstacles in communicating his needs and worries, underlining the
significance of gentle and understanding assistance. This case study will
investigate the complexities of handling anemia and cardiomegaly while
dealing with communication challenges related to aging.
Both anemia and cardiomegaly create considerable obstacles for Mr. D

health and well-being. Fatigue, shortness of breath, and reduced ability to
exercise can result from anemia, while cardiomegaly raises the likelihood of
heart failure and other heart-related problems. Dealing with these issues
necessitates a comprehensive strategy that takes into account his medical
and social requirements.
This case study will examine the complexities of treating anemia and
cardiomegaly in an elderly patient. It will underscore the significance of
delivering inclusive care that includes both medical intervention and social
assistance along with advocacy. By carefully reviewing Mr. Bernardino's
case, our goal is to find ways to enhance his health results and general
well-being, as well as tackle the broader challenges faced by vulnerable
populations.
o To Recognize and resolve any root causes or factors influencing his

health, such as inadequate diet, possible long-term illnesses, and the
effects of his living environment.
o To screen for and manage any comorbid conditions that may
complicate the cardiomegaly or recovery process. Assess Mr.
Bernardino's anemia and cardiomegaly by conducting a thorough
review of his medical history, physical exam, and necessary
diagnostic tests and Create and execute a customized treatment
strategy involving optimizing medication, making dietary changes,
and adjusting lifestyle habits, with an emphasis on addressing his
anemia and heart enlargement.
o To Create a physical activity plan that is safe and achievable based
on his cardiomegaly and overall health, while also enhancing
cardiovascular health and overall fitness.
o To Evaluate and tend to Mr. D psychosocial requirements, offering
assistance and aids to enhance mental and emotional health,
recognizing the possible consequences of his
homelessness/Loneliness. Advocate also for his needs and connect
him with available community resources to address the challenges
associated with aging.
o To evaluate the impact of Cardiomegaly on the patient’s functional
status and ability to perform activities of daily living (ADLs), and
provide support or adaptations as needed.
General Objectives:
This case study seeks to thoroughly evaluate and address the medical
needs of Mr. D, a 64-year-old man living at Bgy 319, who has a medical
record of anemia and cardiomegaly. We will pinpoint and resolve factors
influencing his conditions, develop a customized treatment plan, and
provide him with the required assistance. In the end, the main goal of this
case study is to enhance Mr. Bernardino’s quality of life and maximize his
health results in his existing living conditions.
II. Introduction
Iron-deficiency anemia is the most common form of anemia, a blood

disorder that affects your red blood cells. Iron-deficiency symptoms develop
over time. Healthcare providers may treat iron-deficiency anemia by
diagnosing and treating the condition that caused anemia and/or by
prescribing iron supplements.
 Fatigue and Weakness: Resulting from reduced oxygen delivery to

tissues due to low hemoglobin levels.
 Pallor: Noticeable in the skin, mucous membranes, and nail beds.
 Shortness of Breath: Particularly during exertion, due to decreased
oxygen-carrying capacity.
 Dizziness or Lightheadedness: Often caused by inadequate
oxygen perfusion to the brain.
 Cold Hands and Feet: Related to poor circulation and low
hemoglobin.
IV. Anatomy
Iron
deficiency anemia is a common type of anemia. It is a condition in which
blood lacks adequate healthy red blood cells. Red blood cells carry oxygen
to the body’s tissues. Iron deficiency is due to insufficient iron. Without
enough of a substance in red blood cell that enables them to carry oxygen
(hemoglobin)
Hemoglobin in red blood cells carries oxygen, in iron deficiency anemia,

reduced hemoglobin means less oxygen is delivered to tissues including
the heart. To compensate for the low oxygen levels, the heart increases its
output, leading to hypertrophy of the myocardium or the muscle of the
heart. The left ventricle is particularly affected, causing it to enlarge.

VI. Diagnostic and Laboratory Test
Complete Blood Count (CBC) - To assess hemoglobin, hematocrit, red

blood cell count, and indices like MCV, MCH, and MCHC.
Iron Studies - To evaluate for iron deficiency anemia (includes serum iron,
ferritin, transferrin, and total iron-binding capacity).
Vitamin B12 and Folate Levels - To rule out megaloblastic anemia.
Reticulocyte Count - To assess bone marrow function and the body’s

response to anemia.
Peripheral Blood Smear - To visually examine red blood cells for any
abnormalities in shape or size.
Renal Function Tests (BUN, Creatinine) - To check if anemia is related to

chronic kidney disease.
VII. Drug Study
Drug Mechanis Indicati Adverse Action Nursing

order m of ons effects responsibilit
action ies
Losarta Inhibits Hyperte Hypotensio Reduces Monitor blood

n
the action nsion n blood pressure
50mg, of pressure before
1tab
angiotensi and administering
Oral
n II, a improves to ensure it is
chemical blood flow within safe
that by dilating ranges.
causes blood
blood vessels.
vessels to
constrict,
thereby
reducing
blood
pressure
and
improving
blood
flow.
Inhibits Preventi Bleeding on Prevents Assess for

Clopido
grel platelet on of gastrointest blood clots, signs of
aggregati thrombot inal reducing bleeding,
75mg,
1tab on by ic events bleeding the risk of such as
Oral irreversibl and stroke or unusual
y blocking bruising. hear bruising,
the black or tarry
P2Y12 stools, or
compone prolonged
nt of ADP bleeding.
receptors
on
platelet
surfaces.
Assess Nursing Planning Implement Rationale Evaluat

ment Diagnosi ation ion
s
Subjecti imbalance After 8 Educate the Iron After 8

ve: d hours pt. will patient on supplement hours
Nutrition: verbalize consuming ation and pt.
"I feel
Less than understandi iron-rich dietary reports
tired all
Body ng of iron- foods changes improve
the time,"
Requirem rich food are d
as Teach the
ents sources and essential to energy
verbalize patient to
related to supplement replenish levels
d by the take iron
inadequat ation. iron stores and
patient. supplement
Objectiv e iron s with and reduced
e: intake as vitamin C- improve fatigue.
evidenced rich oxygen
(+) Pale
by low beverages. transport.
Skin
serum
Advise the Enhancing
ferritin
patient to iron
and
avoid taking absorption
hemoglobi
iron with ensures
n levels.
calcium- more
containing effective
products, treatment
antacids, or outcomes.
tea, which
Monitoring
may inhibit
lab values
absorption.
helps to
Monitor track
laboratory improveme
results nt and
(hemoglobin determine if
, hematocrit, adjustments
and ferritin in therapy
levels) to are needed.
evaluate
Managing
response to
side effects
therapy.
improves
Encourage adherence
adequate to therapy
hydration and
and provide ensures
stool consistent
softeners if treatment.
needed to
manage
constipation
caused by
iron
supplement
s.
Administer
prescribed
iron
supplement
s (e.g.,
ferrous
sulfate) as
per the
healthcare
provider's
order.
Assess for
any side
effects of
iron
therapy,
such as
nausea or
gastrointesti
nal upset.
IX.Nursing Responsibilities
o Administer prescribed iron supplements (e.g., ferrous sulfate) as

ordered.
o Ensure iron is taken with vitamin C-rich fluids (e.g., orange juice) to
enhance absorption.
o Avoid administering iron with calcium, antacids, or tea, which can

reduce absorption.
o Assess for gastrointestinal side effects such as nausea, constipation,
or dark stools.
o Provide interventions like hydration or stool softeners to manage

constipation.
o Teach the patient to incorporate iron-rich foods into their diet (e.g.,
red meat, spinach, beans, fortified cereals).
o Explain how vitamin C can enhance iron absorption, while certain

foods or medications can inhibit it.
o Regularly check vital signs and assess for pallor, fatigue, or

tachycardia as ongoing symptoms of anemia.
o Monitor lab values (hemoglobin, hematocrit, serum ferritin) to

evaluate treatment effectiveness.
o Instruct the patient to adhere to the prescribed regimen, emphasizing

that it may take weeks to notice improvements.
o Advise on the importance of follow-up appointments to reassess iron

levels and adjust therapy as needed.
o Monitor for potential sources of blood loss (e.g., menstrual bleeding,

gastrointestinal bleeding).
o Report abnormal findings to the healthcare provider for further

evaluation.
Pulmonary Tuberculosis
Case Study
Mr. T is a 70-year-old male who presents with a persistent cough lasting

over three months, accompanied by unintentional weight loss, night
sweats, fatigue, and occasional low-grade fever. He has a history of
smoking, which he quit 10 years ago, and a previous diagnosis of chronic
obstructive pulmonary disease (COPD). His family history reveals that his
father had pulmonary tuberculosis (TB) in his 50s. Recently, the patient
attended a family gathering where he consumed alcohol, which he believes
aggravated his cough and caused increased breathlessness. He is
currently on bronchodilators and a multivitamin but has not been taking any
TB-specific medications. A chest X-ray and sputum analysis are planned to
confirm pulmonary tuberculosis and guide further treatment.
 To identify the clinical manifestations and diagnostic findings of PTB.

 To explain the pathophysiology and impact of PTB on the patient's
health.
 To create an individualized care plan addressing the patient’s
physical, emotional, and social needs.
 To implement infection control measures to prevent disease
transmission.
 To educate the patient and family on medication adherence, lifestyle
modifications, and follow-up care.
General Objectives:
To provide holistic nursing care to a patient with Pulmonary

Tuberculosis, focusing on improving respiratory function, preventing
transmission, and promoting recovery.
II. Introduction
Pulmonary Tuberculosis (PTB) is a chronic infectious disease caused by

Mycobacterium tuberculosis. It primarily affects the lungs but can spread to
other organs if untreated. The disease is transmitted via airborne droplets
from an infected individual. PTB is characterized by pulmonary infiltrates,
granuloma formation, and tissue cavitation. Early detection and adherence
to treatment are critical to preventing complications and controlling its
spread.
III. Signs & Symptoms:

● Persistent productive cough lasting more than 3 weeks.
● Hemoptysis (blood-streaked sputum).
● Generalized fatigue and weakness.
● Night sweats.
● Loss of appetite and significant weight loss.
● Complaints of low-grade fever.
● Crackles and wheezing auscultated in the upper lung fields.
● Decreased breath sounds bilaterally.

● Pallor and underweight appearance.
● Elevated body temperature (38.2°C).
● Respiratory rate of 25 breaths per minute.
IV. ANATOMY
The lungs are located in the thoracic cavity, flanking the heart. Each lung is
protected by the ribcage and is separated by the mediastinum, where the
heart, trachea, esophagus, and major blood vessels are located. The lungs
are cone-shaped with a broad base that rests on the diaphragm and a
tapered apex that extends slightly above the clavicle.
The lungs are divided into 2 lobes, the right lung has 3 lobes which are
upper, middle, and lower while the left lung has 2 lobes which are upper
and lower. The trachea is the airway that connects the larynx to the lungs,
located in front of the esophagus. On the other hand, bronchi The trachea
divides into the left and right main (primary) bronchi, each entering a lung.
Alveolar ducts lead to clusters of alveoli, which are tiny, balloon-like
structures where the primary gas exchange occurs. Each alveolus is
surrounded by a network of capillaries, and the thin walls of the alveoli
allow oxygen to pass from the air into the blood and carbon dioxide to be
expelled.The lungs have a network of lymphatic vessels and nodes that
help remove waste products, pathogens, and excess fluid.
V. PATHOPHYSIOLOGY AND CONCEPT MAP
VI. Diagnostic and Laboratory Test

Ayoko na

Uploaded by

Copyright:

Available Formats

Ayoko na

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Ayoko na

Uploaded by

Copyright:

Available Formats

Perpetual Help College of Manila

1240 V Conception St., Sampaloc Manila, Philippines, 1008

BSN III - N22A

Mr. Darwin Tan, RN

During his review of systems, he relates several recent episodes of not

His medications include furosemide 20 mg daily, atenolol 50 mg daily, and

I. Specific and General Objectives

o To detect and classify atrial fibrillation using diagnostic tools like

o To prevent stroke and other thromboembolic events using risk

o To improve patients’ quality of life and treatment adherence.

o To identify key risk factors and the prevalence of atrial

The overarching goal of atrial fibrillation (AFib) treatment is to

III. Signs and Symptoms

Heart palpitations - A feeling of a rapid, fluttering, or pounding

Fatigue - Feeling tired or weak.

Shortness of breath - Difficulty breathing, especially during physical

Dizziness or lightheadedness - A sensation of spinning or

Chest pain - Discomfort or pressure in the chest.

ConfusionDifficulty thinking clearly.

Anxiety - Feeling nervous or uneasy.

Atrial Fibrillation (AFib) is a heart rhythm disorder characterized by rapid

Normal Heart Rhythm

Sinus Rhythm -The heart's electrical impulses originate from the

Regular P-wave - The P-wave on an electrocardiogram (ECG)

Regular QRS complex - The QRS complex represents the electrical

Irregular Ventricular Response - The ventricles receive a rapid and

Pulmonary Veins - These veins return oxygenated blood from the

V. Pathophysiology and Concept Map

Shortening of the refactory period, ionic channels,

Increase in intra-atrial pressure

Atrial and ventricular extrasystoles, atrial

Atrial fibrosis and inflammation

Decompensated Frank Starling

Pre-existing coronary , myocardial

 Electrocardiogram (ECG or EKG)

o Standard 12-Lead ECG: This is the most common test used to

o Holter Monitor: This portable device records the heart's electrical

 Echocardiogram: This test uses sound waves to create images of the

 Electrophysiology Study (EPS): This invasive procedure involves

 Complete Blood Count (CBC): To check for anemia or infection.

 Basic Metabolic Panel: To assess kidney function, electrolyte

 Lipid Panel: To assess cholesterol levels and identify risk factors

 Cardiac Enzymes: To rule out heart damage, especially in cases

 Coagulation Tests: To assess blood clotting factors, particularly if

VII. Drugs Study

Drug Mechanis Indicatio Adverse Action Nursing

Furosemi Acts on Edema on headache, Increas Observe 10

electrolyte diarrhea, nocturia, give

chloride, in the morning

causing Give second

excretion dose in early

Use can lead

Atenol Atenolol is Hypertensi Bradycardi Reduces Monitor heart

l oxygen with Caution when

Drug Mechanism Indications Adverse Action Nursing

Aspirin 81 Aspirin Cardiovascul Gastrointes Reduces Monitor for

VIII. Nursing Care Plan

Assessm Nursing Planning Implementa Rationale Evaluatio

Subjectiv Decreas After 8 Regularly Monitoring After 8

IX. Nursing Responsibilities