● Cardiovascular Disorders:

○ Performing a Cardiovascular Assessment:

■ Chief Complaints: primary symptoms of heart disease
● Chest discomfort
● Dyspnea (with or without cough)
● Syncope
● Palpitations
● Edema (causing weight gain and abdominal distension)
● Fatigue
● Changes to the extremities
■ Biographical Data and Health History:
● Age: the risk increases with age
● Gender: more common in men than women
○ Women have different symptoms than men
● Ethnic background: black men have a higher incidence of
hypertension
● Occupation: stress, disability
● Chronic disease
● Family history: genetic factors can predispose patients (take note
of the age and type that occurred)
● Review of the systems
● Psychosocial profile: ask about lifestyle to help identify risk
factors and changes driven by chronic disease
■ Focused Cardiovascular History:
● What to ask the patient:
○ *Do you have chest pain? When did it start? What makes it
worse or better? Have you ever had this pain before? What
does it feel like? Show me where it hurts. How bad does it
hurt on a scale of 1-10?*
■ *If the patient has chest pain, the FIRST thing you
do is an EKG*
○ Do you have a history of cardiovascular disease? Do you
take medication and, if so, why? Are the medications
prescribed or over the counter?
○ Do you have any other medical problems? Any difficulty
breathing? Any allergies and, if so, what kind of reaction
do you have?
○ Most important questions: always ask if there's a family
history of heart disease and if the patient is taking sexual
enhancing medication
■ Older Adult Considerations:
● Have increased systolic blood pressure
● Incidence of cardiovascular disease increases with age
● Have postural hypotension due to decreased sensitivity to
baroreceptors

■ Inspection:
● General appearance: is the patient alert and oriented? Are they thin
or obsese?
● Skin: color, temperature, turgor, texture, clubbing
○ Clubbing is a late sign of disease
● Critical landmarks: pulsations, symmetry of movement,
retaractions, heaves, point of maximal impulse
○ Diagnostic and Laboratory Tests for Cardiac Disorders:
■ Electrocardiography (ECG or EKG): used to diagnose dysrhythmias,
conduction abnormalities, chamber enlargement, myocardial ischemia,
injury or infarction; can also suggest cardiac effects of electrolyte
disturbances
■ Telemetry: wires attached to the chest to continuously monitor the heart
while the patient is in the hospital; patient can walk around and the nurse
watches the heart rhythm
■ Holter Monitor: patient wears a recorder for 24-48 hours (sometimes up
to 2 weeks); the patient goes home with it
● If the patient experiences symptoms, they must activate the event
marker and keep a diary of the date and time of symptoms or
performances of unusual activities
■ Cardiac Stress Testing: the patient walks on a treadmill while being
attached to an EKG; intensity is gradually increased
● Provides information regarding the workload of the heart
● The test is discontinued once the heart rate reaches a certain rate
and the patient begins to have chest pain (give nitroglycerin)
● A chemical (pharmacological) stress test can be done if the patient
is unable to finish the test
 ● Nursing Interventions:
○ Assist the provider in obtaining a signed consent form and
explain that they will be walking on a treadmill
○ Instruct them to wear comfortable athletic shoes and
clothing
○ Instruct the patient to fast 2-4 hours before the procedure
and to avoid alcohol, caffeine, and tobacco before the test
○ Instruct the patient to get adequate rest the night before the
procedure
■ Echocardiogram: an ultrasound of the heart; used to diagnose valve
disorders and cardiomyopathy
● Pre-Procedure: explain the reason for the test and that it is a
non-invasive test that takes up to 1 hour
● Intra-Procedure: patient should lie on the left side and remain still
● Post-Procedure: provider reviews test results (not the tech or
nurse) and a plan for care with the patient
■ Transesophageal Echocardiogram: numb the patient, pass the
ultrasound through their throat, and goes to the heart
■ Cardiac Catheterization: a percutaneous insertion of a radiopaque
catheter into a large vein or artery (femoral or radial; radial is done more
because there are less complications); fluoroscopy (injected dye) is used
to guide the advancement of the catheter through the right and left heart;
extremely invasive procedure
● Nursing Interventions:
○ Maintain an NPO status for at least 8 hours due to the risk
of aspiration while the patient is lying flat
○ Ask the patient if they are allergic to iodine or shellfish
(give benadryl, prednisone, or solumedrol to suppress the
immune system)
○ Obtain vital signs, auscultate heart and lung sounds, and
assess peripheral pulses
○ Ensure that a consent is signed
○ Assess renal function before giving contrast dye (it is toxic
to the kidneys)
● Nursing Interventions Post-Procedure:
○ Observe catheterization site for bleeding/hematoma and
assess peripheral pulses
○ Check temp, color, and capillary refill of affected extremity
○ Screen for dysrhythmias (pt should be on a cardiac
monitor)
 ○ PATIENT IS ON BED REST FOR 2 to 6 HOURS
■ Patient should call for help out of bed
○ Instruct patient to report chest pain and bleeding
○ Monitor for contrast-induced nephropathy
○ Monitor urine output and administer IV fluids for
hydration and flush out contrast
○ Encourage patient to ask for help when getting OOB for the
first time after procedure
○ *Instruct the client to leave the dressing in place for the
first 24hrs following discharge, avoid strenuous exercise,
restrict lifting to less than 10lbs for the prescribed period of
time*
○ Lifestyle guidelines for patients: manage weight,
low-fat/low-sodium diet, exercise, stop smoking, decrease
alcohol intake
■ Cardiac Biomarkers: troponin levels are the most important*
■ Blood Chemistry: BUN, creatinine, electrolytes
■ Coagulation Studies: partial thromboplastin time (PTT), activated partial
thromboplastin time (aPTT), international normalized ratio (INR)
■ Hematology: CBC, hematocrit, WBC, platelets
■ Lipid Profile: to check LDL and HDL cholesterol
● If cholesterol is high, patient should make diet and exercise
changes and take statins: atorvastatin [Lipitor], simvastatin
[Zocor]
■ If the artery is 100% occluded, the patient needs to go to the OR right
away for a coronary bypass
○ Coronary Artery Disease: Atherosclerosis
■ Atherosclerosis is the most common cause of cardiovascular disease; CAD
is the most prevalent cardiovascular disease in adults
■ Atherosclerosis is an abnormal accumulation of lipid deposits and fibrous
tissue within arterial wall lumen
● The plaque in the artery can rupture and causes the wbcs to go to
the site and occludes the site, which can cause an MI
■ Blockages and narrowing of the coronary vessels reduce blood flow to the
myocardium
■ Manifestations of CAD: depends on location and degree of obstruction
● Narrowing of the arterial lumen
● Thrombus formation
● Progressive impediment of blood flow
 ● ANGINA PECTORIS IS THE MOST COMMON
MANIFESTATION
● Epigastric distress
● Pain that radiates to the jaw or left arm
● Shortness of breath
● Atypical symptoms in women (women may just feel discomfort or
nothing at all)
● Myocardial infarction, Heart failure, Sudden cardiac death
■ Modifiable Risk Factors for CAD: something that you can change
● Hypertension
● Smoking
● Diabetes
● Obesity
● Hyperlipidemia
○ Total cholesterol = less than 200mg/dL
○ LDL cholesterol = less than 100mg/dL (less than 70mg/dL
for a very high-risk patient)
○ HDL cholesterol = greater than 40mg/dl for males and
greater than 50 mg/dL for females
● Sedentary Lifestyle (physical inactivity)
■ Non-Modifiable Risk Factors for CAD:
● Family history
● Age
● Gender
● Race
○ Acute Coronary Syndrome:
■ Characterized by an acute onset myocardial infarction that results in
myocardial death (heart tissue will die)
● IT IS AN EMERGENCY SITUATION
■ Symptoms: unstable angina, non-Q wave MI, Q wave MI
● UNSTABLE ANGINA AND NON-ST ELEVATION
MYOCARDIAL INFARCTION ARE THE MOST COMMON
■ Symptoms are caused by an imbalance of myocardial oxygen supply and
demand (which is why the tissue begins to die)
● If the tissue is being deprived of oxygen, and it will begin to die if
it is without oxygen for too long, it is very possible that a priority
intervention will be to supply the patient with oxygen
● Remember that this is an EMERGENCY, so questions based on
this will likely, *NOT DEFINITELY* (so don’t come for me), be
an ABC question, but it still depends on the question
○ Angina Pectoris:
■ Characterized by pain or pressure in the anterior chest
■ A WARNING SIGN OF AN IMPENDING ACUTE MI
● Women and older adults may not experience symptoms typically
associated with angina or MI
■ When blood flow to the heart is compromised, ischemia causes chest pain.
■ Symptoms: angina pain is often described as a tight squeezing, heaving
pressure of constricted feeling in the chest; it can radiate to the jaw, neck
or arm
■ Myocardial oxygen demand exceeds supply (what I wrote above about
ACS applies here too; the tissue is being deprived of oxygen)
■ Risk Factors: history of angina, cardiac disease, hypertension, diabetes
mellitus, congestive heart failure, cocaine or methamphetamine use,
hyperlipidemia, hyperthyroidism, alcohol use, male gender,
post-menopausal women, obesity, stress
■ Stable Angina: occurs with exercise and emotional stress and is relieved
by rest or nitroglycerin*
■ Unstable Angina: also called pre-infarction; occurs with exercise or at
rest but increases with occurrence, severity, and duration over time;
nitroglycerin does not help
■ Variant Angina: also called Prizmental’s; due to coronary artery spasm,
often occurs when resting
● Cardiac catheterization is indicated when there is unstable and
variant angina; DO NOT DO A STRESS TEST
■ Health Promotion and Disease Prevention:
● Maintain an exercise routine to remain physically active; consult
with a provider before starting any exercise regime
● Have cholesterol level and blood pressure checked regularly
● Consume a diet low in saturated fats and sodium
● Promote smoking cessation
■ Lab Tests: cardiac enzymes are released with cardiac injury
● Myoglobin: earliest marker of injury to cardiac or skeletal muscle;
levels are no longer evident after 24hrs
● Creatine Kinase-MB: peaks around 24hrs after onset of chest
pain; levels no longer evident after 3 days
● Troponin I or T: any positive value indicates damage to cardiac
tissue and should be reported
○ Troponin I: levels no longer evident after 7 to 10 days
○ Troponin T: levels no longer evident after 10 to 14 days
■ Treatment:
 ● Administer 2 to 4L/min of oxygen
● Nitrates: Nitroglycerin – given sublingual or IV
○ Prevents coronary vasospasm & reduces preload and
afterload, which decreases myocardial O2 demand
○ Can cause hypotension
● Beta Blocking Agents: Metoprolol [Lopressor]
○ They decrease the workload of the heart
○ Has antidysrhythmic and anti-hypertensive properties that
decreases the imbalance between myocardial O2 supply
and demand by reducing afterload and slowing heart-rate
○ Side Effects: hypotension and bradycardia
■ Hold medication if the apical pulse is less than 60
min and notify the provider
■ Monitor for decreased level of consciousness and
crackles in the lungs
○ *Do not give to clients who have asthma*
● Calcium Channel Blocking Agents: Amlodipine [Norvasc] and
Diltiazem [Cardizem] - slower heart rate and a decrease in
strength of myocardial contraction causing decrease in workload of
the heart
● Antiplatelet Agents: Aspirin and Clopidogrel [Plavix] -
prevents platelets from forming together which can produce
arterial clotting; aspirin prevents vasoconstriction
○ ASPIRIN SHOULD BE ADMINISTERED WITH
NITROGLYCERIN AT THE ONSET OF CHEST PAIN
○ Nursing Considerations:
■ Can cause GI upset
■ Use cautiously with clients who has history of GI
ulcers
■ Tinnitus (ringing of the ear) can be a sign of aspirin
toxicity
● Anticoagulants: Heparin [Hep-Lock] and Enoxaparin
[Lovenox] - prevent clots from becoming larger or other clots from
forming
● Cholesterol Medications: Statins like Simvastatin [Zocor]
-lowers the LDL and increases HDL

■ Nursing Process: Care of Patient with Angina Pectoris

● Assessment: Symptoms, Activities , Risk Factors, Knowledge
 ● Diagnosis: risk for decreased cardiac tissue perfusion; anxiety
related to cardiac symptoms and possible death; deficient
knowledge about the underlying disease and methods for avoiding
complications; noncompliance, ineffective management of
therapeutic regimen related to failure to accept necessary lifestyle
changes
● Goals: minimize myocardial damage by reestablishing coronary
flow, preserve myocardial function by minimizing myocardial
damage (by reducing myocardial oxygen demand and increasing
oxygen supply) and prevent of complications
● Interventions: treat angina: reduce anxiety; prevent pain; educate
about self-management; follow up care
○ Acute Myocardial Infarction:
■ Characterized by acute onset of myocardial ischemia (ischemia means
there is reduced blood flow) that results in myocardial death
● The heart muscle cannot survive to do an occlusion, causing cell
death
■ Most common site of an MI is the left anterior descending coronary; it is
the biggest and supplies oxygenated blood to the rest of the body
■ If the ST segment is depressed, it means there's ischemia (lack of oxygen)
■ If the ST segment is elevated, it means there's an infarct/injury and the
tissue is starting to die
■ Dysrhythmias account for most deaths; can be preventable with
early-access to hospital care
■ Progression from CAD to AMI:
● A lesion is formed
● Fibrous cap: thick fibrous cap, thin fibrous cap (more vulnerable
plaque), lipid cores

● Plaque ruptures
● Thrombotic cascade (the process of forming a blood clot)
■ Progression of AMI: (1) ischemia, (2) injury, (3) infarct
 ● You will see this progression on a 12 Lead EKG and the occluded
coronary artery can be identified
■ Patient Assessment: assess patient history
● Physical Assessment
○ Include all cardiac assessments previously discussed
○ Carefully evaluate patient appearance
○ Vital signs and12 lead EKG
● Labs: cardiac biomarkers
○ Troponin I or T is the most definitive biomarker: indicates
damage to cardiac tissue and should be reported
■ Troponin I: levels no longer evident after 7 to
10days
■ Troponin T: levels no longer evident after 10 to
14days
○ Myoglobin: earliest marker; levels no longer evident after
24hrs
○ Creatine Kinase-MB: peaks around 24hr after onset of
chest pain; levels no longer evident after 3days
■ Manifestations:
● PAIN IS THE MAIN SYMPTOM
○ Do not drive yourself to the hospital if you feel chest pain,
take nitroglycerin, call an ambulance, if it doesn't work take
another dose of nitroglycerin 5 minutes later, then if that
doesn't work, take a 3rd dose
○ Nitroglycerin can only be given 3 times, 5 minutes apart
● Diaphoresis
● Nausea and vomiting
● Confusion/agitation
● Dyspnea
● Syncope
● Urge to defecate
● Feeling of impending doom
● Palpitations
● Some patients may not have any pain – just not feeling well
■ Treatment for AMI:
● MONA:
○ Morphine
○ Oxygen
○ Nitroglycerin
○ Aspirin
● Beta-Blockers: drugs ending in -olol
● Ace Inhibitors: drugs ending in -pril (Captopril, Lisinopril,
Enalopril)
● Anticoagulants: Heparin, Enoxaparin
● Statins: drugs ending in -statin (Simvastatin, Atorvastatin)
○ If the patient feels muscle pain, report it to the provider
immediately because rhabdomyolysis is a side effect
● Thrombolytics: drugs ending in -ase (Alteplase)
● Reperfusion Therapy:
○ Percutaneous Coronary Intervention: a procedure
performed to open coronary arteries through one of the
following means; also called cardiac catheterization
■ Atherectomy: used to break up and remove plaques
within the cardiac vessels
■ Stent: placement of a mesh-wire device to hold an
artery open and prevent restenosis
■ Percutaneous Transluminal Coronary Angioplasty:
aka an angioplasty; involves inflating a balloon to
dilate the arterial lumen and the adhering plaque,
which widens the arterial lumen
● This can include stent placement to prevent
artery reocclusion and to dilate the coronary
artery
■ *Nursing interventions for PCI are the same as the
ones under cardiac catheterization*
■ Goals:
● Relief of pain or ischemic signs (ex: ST-segment changes) and
symptoms
● Prevention of myocardial damage
● Maintenance of effective respiratory function, adequate tissue
perfusion
● Reduction of anxiety
● Adherence to the self-care program
● Early recognition of complications
 ■ Nursing Interventions:
● Relieve pain and symptoms of ischemia
● Improve respiratory function
● Promote adequate tissue perfusion
● Reduce anxiety
● Monitor and manage potential complications
● Educate patient and family
● Provide continuing care
■ Nursing Management:
● Oxygen and medication therapy
● Frequent vital sign assessment
● Physical rest in bed with head of bed elevated
● Relief of pain helps decrease workload of heart
● Monitor I&O and tissue perfusion
● Frequent position changes to prevent respiratory complications
● Report changes in patient’s condition
● *Evaluate interventions*
○ Differences between Angina and a MI:
■ Angina:
● Caused by exertion (like exercise) or stress
● Relieved by rest or nitroglycerin
● Symptoms last less than 15 mins
● Not associated with nausea, epigastric distress, dyspnea, anxiety,
diaphoresis*
■ Myocardial Infarction:
● Can occur without cause, often in the morning after rest
● Relieved only by opioids
● Symptoms last more than 30mins
● Associated with nausea, epigastric distress, dyspnea, anxiety,
diaphoresis*
○ Heart Failure:
■ A clinical syndrome resulting from structural or functional cardiac
disorders that impair the ability of the ventricles to fill or eject blood
● Results in inadequate cardiac output, myocardial hypertrophy and
pulmonary/systemic congestion
■ Inability of the heart to pump blood fast enough to meet the needs of the
peripheral tissues
■ Characterized by signs and symptoms of fluid overload or inadequate
tissue perfusion
■ Etiology of Heart Failure:
● The loss of a critical quantity of functioning myocardial cells after
injury to the heart due to:
○ Ischemic Heart Disease
○ Hypertension (systemic or MI pulmonary hypertension)
○ Idiopathic Cardiomyopathy
○ Infections (viral myocarditis, Chagas’ disease)
○ Toxins (alcohol or cytotoxic drugs)
○ Valvular Disease
○ Prolonged Arrhythmias
○ Pericarditis
○ Dysrhythmias
■ Pathophysiology:
● Initial stressors to the heart cause the heart to eventually change
over time (from neurohormone and other molecular release)
● Two types:
○ Systolic: ventricles are weakened
○ Diastolic: ventricles can’t fill appropriately
■ Manifestations:
● Left Sided: *think of the lungs*
○ Pulmonary congestion and crackles in the lungs
○ S3 or “ventricular gallop”
○ Dyspnea on exertion (DOE)
○ Low O2 sat, fatigue, altered mental status
○ Dry, nonproductive cough initially
○ Oliguria (decrease in urine output)
● Right Sided: *think of the rest of the body*
○ Viscera and peripheral congestion
○ Jugular venous distention (JVD)
○ Dependent edema (which means edema in one area like the
leg)
○ Hepatomegaly (liver enlargement)
○ Ascites, fatigue, weakness
○ Weight gain, nausea, anorexia
■ Diagnostic and Lab Testing:
● Human B-type Natriuretic Peptides (hBNP): in patients with
dyspnea, elevated hBNP confirms a diagnosis of heart failure
rather than a problem originating in the respiratory system
○ hBNP is the most definitive test for heart failure; it tells
you how stressed your ventricle is; it should less than 100
 ● Transesophageal echocardiography (TEE): uses a transducer
placed in the esophagus behind the heart to obtain a detailed view
of cardiac structures
● Ultrasound or Echocardiogram: used to measure the systolic and
diastolic functioning of the heart
● Chest X-Ray: can reveal cardiomegaly and pleural effusions
● EKG, Cardiac enzymes, electrolytes and ABGs
■ Lifestyle Modifications:
● Stop smoking
● Avoid alcohol and other cardio-toxic substances
● Maintain an exercise routine to remain physically active, and
consult with the provider before starting any exercise regime
● Have a low-sodium diet, along with fluids restrictions, and consult
with the provider regarding diet specifications
● Follow medication regime and follow up with the provider
■ Pharmacologic Management:
● Inotropic Agents: Digoxin [Lanoxin], Dopamine, Dobutamine are
used to increase contractility and thereby improve cardiac output
○ For digoxin, take the apical pulse for 1 min; hold
medication if apical pulse is less than 60/min, notify
provider
○ Observe client for nausea and vomiting
● Patient Education for Digoxin:
○ Count pulse for 1 min before taking medication
○ Take the digoxin dose at the same time every day
○ Do not take digoxin at the same time with antacids
■ Separate both medications by at least 2hrs apart
○ Report signs of toxicity, including fatigue, muscle
weakness, confusion and loss of appetite, vision changes
■ Halos are a common side effect of digoxin
○ Regularly have digoxin and potassium levels checked:
digoxin toxicity is worse when potassium levels are low
■ If the potassium is low, the EKG will have ST
depression
● Diuretics: check potassium levels BEFORE giving
○ Loop diuretics: Furosemide [Lasix]
○ Thiazide diuretics: Hydrochlorothiazide [Urozide]
○ Potassium-sparing diuretics: Spironolactone [Aldactone]
○ Used to relieve fluid retention, decrease preload, and
improve exercise tolerance
 ○ Facilitates the use of other drugs indicated for heart failure
(it should never be used alone to treat heart failure)
○ Patients can be taught to adjust their diuretic dose based on
changes in body weight
○ Electrolyte depletion a frequent complication
○ Higher doses of diuretics are associated with increased
mortality
● Ace Inhibitors:
○ Blocks conversion of angiotensin I to angiotensin II and
prevents functional deterioration
○ Recommended for all patients with heart failure
○ Relieves symptoms and improves exercise tolerance
○ Benefits may not be apparent for 1-2 months
○ Nursing Considerations:
■ Causes angioedema (swelling of the tongue and
throat), decreased sense of taste and/or skin rash
■ Monitor for hypotension following initial dose
■ Monitor for increased level of potassium
○ Patient Education:
■ Inform the patient that it can cause a dry cough (the
most common side effect)
■ Notify the provider if the patient gets a rash or has a
decrease in taste
■ Notify the provider if swelling of the face or
extremities occurs
■ Remind the client that B/P needs to be monitored
for 2hrs after the initial first dose to detect
hypotension
● Angiotensin Receptor II Blockers: aka ARBs
○ Drugs that end in -sartan like Losartan [Cozaar]
○ This drug is for patients who cannot tolerate ACE
inhibitors and is not associated with dry hacking and cough
● Beta Blockers: like Carvedilol [Coreg] or Metoprolol [Lopressor]
○ Improves the condition of the patient who has sustained
increased levels of sympathetic stimulations and
catecholamines
○ Nursing Considerations:
■ Monitor blood pressure, pulse, activity tolerance
and orthopnea (discomfort when breathing while
lying down flat)
 ■ Check for orthostatic blood pressure reading
■ When a patient has acute systolic heart failure, do
NOT give them a beta blocker because it will slow
down the myocardial contraction
■ When a patient has diastolic failure, give a beta
blocker to slow myocardial contraction, so it gives
the heart enough time to fill up before it pumps
○ Client Education:
■ Instruct the client to check weight daily
■ Advise the client to regularly check blood pressure
■ Tell the client to follow the provider’s instructions
for increasing medication dose
○ Assessment of the Vascular System:
■ Health History: pain when resting, location of the pain, and intermittent
claudication
■ Physical Assessment: skin (cool, pale, pallor, rubor (flushing), loss of hair,
brittle nails, dry or scaling skin, atrophy, and ulcerations) and peripheral
pulses
● Most important peripheral pulses to asses: popliteal, dorsalis pedis,
and posterior tibial
● Always ask the patient if pain only happens when they are active
or also when they are at rest
○ Peripheral Arterial Disease (PAD):
■ Remember that arteries carry blood away from the heart, so blood is
having a hard time getting down to the lower extremities
■ Risk Factors: hypertension, hyperlipidemia, smoking, obesity, diabetes
mellitus, sedentary lifestyle, sedentary predisposition, older adults
■ PAD results from atherosclerosis that usually occurs in the arteries of the
lower extremities and is characterized by inadequate flow of blood
■ INTERMITTENT CLAUDICATION IS THE HALLMARK SYMPTOM:
it is described as aching, cramping, or inducing fatigue or weakness;
occurs with some degree of exercise or activity
■ DEPENDENT POSITION (dangling the legs) RELIEVES PAIN
■ Pain is associated with critical ischemia of the distal extremity and is
described as persistent, aching, or boring (rest pain)
■ Expected Findings: pain and paresthesia are early signs
● Burning, cramping, and pain in the legs during exercise
(intermittent claudication)
● Numbness or burning pain primarily in the feet when in bed
● Decreased capillary refills or toes (greater than 3 seconds)
 ● Diminished or no palpable pulses
● Loss of hair on lower calf, ankle, and foot
● Cold and cyanotic extremity
● Pallor of extremity with elevation
● Ulcers and possible gangrene (aka ascar) of toes; amputation may
be needed
● Thick toenails and dependent rubor (redness) of the extremity
■ Diagnostic Evaluation:
● Doppler Ultrasound: to visualize blood flow
● Ankle brachial index (ABI): normal is 0.9- 1.3: an ABI of less than
0.9 is either leg is diagnostic of PAD
○ BP cuff is placed on the same side of the affected extremity
● Exercise Testing: to evaluate claudication during exercise
○ It is used to determine how long a patient can walk and to
measure the ankle systolic blood pressure in response to
walking
● Computed Tomography Scanning
● Angiography and Magnetic Resonance Angiography
● Contrast Phlebography (venography)
● Continuous-Wave Doppler Ultrasound: detects blood flow,
combined with computation of ankle or arm pressures; this
diagnostic technique helps characterize the nature of peripheral
vascular disease
■ Nursing Interventions and Patient Education:
● Encourage the client to exercise to build up circulation
● Initiate exercise gradually and increase slowly
● Instruct the client to walk until the point of pain, stop and rest, and
than walk a little farther (to improve endurance)
● Avoid cold temperature to avoid vasoconstriction
● Provide a warm environment for the client to promote vasodilation
● Have the client wear insulated socks (keep legs warm to improve
blood flow)
● Tell the client to never apply direct heat, such as a heating pad, to
the affected extremity because sensitivity is decreased, and this can
cause burns
● Instruct the client to avoid stress, caffeine (coffee, tea, sodas,
chocolate, energy drink), nicotine which can cause
vasoconstriction
■ Patient Positioning:
● Instruct the client to avoid crossing the legs
 ● Tell the client to refrain from wearing restrictive garments
● Tell the client to elevate the legs to reduce swelling but DO NOT
ELEVATE THEM ABOVE HEART LEVEL because it slows
arterial blood flow to the feet
● Hang the legs over the bed (dependent position)
■ Pharmacologic Therapy for PAD:
● Antiplatelet Medications: Aspirin and Clopidogrel [Plavix]
reduce blood viscosity by decreasing blood fibrinogen levels,
enhancing erythrocyte flexibility and increasing blood flow in the
extremities
● Statins (simvastatin, atorvastatin): can relieve manifestations
associated with PAD (intermittent claudication)
○ Monitor liver function and avoid grapefruit juice
■ Therapeutic Procedures:
● Percutaneous Transluminal Angioplasty: an invasive intra-arterial
procedure using a balloon and stent to open and help maintain the
patency of the vessel
○ Nursing considerations:
■ OBSERVING FOR BLEEDING AT THE
PUNCTURE SITE IS PRIORITY
■ Monitor vital signs, peripheral pulses and capillary
refill
■ Keep the patient on bed rest (lying flat) with the
limb straight for 2 to 6 hrs before ambulation
■ Anticoagulant therapy is used during the procedure
and followed by antiplatelet therapy for 1 to 3
months
● Peripheral By-Pass Graft: reroutes circulation around the arterial
occlusion; done if the angioplasty does not work
○ Peripheral Venous Disorder:
■ Peripheral venous disorders are problems with the veins that interfere with
adequate return of blood flow from the extremities; superficial and deep
veins in the lower extremities that have valves that prevent backflow of
blood as it returns to the heart
■ 3 Peripheral Venous Disorders: venous thromboembolism (VTE), venous
insufficiency, and varicose veins
■ VTE: is a blood clot believed to form as a result of venous stasis, or
hypercoagulability
● Thrombus formation can lead to a pulmonary embolism which is
a life-threatening complication
 ● Thrombophlebitis refers to a thrombus that is associated with
inflammation
● Expected Findings:
○ Calf or groin pain, tenderness and a sudden onset of edema
of the extremity
○ Warm, edema and induration and hardiness over the
involved blood vessels
○ Changes in the circumferences of right and left calf and
thigh over time, localized edema over the affected area
■ Venous Insufficiency: occurs secondary to incompetent valves in the
deeper veins of the lower extremities which allows pooling of blood and
dilation of the veins
● The veins inability to carry fluids and wastes from the lower
extremities precipitates the development of swelling, venous stasis
ulcers and, in advanced cases, cellulitis
● Expected Findings:
○ Stasis dermatitis is a yellowish-brown discoloration along
the ankles that extends up the calf relative to the level of
insufficiency
○ Edema/swelling
○ Stasis ulcers (typically found around ankles, moist and
irregular with yellowish-brown discoloration)
○ Aching pain and feeling of fullness or heaviness in the legs
after standing
■ Diagnostic and Lab Testing:
● D-Dimer Test: measures fibrin degradation products present in the
blood produced from fibrinolysis
○ A positive test indicates a thrombus formation possibly
occurred
● Venous Duplex Ultrasound: high-frequency sound waves to
provide a real-time picture of the blood flow through a blood
vessels
● Doppler Slow Study: produces an audible sound when venous
circulation is normal and little or no sounds when veins are
thrombosed
● Venogram: uses contrast dye for an accurate diagnosis; is needed
if the above tests are negative for DVT, but one is still suspected
■ Nursing Interventions and Patient Education:
● DVT and Thrombophlebitis:
 ○ Encourage the client to rest (facilitate bedrest and elevation
of the extremity above the level of the heart as prescribed)
○ *Do not massage the affected limb*
○ Avoid using a knee gatch or pillow under knees
○ Provide thigh-high compression or anti-embolism stockings
(put it on in the morning)
○ Prepare the client for an inferior vena cava interruption
surgery (a filter traps emboli and prevents them from
reaching the heart) as indicated
● Venous Insufficiency:
○ Elevate legs for at least 20 mins four to five times a day
○ Elevate the legs above the heart when in bed
○ Instruct the clients to avoid crossing legs and wearing
constrictive clothing or stockings
○ Instruct the client to wear elastic compression stockings
and apply them after the legs have been elevated and when
swelling is at a minimum
■ Treatment: anticoagulants
● Unfractionated Heparin: given IV to prevent formation of other
clots and to prevent enlargement of the existing clots
○ Protamine sulfate is the antidote
● Low-Molecular Weight Heparin: given subQ and is based on the
client’s weight
○ Enoxaparin is used for prevention and treatment of DVT
● Warfarin [Coumadin]: inhibits synthesis of the four vitamin
K-dependent clotting factors
○ Therapeutic effects take 3 to 4 days to develop, so the
administer while the patient is still on heparin
○ Vitamin K is the antidote for warfarin
○ Hypertension:
■ Occurs when the systolic blood pressure is or greater than 140 mmHg or
diastolic blood pressure is at or greater than 90 mmHg for two or more
assessments of B/P
■ For patients older than 60 years: BP should be less than 150/90
■ Essential Hypertension: also called primary HTN, accounts for most
cases of HTN; there is no known cause
■ Secondary Hypertension: can be caused by disease states, such as kidney
disease, or as an adverse effect of some medications
● Treatment occurs by removing the cause (adrenal tumor,
medication)
■ Health Promotion and Disease Prevention:
● Maintain body mass index of less than 30
● Clients who have diabetes should keep blood glucose within a
recommended reference range
● Limit caffeine and alcohol intake
● Use stress-management techniques during times of stress
● Stop smoking (nicotine patches or engaging in a smoking cessation
are potential strategies)
● Limit sodium and fat intake
■ Incidence of Hypertension:“The Silent Killer”
● About 33% of the adult population of the U.S. has hypertension
● About 46% do not have it under control
● Highest prevalence in African Americans
● Clients who have systolic blood pressure of 120 to 39 mmHg or a
diastolic blood pressure of 80 to 89 mmHg are considered to have
pre-hypertension
● Complications include peripheral vascular disease that primarily
affects the heart, brain, eyes and kidneys
■ Risk factors for Essential Hypertension:
● Positive family history and stress
● Excessive sodium and alcohol intake
● Physical inactivity
● Obesity and hyperlipidemia
● African Americans
● Smoking
● Age greater than 60 or postmenopausal women
■ Risk Factors for Secondary Hypertension:
● Kidney disease
● Pregnancy
● Medications such as estrogen, steroids
● Brain tumors, encephalitis
● Primary aldosteronism (causes hypertension and hypokalemia)
■ Expected Findings: headaches, facial flushing, dizziness, fainting, retinal
changes, visual disturbances, nocturia
● Symptoms related to organ damage are seen late and are serious
such as myocardial infarction, cardiac hypertrophy, and stroke
■ Patient Positioning: when a blood pressure reading is elevated, take it in
both arms with the client sitting or sitting
● Pre-Hypertension: systolic 120 to 139 mm Hg. Diastolic 80 to 89
mmHg
● Stage 1 Hypertension: systolic 140 to 159 mm Hg; Diastolic 90 to
99 mmHg
● Stage II Hypertension: systolic greater than or equal to 160 mmHg
and diastolic greater than or equal to 100 mm Hg
■ Patient Assessment:
● Patient history
● Physical examination with a retinal exam
● No lab tests exist to diagnose HTN, but several lab tests can
identify the causes of secondary HTN and target organ damage
such as: BUN, creatinine, elevated serum corticoids, blood glucose
and cholesterol levels
● ECG: evaluates cardiac function
● Chest X-Ray: can show cardiomegaly
■ Treatment and Management:
● Maintain blood pressure
○ <140/90 mm Hg
○ <150/90 mm Hg for older adult patients
● Lifestyle modifications BEFORE medication
● Physical activity for weight reduction
● Encourage DASH diet (dietary approaches to stop hypertension)
low-fat dairy foods and decreased sodium intake of less than
2.3g/day
● Medications are added to treat HTN that is not responsive to
lifestyle changes alone:
○ Diuretics are often first-line medications:
■ Thiazide diuretics: Hydrochlorothiazide - inhibit
water and sodium reabsorption and increases K+
excretion
■ Beta-Blockers, Alpha1-Blockers, Combined Alpha-
and Beta-blockers, Vasodilators, ACE inhibitors,
ARBs, Calcium Channel Blockers,
 Dihydropyridines, and direct renin inhibitors are
also used
● Patients on beta blockers need to constantly
check their sugar levels because they won't
feel symptoms of hypo/hyperglycemia
○ The aim of the medications are to:
■ Decrease peripheral resistance, blood volume
■ Decrease strength and rate of myocardial
contraction
■ Diuretics, beta-blockers, alpha1-blockers, combined
alpha- and beta-blockers, vasodilators, ACE
inhibitors, ARBs, calcium channel blockers,
dihydropyridines, and direct renin inhibitors
■ Patient Education:
● Express to the client and family the importance of adhering to the
medication regime, even if the client does not have any
manifestations of hypertension
● Provide verbal and written education to the client regarding
medications and their adverse effects
● Encourage the client to schedule regular provider appointments to
monitor hypertension and cardiovascular status
● Ensure that the client has the resources necessary to pay for and
obtain prescribed antihypertensive medications
● Treatment involves the client making lifestyle changes
● Older adult clients are more likely to experience medication
interactions and orthostatic hypotension
● Weight reduction and maintenance: begin slowly and gradually
advance the program with the guidance of the provider and
physical therapist
● Exercise at least three times a week in a manner that provides
aerobic benefits
● Smoking cessation: explore smoking cessation options such as
nicotine replacement therapy or support groups
● Stress reduction: encourage the client to try yoga, massage,
hypnosis or other forms of relaxation
● Rebound hypertension: if they skip the medication, the medication
will not work anymore
■ Gerontologic Considerations:
● Medication regimen can be difficult to remember
● Expense can be a challenge
 ● Monotherapy, if appropriate, may simplify the medication regimen
and make it less expensive
● Ensure that older adult patients understand the regimen and can
see and read instructions, open medication containers, and get
prescriptions refilled
● Include family and caregivers in educational program
■ Nutritional Education:
● Consume less than 2.3g/day of sodium and a diet low in fat,
saturated fat, and cholesterol
● Limit alcohol intake to 2 servings per day for men and 1 serving
per day for women; a serving of alcohol is equivalent to 1.5oz
liquor, 5oz wine or 12 oz beer
● Dietary approaches to stop hypertension (DASH) are effective in
the prevention and treatment of hypertension
○ The DASH diet is high in fruits, vegetables, and low-fat
dairy foods
● Clients not taking a potassium-sparing medications should
increase potassium consumptions
■ Complications: hemorrhagic stroke, heart failure and vision problems
● Endocrine Disorders:
○ Diabetes Insipidus: results from a deficiency of ADH, which is secreted by the
posterior lobe of the pituitary gland; THINK DRY INSIDE
■ Decreased ADH reduces the ability of the renal tubules in the kidneys to
collect and concentrate urine
■ Resulting in excessive diluted urination, excessive thirst, electrolyte
imbalance, and excessive fluid intake
■ Risk Factors:
● Patients who have a head injury, tumor, surgery or irradiation near
or around the pituitary gland, or infection
● Patients who are talking lithium carbonate or demeclocycline
■ Expected Findings: polyuria, polydipsia, fatigue, dehydration (weight
loss, muscle weakness, headache, constipation and dizziness)
■ Physical Assessment: sunken eyes, tachycardia, hypotension, loss or
absence of skin turgor, decreased cognition
■ Laboratory Tests:
● Electrolyte imbalances: they will be increased
● Urine Chemistry: think DILUTE
● Decreased urine specific gravity (less than 1.005)
● Decreased urine osmolality (less than 200 mOsm/L)
 ■ Medications:
● ADH replacement agents: Desmopressin [DDAVP] and
Vasopressin [Vasostrict] administered intranasally, orally or
parenterally
○ Results in increased water absorption from kidneys and
decreased urine output
○ Remember that a side effect of these medications are water
intoxication: headache, confusion, dizziness are s&s
■ Nursing Considerations:
● Monitor vital signs, I&O, specific gravity and laboratory studies
(potassium, sodium, BUN, creatinine, specific gravity and
osmolarity)
○ Urine output will tell you if you need to increase or
decrease dose of medication
● Dose can be adjusted depending in urine output
● Use vasopressin cautiously in patients who have CAD because the
medication can cause vasoconstriction --- ANGINA!!
■ Patient Education:
● Educate patient on lifelong self-administration of vasopressin
● For an intranasal dose, teach the client to clear nasal passage and
sit upright prior to inhalation
● Instruct patient to monitor weight daily (on the same scale
everytime), I&O, and notify the provider of a gain greater than
2lbs in 24hrs
● Eat a high-fiber diet
● Instruct the client to restrict fluids if directed and notify the
provider of headache or confusion
○ Syndrome of Inappropriate Antidiuretic Hormone (SIADH):
■ It is an excessive release of ADH, also known as vasopressin, secreted by
the posterior lobe of the pituitary gland; THINK SOAKED INSIDE
■ Risk Factors: malignant tumors, lung cancer, head injury, meningitis,
stroke, TB and medications (opioids, chemotherapy agents etc.)
■ Early Manifestations: headache, weakness, anorexia, muscle cramps, and
weight gain
● As the serum level decreases, the patient experiences personality
changes, hostility, diarrhea, nausea, vomiting and oliguria
■ Physical Findings: hypertension, crackles in lungs, distended neck veins,
tachycardia, seizures, coma and death can occur
 ■ Laboratory Tests:
● Urine chemistry (Think Concentration): increased urine
osmolarity; specific gravity will be high
● Blood chemistry (Think Dilute): electrolytes will be decreased
■ Medications:
● Tetracycline derivative: Demeclocycline
● Loop diuretics: Furosemide [Lasix]
● Hypertonic 3% normal saline IV fluids: to elevate the sodium level
enough to alleviate neurologic compromise
○ Patient needs to be in critical care and the saline needs to be
given slowly
○ If the patient has a tube, flush it with normal saline instead
of regular water to help replace sodium
■ Nursing Interventions:
● RESTRICT ORAL FLUID TO 500 TO 1,000 ml/day IS
PRIORITY: prevents further hemodilution; if you give them ice,
calculate it into the water that was given
○ During fluid restriction, provide comfort measures for
thirst, such as mouth care, ice chips, lozenges, and
staggered water intake
● Flush all enteral and gastric tunes with 0.9% sodium chloride,
instead of water to replace sodium and prevent further
hemodilution
● Monitor I&O and report decreased urine output
● Mouth care
● Monitor vital signs for increased blood pressure and tachycardia
● Auscultate lung sounds to monitor for pulmonary edema, which is
a medical emergency
● Provide a safe environment for clients who have altered levels of
consciousness and maintain seizure precautions
● Monitor for indications of heart failure, which can occur from fluid
overload (use of a loop diuretic if indicated)
○ Function of the Thyroid Gland:
■ T3 and T4 affect all body systems by regulating overall body metabolism,
energy production, and controlling tissue use of fats, proteins and
carbohydrates
■ Calcitonin inhibits mobilization of calcium from the bone and reduces
blood calcium levels
 ■ When serum T3 and T4 levels decrease, thyroid-stimulating hormone
(TSH) is released by the anterior pituitary, which stimulates the thyroid
gland to secrete more hormones until normal levels are reached
● Remember, this process cannot occur without Iodine in the body
found in diet
■ Protein and iodine in the diet are needed for the production of the thyroid
hormones (T3, T4, and calcitonin)
○ Hyperthyroidism: caused by excess thyroid hormones
■ Normal body functions are exaggerated; affects women more than men
■ Graves’ Disease: most common cause; is a autoimmune disease; trait
passed onto females
■ Thyrotoxicosis: excessive output of thyroid hormone (causes thyroid
storm; exaggerated symptoms of hyperthyroidism)
● Fever and hypertension are common symptoms
■ Toxic Nodular Goiter: less common form of hyperthyroidism; is caused
by independent overproduction of thyroid hormone due to the presence of
thyroid nodules
■ Exogenous Hyperthyroidism: caused by excessive dosage of thyroid
hormone
■ Hyperthyroidism is also caused by excess consumption of iodine rich
foods
■ Clinical Manifestations: nervousness, rapid pulse, heat intolerance,
tremors, skin flushed (also warm, soft, and moist), exophthalmos (bulging
eyes), increased appetite, weight loss, elevated systolic BP, cardiac
dysrhythmias (A-fib), frequent diarrhea, hair thinning or loss, insomnia
● Think of it like metabolism, everything is high and fast*

■ Diagnostic Procedures and Labs:

● Serum TSH test: decreased in the presence of Graves disease
● Free T4 index, T4 (Total) T3: will be elevated
 ● Ultrasound: used to obtain images of the thyroid gland and
surrounding tissue (it will be big)
● Electrocardiogram: used to evaluate the effects of excessive
thyroid hormone on the heart (tachycardia, dysrhythmias)
● Radioactive Iodine Uptake: nuclear medicine test
○ Clarifies the size and function of the gland
○ The uptake of radioactive iodine, administered orally 24hrs,
is measured
○ An elevated uptake is indicative of hyperthyroidism
■ Medications: NEVER GIVE ASPIRIN FOR HYPERTHYROIDISM
● Methimazole [Tapazole] and Propylthiouracil [PTU]: inhibit the
production of thyroid hormone (they do not damage the thyroid)
● Methimazole is used to treat Graves disease as an adjunct to
radioactive iodine therapy, to decrease hormone levels in
preparation for surgery and to treat thyrotoxicosis
○ Do not give methimazole to patients in the first trimester of
pregnancy, they get PTU instead
○ Nursing Considerations: Monitor for CBC for leukopenia
or thrombocytopenia (they are at risk for infection); PTU
causes severe liver injury (get LFTs)
● Beta Blockers: treat sympathetic nervous system effects
(tachycardia, palpitations).
○ It counteracts the effects of increased thyroid hormones but
does not alter the levels of the hormones
○ Nursing Considerations: Monitor BP, HR, and for
hypoglycemia in clients who have diabetes mellitus
○ Contraindicated in patients with asthma
● Lugol’s Solution: is a nonradioactive 5% elemental iodine in 10%
potassium iodine that inhibits the release of thyroid hormone
■ Therapeutic Procedures:
● Radioactive Iodine Therapy: is taken up by the thyroid and
destroys some of the hormone-producing cells (it is a permanent)
○ One dose can be sufficient, but a second or third dose might
be needed
○ The degree of thyroid destruction varies and can require
life-long thyroid replacement
○ Nursing Considerations: contraindicated in women who
are pregnant; monitor for manifestation of hypothyroidism
(edema, intolerance to cold, bradycardia, increase in weight
and depression), tell patient to continue to take the
medication as directed
○ Patient Education: advise the pt that the effects of therapy
might not be evident for 6 to 8 weeks; advise the client to
stay away from pregnant women, infants, or small children
for the first week following treatment; although a low dose
of radiation is used, provide the patient with precautions to
prevent radiation exposure to others
● Thyroidectomy: the surgical removal of part or all of the thyroid
gland
○ Subtotal Thyroidectomy: can be performed when
medication therapy fails, or radiation therapy is
contraindicated.
■ After a subtotal thyroidectomy, the remaining
thyroid tissue usually supplies enough thyroid
hormone for normal function
○ Total Thyroidectomy: the patient will need thyroid hormone
replacement therapy
○ Remember to monitor for parathyroid complications after
surgery which will cause low calcium levels*
○ Post Procedure Considerations:
■ Patient is in semi-fowler’s position and support the
head and neck with pillow to avoid neck extension
■ Check for surgical dressing and back of the neck for
excessive bleeding
● Respiratory distress can occur from
compression of trachea due to hemorrhage;
mostly likely to occur in the first 24 hours
 ■ Check for laryngeal nerve damage by asking the
client to speak as soon as they awake from
anesthesia and every 2 hrs thereafter
■ Respiratory disease also can occur due to edema, so
ensure that tracheostomy supplies are at the bedside
■ Hypocalcemia and tetany (intermittent muscular
spasms) can occur if parathyroid glands are
damaged or removed
● S&S: tingling of toes or around mouth, and
muscle twitching
● Check for positive Chvostek’s and
Trousseau’s signs
● Ensure that IV calcium gluconate or calcium
chloride are immediately available
■ Monitor for signs of thyroid storm: symptoms are
exacerbated; fever and extremely high HR
○ Hypothyroidism: an inadequate amount of circulating thyroid hormones
■ Risk Factors: women 30 to 60 years old, use of certain medications
(lithium, amiodarone), inadequate intake of iodine, radiation therapy to the
head/neck, complication of medical treatment
■ It can contribute to an acceleration of atherosclerosis
■ Hashmimoto’s Thyroiditis: is autoimmune; caused by low iodine diet,
pituitary tumor, medication for hyperthyroidism
■ Expected Findings: fatigue, lethargy, irritability, constipation, depression,
weight gain, pale skin, cold intolerance, bradycardia, hypotension,
dysrhythmias, dry and flaky skin, hoarse and raspy speech, abnormal
menstrual periods, goiter on the neck
■ Medications: Levothyroxine [Synthroid]: give it on an empty stomach
one hour before meals

■ Nursing Interventions:
● Monitor for Myxedema: a life-threatening condition that occurs
when hypothyroidism is untreated or due to a stressor (ex: acute
 illness, surgery, chemo, discontinuing of thyroid replacement
therapy)
○ Manifestations: respiratory failure, hypotension,
hypothermia, bradycardia, coma, hypoglycemia,
hyponatremia
● Monitor vital signs and weight
● Keep client warm
● Remember these patients are very sensitive to sedatives and
opioids (do NOT administer sedatives and opioids because it
would lead to myxedema)
○ Addison’s Disease: is an adrenocortical insufficiency
■ It is caused by damage or dysfunction of the adrenal cortex
■ The production of the mineralocorticoids (Aldosterone) and
glucocorticoids (Cortisol) is diminished
● ACTH is released to stimulate the release of hormones: cortisol
(infection is internal stress; external is school)
● Cortisol helps us deal with stress; it raises blood sugar when raised
■ Mineralocorticoids: aldosterone increases sodium absorption and causing
potassium excretion in the kidney
■ Glucocorticoids: cortisol affects glucose, protein, and fat metabolism; the
body’s response to stress and the body’s immune function
■ Sex Hormones: androgens and estrogens

■ Risk Factors: adrenalectomy, TB, cancer, radiation therapy of the

abdomen
● Secondary Risk Factors: steroid withdrawal, hypophysectomy,
pituitary neoplasm
■ Addisonian Crisis: aka acute adrenal insufficiency, is a medical
emergency; *risk for shock*
● Expected Findings: weight loss, craving for salt, weakness,
tiredness and fatigue, hyponatremia, hyperkalemia, hypercalcemia,
hypoglycemia, dehydration, constipation or diarrhea, abdominal
 pain/cramping, nausea, vomiting, hypotension, hyperpigmentation
(brownish discoloration of skin)
● Treatment: Hydrocortisone [Cortef], Prednisone [Deltasone],
Cortisone [Cortone], Fludrocortisone [Florinef] (mineralocorticoid
replacement)
○ Since these are corticosteroids, the dose will need to be
increased when the patient is stressed
■ Assessment:
● Note any illness or stressors that may precipitate problems
● Note signs and symptoms related to adrenocortical insufficiency:
weight changes, muscle weakness, fatigue
● Medications patient is taking
● Monitor for signs and symptoms of addisonian crisis
■ Nursing Interventions:
● Monitor for dehydration and electrolyte imbalances
● Administer saline infusions to restore fluid volume and obtain
orthostatic vital signs
● Administer hydrocortisone IV bolus and a continuous infusion or
intermittent IV bolus
● Monitor for and treat hyperkalemia: a) obtain serum K+ levels and
EKG b) administer sodium polystyrene sulfonate [Kayexalate],
insulin calcium, glucose and sodium bicarbonate
○ IF POTASSIUM LEVELS ARE HIGH, GETTING AN EKG
IS PRIORITY
● Monitor and treat hypoglycemia: perform frequent checks for
neurologic status and check serum glucose
● Maintain safe environment: provide assistance ambulating and
prevent falls by keeping floors clear
■ Complications of Addison's Disease:
● Bone fractures due to hypocalcemia
● Infections due to immunosuppression
● Adrenal crisis
○ Cushing’s Syndrome/Disease: increased cortisol levels
■ Risk Factors: women between ages 20-40
■ Cushing’s Disease: due to an endogenous cause like pituitary carcinoma
secreting adrenocorticotropic hormone (ACTH), adrenocortical carcinoma
● Remove the tumor on the adrenals or pituitary or remove the gland
itself to treat it
● They have to be on therapy for the rest of their lives
■ Cushing’s Syndrome: exogenous cause like use of glucocorticoids for the
following: organ transplant, chemotherapy, autoimmune disease, asthma,
allergies, chronic inflammatory disease
● Stop taking the steroid if it is external, but never abruptly withdraw
it
■ Expected Findings:
● “Moon-face” and “buffalo-hump”
● Hyperglycemia, sodium retention, hypokalemia, hypertension,
tachycardia, weight gain, irregular menses
● Central-type obesity between the shoulders
● Bone fractures (Osteoporosis)
● Fragile, thin skin, ecchymosis, acne
● Striae (pink or purple stretch on the skin)
● Bruising and petechiae (fragile blood vessel)
● Hirsutism (excessive body hair) or balding
● Decreased inflammatory response and impaired wound healing

■ Nursing Considerations:
● Must wash your hands before treating them
● Decreased risk of injury to minimize the risk of pathological
fractures and skin trauma
● Improve body image and improve mental function
● Increased ability to carry out self-care activities
● Encourage weight bearing exercise to strengthen bone and prevent
fractures
● Decreased risk of infection by avoiding crowds and proper
handwashing
● Improved skin integrity by providing meticulous skin care and
reposition every 2 hours
● Absence of complications
● Monitor WBC count daily
 ■ Treatments:
● Hydrocortisone [Cortef] for replacement therapy for clients who
have adrenocortical insufficiency
● Hypophysectomy: surgical removal of the pituitary gland
depending on the cause of Cushing's disease
● Adrenalectomy: surgical removal of the adrenal gland
■ Patient Education:
● Instruct the patient to carry emergency identification about
corticosteroid use
● Inform the client to notify provider for any signs of infection
● Instruct client to take the medication without skipping any doses
● Advise the client to consume a diet high in calcium and vitamin D
● Never wear sandals, only good fitting shoes
● Diabetes: characterized by elevated levels of glucose in the blood
○ Resulting from either an inadequate production of insulin (type 1) or an inability
of the body’s cells to respond to insulin (type 2) or both
○ Normal blood glucose: 70-110
○ Insulin the the key to let glucose into the cell because it needs it for energy
○ Minority populations and older adults are disproportionately affected
○ Risk Factors: family history, obesity, race (Africans Americans, Hispanic
Americans, Native Americans and Pacific Islanders), age >45 years, hypertension,
high cholesterol, history of gestational diabetes, more common in men than
women
○ Insulin: a hormone produced by the pancreas
■ It controls the levels of glucose in the blood by regulating the production
and storage of glucose
■ Stimulates storage of glucose in the liver and muscle as glycogen
■ Signals the liver to stop the release of glucose
■ Enhances storage of dietary fat in adipose tissue
■ Accelerates transport of amino acids into cells
■ Inhibits the breakdown of stored glucose, protein, and fat
○ Diabetes Mellitus Type 1: insulin-producing pancreatic beta cells are destroyed
by a combination of genetic, autoimmune, or environmental factors
■ As a result, the beta cells produce little or no insulin
■ Requires insulin injections to control blood glucose
■ Characterized by an acute onset usually before age 30
■ Main Clinical Features: hyperglycemia, dehydration, electrolyte loss,
acidosis, possible sudden weight loss
■ Diabetic Ketoacidosis- caused by an absence of inadequate amounts of
insulin; rapid onset and the mortality rate is up to 10%
 ● An acute life-threatening condition characterized by uncontrolled
hyperglycemia (more than 300 mg/dl) resulting in the breakdown
of body fat for energy, dehydration, metabolic acidosis and an
accumulation of ketones in the blood and urine
● Manifestations of DKA:
○ Polydipsia: excessive thirst
○ Polyuria: excess urine production and frequency
■ Loss of skin turgor, skin warm and dry
■ Dry mucous membranes
■ Weakness
○ Polyphagia: excessive hunger and eating caused from
inability of cells to receive glucose (because of a lack of
insulin or cellular resistance to available insulin) and the
body’s use of protein and fat for energy (which causes
ketosis)
○ Fatigue, weakness, vision changes, tingling or numbness in
hands or feet, dry skin, lesions or wounds that are slow to
heal, recurrent infections
○ Seizures leading to coma, decreased LOC, inability to
concentrate, headache, vomiting, abdominal pain
■ Treatment of DKA:
● Rehydration with IV fluids
○ Rehydration leads to increased plasma volume and
decreased potassium; insulin causes movement of
potassium from extracellular fluid into the cells
● IV continuous infusion of regular insulin
● Reverse acidosis and restore electrolyte balance
● Monitor blood glucose, renal function and urinary output, EKG,
electrolyte levels, vital signs
● Lung assessments for signs of fluid overload
○ Diabetes Mellitus Type 2: insulin resistance and impaired beta cell functioning
results in decreased insulin production; onset over age 30 years
■ Slow, progressive glucose intolerance and may go undetected for years
■ Insulin resistance may lead to metabolic syndrome: hypertension,
hypercholesterolemia, abdominal Obesity
■ Hyperglycemic Hyperosmolar Syndrome (HHS): is an acute, life
threatening condition characterized by profound hyperglycemia (greater
than 600mg/dl)
● Hyperosmolarity leads to dehydration and absence of ketosis
 ● ONSET GENERALLY OCCURS GRADUALLY OVER
SEVERAL DAYS AND IF LEFT UNTREATED CAN LEAD TO
COMA OR DEATH
■ Manifestations of HHS: hypotension, profound dehydration (dry mucous
membranes, poor skin turgor), tachycardia, neurologic signs (seizures,
altered mental status), insulin deficiency, persistent hyperglycemic,
polyuria with inadequate fluid intake
■ Treatment of HHS:
● Rehydration with isotonic fluids (0.9 NS sodium chloride)
● Insulin administration via IV rather than subQ to provide
immediate treatment
○ Remember, the patient will absorb SQ slowly and
erratically, making it difficult to adjust dosages of insulin
appropriately
● Monitor blood glucose hourly
● Monitor fluid volume and electrolyte status, especially potassium
○ Potassium levels will initially be increased but with insulin
therapy; they will need to be monitored for hypokalemia
■ Prevention of HHS: blood glucose self-monitoring (BGSM), diagnosis
and management of diabetes
○ Distinguishing Between HHS from DKA: ketosis and acidosis do not occur in
HHS and the loss of water in HHS makes the blood more concentrated than
normal (called hyperosmolarity – a condition in which the blood has a high
concentration of sodium and glucose which draws water out of the body)
■ In DKA, no insulin is present, and this promotes the breakdown of stored
glucose, protein and fat which leads to the production of ketone bodies
and ketoacidosis
○ Diagnostic Criteria for Diabetes: two findings (on separate days) of at least 1 of
the following
■ Manifestations of diabetes plus casual blood glucose concentration greater
than 200mg/dl (without regard to time since last meal)
■ Fasting blood glucose greater than 126 mg/dL
■ 2-hr glucose greater than 200mg/dl with oral glucose tolerance test (often
used to diagnose gestational diabetes mellitus during pregnancy)
■ Glycosylated hemoglobin (A1C) greater than 6.5%: expected reference
range is 4% to 6% but an acceptable reference range for clients who have
diabetes can be 6.5% to 8% with a target goal of less than 7%
○ Long-Term Complications of Diabetes:
■ Cardiovascular disease, HTN, kidney disease, peripheral neuropathy,
retinopathy, stroke, nephropathy, autonomic neuropathies, hypoglycemic
 unawarness, sexual dysfucntion; accelerated atherosclerosis changes,
CAD, cerebrovascular disease, and peripheral vascular disease
○ Patient Education for Diabetes:
■ Encourage yearly eye exams to ensure the health or the eyes and to protect
vision
■ Encourage the management of blood glucose levels
■ Encourage annual exams by a podiatrist
■ Encourage regular follow-up with provider to assess and treat neuropathy
■ Encourage yearly urine analysis, BUN, micro albumin and serum
creatinine screenings
■ Encourage the client to avoid soda, alcohol and toxic levels of
acetaminophen or NSAIDS
■ Teach the client to consume 2 to 3L/day of fluids
■ Teach the client to report decrease in output to the provider
■ Foot Care:
● Inspect and wash feet daily with mild soap and warm water
● Pat feet dry gently, especially between toes and avoid lotions
between toes to decrease excess moisture and prevent infection
● Consult with a podiatrist and never cut your own toenails
● Avoid open toe, open heel shoes; never go barefoot
● Leather shoes are preferred to plastic
● Wear shoes that fit correctly and slippers with soles
○ Management of Diabetes:
■ Main goal is to normalize insulin activity and blood glucose levels to
reduce the development of complications
■ HgbA1c less than 7% is now recommended
■ Five components: nutritional therapy, exercise, monitoring, pharmacologic
therapy, an education
○ Insulin Therapy: the abdomen is the best place to inject insulin
■ Blood glucose monitoring should be done before giving insulin and never
give it if there is no food in front of the patient
■ Rapid Acting: lispro, aspart, glulisine
● Administer before meals to control postprandial rise in blood
glucose
● Onset is rapid (10-30mins) depending in which is given
● Administer in conjunction with immediate-or long acting insulin to
provide glycemic control between meals and at night
■ Short Acting: regular insulin
● Administer 30 -60 mins before meals to control postprandial
hyperglycemia
 ● Regular is available in two concentrations:
○ U-500 is reserved for the client who has insulin resistance;
never administered IV
○ U-100 is prescribed for most clients and may be
administered IV
■ Intermediate Acting: NPH insulin
● Administered for glycemic control between meals and at night
● Not administered before meals to control postprandial rise in blood
glucose
● Administer NPH insulin sub Q only and as the only insulin to mix
with short-acting insulin
■ Long Acting: glargine [Lantus] and detemir [Levemir]
● Administered once daily, anytime during the day, but always at the
same time each day; administered subQ only
○ Administration at night is best, especially when the patients
sugar typically goes higher in the morning
● It forms micro-precipitates that dissolves slowly over 24 hrs and
maintains a steady blood sugar level with no peaks
■ Nursing Considerations:
● Observe the patient perform self-administration of insulin and offer
additional instructions as indicated
● Monitor for hypoglycemic reactions such as sweating, weakness,
dizziness, confusion, headache, tachycardia, slurred speech
● Dosage can be adjusted when the client is scheduled for procedures
that requires fasting

■ Patient Education for Insulin Management:

● Educate clients to rotate injection sites to prevent lipohypertrophy
○ Inject at a 90 degree angle (45 degree angle if the client is
thin)
○ When mixing a rapid – or short insulin with a longer
–acting insulin, draw up the shorter-acting insulin into the
syringe first and then the longer-acting insulin
 ● Advise patients to eat at a regular intervals, avoid alcohol intake
and adjust insulin to exercise and diet to avoid hypoglycemia
● Encourage the client to wear a medical identification wristband
○ Hypoglycemia: occurs if blood sugar is less than 70 mg/dL
■ Symptoms: altered mental status, fatigue, pale/clammy skin, shakiness,
diaphoresis, tachycardia, irritability, tingling or numbness of the lips,
tongue or cheek, confusion, blurred vision, seizures, loss of consciousness
● Shakiness is one of the earliest signs
■ Factors Causing Hypoglycemia:
● Overdose of insulin or oral hypoglycemic agents
● Omission of food or too little intake
● GI discomfort such as nausea, vomiting or diarrhea
● Alcohol intake
● Lipodystrophy at injection site (causing decreased absorption of
insulin when injected)
● Strenuous activities or excessive workouts
● Breastfeeding by a diabetic mother
● Poorly designed insulin regimen
■ Nursing Interventions:
● Assess causative factors and degree of impairment
● Check current blood glucose
○ For conscious patients with blood glucose below 60 mg/dl:
give at least 10-15g of fast acting simple carbohydrates
(hard candy, honey, crackers or fruit juice)
○ For unconscious patients and patient unable to swallow:
administer dextrose 50% 50ml bolus intravenously as
ordered
● Repeat the patient blood glucose in 1 hour after administration
● Monitor vital signs and draw blood for baseline electrolytes
● Obtain a complete patient history including the last alcohol intake
and medications
○ Hyperglycemia: blood glucose greater than 140 mg/dL is the main cause of
organ damage and linked to poor patient outcomes
■ Causes: skipping or forgetting medications, eating the wrong food,
infection/illness, stress, medications such as steroids
■ Symptoms: blurred vision, frequent urination, increased thirst/hunger,
numbness and tingling of feet, fatigue, weight loss, vaginal and skin
infections, slow wound healing
● Females are at high risk for vaginal yeast infections
■ Treatment: blood glucose monitoring, insulin (subQ or IV), IV fluids
 ■ Patient Education:
● Notify the doctor if glucose is greater than 150 mg/dl for more than
1 week or 2 consecutive readings of 300 mg/dl
● Avoid non-caffeinated and non-alcoholic beverages
● Read food labels
● Follow meal plan, medication and exercise program
● Cholelithiasis and Cholecystitis:
○ Cholelithiasis: the presence of gallstones in the gallbladder related to the
precipitation of either bile or cholesterol into stones
○ Cholecystitis: inflammation of the gallbladder wall
■ Often caused by gallbladder obstructing the cystic and/or common bile
duct
○ Risk Factors: being female, high-fat diet, obesity, genetic predisposition, older
adults, type 2 diabetes

○ Health Promotion and Disease Prevention: consume a low-fat diet rich in HDL
sources (seafood, nuts, olive oil), regularly exercise, do not smoke
○ Expected Findings:
■ Sharp pain in the right upper quadrant, often radiating to the right shoulder
■ Intense pain and rebound tenderness (Blumberg's and Murphy’s sign
performed by the provider)
● Blumberg’s sign: patient lays down, they inhale and you try to feel
for the gallbladder, and they stop breathing; this is positive
● Murphy’s sign: patient takes a deep breath in and holds it while the
gallbladder is palpated; positive if there is pain on inspiration while
it is being palpated
■ Belching and flatulence
■ Fever, jaundice, clay-colored stools
■ Steatorrhea (fatty stools; it will float on the water)
■ Dark urine
■ Pruritus (from accumulation of bile salts in the skin)
 ○ Therapeutic Procedures:
■ Extracorporeal Shock Wave Lithotripsy: shock waves are used to break
up stones
● This can be used more on nonsurgical candidates of normal weight
who have small, cholesterol-based stones
■ Cholecystectomy: removal of gallbladder with a laparoscopic minimally
invasive, or open approach
● Patient is discharged within 24hrs if it is laparoscopic
● An open approach can require hospitalization for 1 to 2 days: they
should be using an incentive spirometer and be ambulated asap
● Educate patient to slowly incorporate fat into their diet post
operatively, or they can have loose stools
● A T-tube may be placed in the common bile duct so it can drain out
all the bile; there is swelling, so after it stops, we take it out; make
sure the patient is not laying on the bag or kinking it; the patient
should be sitting in a semi-fowlers position; monitor the fluid
● Patient will have pain that while rise to the shoulder; have them
lay on the side (lateral position) and give them pain medication
○ Goals: relief of pain, adequate ventilation, intact skin, improved biliary drainage,
optimal nutritional intake, absence of complications, understands self-care
routines
○ Nursing Interventions:
■ Semi-Fowler’s position
■ NG or NPO until bowel sounds return; then a soft, low-fat,
high-carbohydrate diet
■ Care of biliary drainage system
■ Analgesics, pain management
■ Patient should have a low-fat diet
■ Frequent position changes
■ Cough and deep breathing while splinting (with pillow) to reduce pain
■ Ambulation: many patients c/o shoulder pain from gas
■ Self-care education
● Pancreatitis: an auto digestion of the pancreas by pancreatic digestive enzymes
(amylase, protease, lipase) that activate prematurely before reaching the intestine
○ Inflammation of the pancreatic tissue causes duct obstruction which can lead to
increased pressure and duct rupture causing the release of pancreatic enzymes into
the pancreatic tissue
○ Acute Pancreatitis: is an inflammation process due to activated pancreatic
enzymes auto-digestion the pancreas
○ Chronic Pancreatitis: progressive destructive disease of inflammation and
fibrosis of the pancreas; classified as chronic calcifying (often associated with
alcohol use disorder), chronic obstructive pancreatitis (often associated with
cholelithiasis) and autoimmune pancreatitis and idiopathic and hereditary
pancreatitis
■ Patients do not make the enzymes anymore, so they need to be given the
enzymes PO right before they eat
○ The islets of Langerhans in the pancreas secrete insulin and glucagon; the
pancreatic tissue secretes digestive enzymes that breakdown carbohydrates,
proteins and fats
○ Risk Factors: alcohol use and gallstones are the biggest risk factors
■ Biliary tract disease: gallstones can cause a blockage where the common
bile duct and pancreatic duct meet
■ Alcohol use: primary cause of chronic pancreatitis is alcohol use disorder
■ Increased age: pancreatitis is more common in older adults
■ Genetic predisposition
■ Trauma
■ Medication Toxicity: Valproic acid, Sulfonamides, Tetracycline,
Corticosteroids
■ Viral infections - human immunodeficiency virus
■ Cigarette smoking
○ Clinical Manifestations:
■ Classic presentation of an acute attack: severe, constant, knifelike pain
(left upper quadrant, mid-epigastric and/or radiating to the back)
■ Abdominal Distention: poorly defined palpable mass, rigid (peritonitis)
■ Decreased peristalsis and diminished bowel sounds
■ Nausea, vomiting, weight loss
■ Hypotension and hypovolemia
■ Tachycardia
■ Ecchymosis on the flanks (Turner’s sign)
● Patients will bleed easier because the enzymes eat the tissue and
vessels in the surrounding areas
■ Bluish-gray periumbilical discoloration (Cullen’s sign)
■ Generalized jaundice
○ Nursing Management:
■ Rest the pancreas so it is not stimulated so it would not release enzymes
■ IV opioids: continuous drip (morphine is contraindicated due to spasms)
■ Position the client for comfort (fetal, side-lying, head of the bed elevated,
sitting up or learning forward)
■ PLACE THE PATIENT ON NPO IS THE PRIORITY
 ■ Decrease secretion of pancreatic or gastric enzymes with IV hydration
■ Insert NGT for decompression
■ Monitor of fluid and electrolyte imbalances/ administer fluids and
electrolytes replacement
■ Start total parenteral nutrition (TPN ) therapy as ordered
■ Administer antiemetic as needed
■ No alcohol consumption
■ Administer pancreatic enzymes as ordered
● Administer right before meals and snacks and monitor stool for
effectiveness of pancreatic enzymes (pt will have diarrhea) for
decrease in steatorrhea
■ Improve breathing pattern (Left lung effusion and atelectasis is a
complication)
● Monitor pulse oximetry and ABGs
● Semi-Fowlers position to decrease pressure on diaphragm by a
distended abdomen and increase respiratory expansion
● Frequent position changes to prevent atelectasis
■ Sitting up in bed or learning forward to help ease pain
■ Avoid alcohol or greasy fatty foods; consume foods low in fat and high
protein; limit sugars and refined carbs
○ Complications: pseudocyst (inside or on top of the pancreas; the enzymes begin
to form pockets and collects; which can cause a widespread infection called
peritonitis)
■ Put the patient on NPO because the enzyme will be produced if they eat;
put in an NG tube and connect it to suction to take out all the enzymes