DONT FORGET SIMPLENURSING.

COM has videos for the EGG, Cardiac enzymes,

meds, an and answers most the objective questions if you get stuck!
MI - Tropnin - CPK - Myoglobin (one video)
Cardiac stroke volume 1 of 2
Cardiac stroke volume 2 of 2
Cardiac Glycoside (Digoxin)
CHF Drugs Part 1
CHF Drugs Part 2
Stress Test Cardiac
Acute Coronary Syndrome, Coronary Artery Disease and MI
CAD vs ACS 1 of 2
CAD vs ACS 2 of 2
Post Angio Cath
4 Drugs Given During an MI Heart Attack (MONA) morphine, Oxygen, Nitro, Asa
MI drugs & Beta Blockers
CHF drugs vs. MI (heart attack) 1 of 2
Heart failure Drugs vs. MI drugs 2 of 2
Heart Failure vs. MI drugs (Heart failure Beta Blockers focus)
Heart Failure vs. MI drugs (Calcium Channel blocker focus)
MI heart attack medications
Heart Attack MI drugs MONA & Beta blockers
CHF vs. MI Drugs
CHF vs. MI Drugs PART 2
CHF vs. MI drugs BETA Blockers
CHF vs. MI drugs CALCIUM CHANNEL BLOCKERS
Post Angio Cath
Cardiac Assessment: S1 S2 & APETM
MI (patho, Nursing interventions, drugs, labs)
Cardiac Glycoside (Digoxin) Positive Inotropic Drug
Nursing Students CHF drugs (Part 1)
Nursing Students CHF Drugs (part 2)
Cardiac Glycoside (Digoxin) Positive Inotropic Drug
34-rythems.pdf
EKG intro electrical conduction
EKG A-fib, AV blocks, V- Tach
Atrial Fibrillation part 1
Cardiac Glycoside (Digoxin)
MI
Stress Test Cardiac
 Cardiovascular Assessment
(Objectives)

Identify important history information in a cardiovascular assessment, including risk factor assessment.

**Chest pain can also indicate: non-cardiac conditions: GERD, anxiety, neuromuscular abnormalities, pleurisy,
PE, hiatal hernia,

*Describe pain (if able) Is it different from other episodes of pain?

What were you doing at the time? Arguing, sleeping, running?
Is pain sharp/dull/radiating/crushing? Pain scale?
Diaphoretic?
Dyspnea breathing difficulties with rest? Exertion (an EARLY symptom of HF)?
Orthopnea? - Breathlessness while lying flat?
Paroxysmal nocturnal dyspnea develops when patient lying flat for several hours

Fatigue: Usually described as bone weary. If it develops after mild activity, = indicates inadequate Cardiac
output.

Palpitations: unpleasant feeling in chest like heart skipping beats or has extra beats.
Non cardiac reasons for palpitations are: anxiety, stress, fatigue, hyperthyroidism, caffeine, nicotine, alcohol
Edema: Sudden weight increase = 2.2 pounds = 1 liter extra fluid in interstitial space

Syncope: brief loss of consciousness. Results from brief reduction of cardiac output

Diagnostic test- Troponin, Creatine Kinase, and Myoglobin

Family history
HDH and HDL levels
History of cardiovascular health
ECG

General build
Skin color
Pallor/cyanotic/pink
Moisture (decreased perfusion = cool, pale, moist skin)
Cyanosis
Dark-skinned pts w/ cyanosis may appear grayish
Central cyanosis = oxygenation of arterial blood in lungs bluish tinge of mucus membranes of tongue and mouth
& conjunctiva
Peripheral cyanosis = blood flow to periphery
Skin temperature
blood flow to skin = temperature

Describe the purpose of and the nursing management for the following diagnostic studies.
Chest X-ray: looking for size, silhouette, and position of the heart

Cardiac Catheterization:
Most definitive and most invasive
Can confirm suspected heart disease
(congenital abnormalities, CAD, myocardial and valvular disease/dysfunction
Location and extent of heart disease (look at right side, left side or coronary arteries)
Table and severe angina unresponsive to medical tx
Unstable angina
Uncontrolled heart failure
Determine best therapeutic option
Evaluate side effect of medical treatment
Catheter inserted into artery through the groin or brachial area.
The catheter is guided to heart by use of fluoroscope.
Contrast dye is injected
image captured and recorded.
Images detect arteries that are narrowed or blocked

NURSING MANAGEMENT:
Before procedure
Pt is admitted to hospital the day of the procedure
Fluids may be given before procedure for renal protection (pg 643)
Contrast induced renal dysfunction can result from vasoconstriction and direct
toxic effect of dye on renal tubules.
Hydration and acetylcysteine post study to reduce risk
NPO after midnight or only liquid breakfast if afternoon study
Antiseptically prepare site and clip hair
Vitals, auscultate lungs and heart pre assessment
Assess history of iodine based allergies (shellfish also)
Mild sedative admin before procedure
If on digitalis or diuretic withheld for procedure
Analysis of BNP, coagulation, CBC pre and post procedure
Post procedure
Pt returns to their room lying flat,
5 pound bag of sand on the groin area for 6 hours r/t bleeding risk.
Vitals q 15 mins for the first hour and q1hr thereafter.
You have to get creative if they need to go to the bathroom, they cant get up!!!!
Book slightly dif from Marti Pwpt
Some cardiologist allow HOB at 30 degrees
Can use vascular closure devices that eliminate need for
compression of 5 lb sand.
Assess temperature, color and pulses each VS check
Contrast medium is an osmotic diuretic, assess urination and adequate fluid
intake to make sure pt. Can excrete it.

Critical rescue box :

If s/s of cardiac ischemia
chest pain, dysrhythmia, bleeding, hematoma formation, or dramatic
change in peripheral pulses in affected extremity. Could be acute MI
call rapid response team!
If neurologic changes
Visual disturbance, extremity weakness, slurred speech, swallowing
difficulties, report immediately could be s/s of stroke. Report to Dr.

COMPLICATIONS:
Right sided catheterization
Thrombophlebitis
Pulmonary embolism
Vagal response (vitals drop)
Left sided catheterization
Myocardial infarction
Stroke
Arterial bleeding or thromboembolism
Dysrhythmias
Happens for each side
 Cardiac tamponade- type of pericardial effusion (fluid, pus, blood, clots, or gas
accumulates in the pericardium)
Hypovolemia
Pulmonary edema
Hematoma or blood loss at insertion site
Reaction to contrast medium
Risk of MI or stroke

ECG (electrocardiography)
Recording of the heart's electrical functioning
Electrodes placed on 12 sites (hence 12 lead)
as opposed to tele in hospital using 6 lead
Provided MD with 12 view of heart's electrical activity

Echocardiography
Non-invasive
Checks function of heart muscles under stress
Exercise tolerance testing
Use of treadmill
IV drugs usually dobutamine (whips the heart muscle)
Assess/dx cardiomyopathy, valvular disorders, pericardial effusion, left ventricular function,
ventricular aneurysms, cardiac tumors

Transesophageal Echocardiography
Uses sound waves to create high-quality moving pictures of the heart and blood vessels.
Used if other methods do not create a clear enough picture

BLOOD TEST

Acute coronary syndrome (AMI) confirmed by abnormally high levels of 3 Cardiac Markers:
Troponin, Creatine Kinase, and Myoglobin

Troponin myocardial muscle protein released into blood stream with injury to heart muscle.
Myocardial muscle protein released during injury
Not found in healthy persons ANY rise indicates cardiac necrosis or MI
Cardiac troponin T = <0.10 ng/ml
Cardiac troponin I = <0.03 ng/ml
Rise - 4-6 hours; peak 10-24 hours; return to normal in 10-14 days; drawn q 8 hrs x 3.
Any rise is treated aggressively
Can be tested at bedside in ER and results back within 15-20 min.
 Creatine Kinase (CK)-MB
Enzyme specific to brain, myocardium, and skeletal muscle
Cardiac specificity determined by 3 isoenzymes activity:
CK-MM found in skeletal muscle
CK-BB found in the brain
CK MB most specific for MI.
Rise 3-8 hours; peak 12-24 hours; return to normal 2-3 days; drawn q8 hours x 3.
< 1 mg/dL = low risk
> 3 mg/Dl = high risk
Myoglobin
<90mcg/ml normal, greater values indicate MI
Found in cardiac and skeletal muscle Earliest marker detected
Rise 2-3 hours; peak 6-9 hours; return to normal in 24 hours
Clinical usefulness more limited than troponin

Homocystine
Amino acid produced when proteins break down
Elevated levels may be risk factor for CVD
The link is controversial but elevated levels may be as big of risk factor as smoking and
hyperlipidemia especially in women.
High-risk patients with personal or family history of premature heart disease should be tested
for this amino acid
Levels in the blood between 4 and 15 micromoles/liter (mol/L).
Any measurement above 15 is considered high

C-Reactive Protein (CRP)

Most studied marker for inflammation
Elevations seen in HTN, smoking, and infection
Levels over 3 mg/dL indicate high risk for heart disease
CRP levels are helpful in managing statin therapy post MI

Brain natriuretic peptide (BNP)

Secreted by ventricles of the heart in response to increase blood volume and pressure
(stretch receptor in heart)
Normal levels = 100 pg/ml; levels over 100 pg/ml may indicate heart failure
Increased urine output; decreased blood volume
Has opposite effects opposite that of aldosterone.
BNP helps reduce the stress on the heart, and does so by diuresis, vasodilation, and
inhibiting the renin-angio

Valvular and Inflammatory Cardiac Disorders

Chart 35-6 page 692
Correlate common signs and symptoms with the pathophysiology of following valvular disorders:

Mitral stenosis (narrows) page 692

 Usually from rheumatic carditis (rheumatic fever)
Mitral valve thickens by fibrosis and calcification

What happens:
Valve leaflets fuse, become stiff,
Chordae tendineae contract and shorten
Valve opening narrows
Prevents normal flow from left atrium to left ventricle.
L/T left atrial pressure , left atrium enlarges (L/T=leads to)
Pulmonary artery pressure increase
Right ventricle hypertrophies

Pulmonary congestion and Right -Sided heart failure occur first

What it looks like:
Mild stenosis is asymptomatic
As it worses (valve opening narrows more)
Pressure in lungs , dyspnea on exertion, orthopnea
paroxysmal nocturnal dyspnea (night waking dyspnea),
palpitations, dry cough As progresses: hemoptysis (cough up blood)
Pulmonary edema, enlarged liver, neck vein distention,
pitting edema (late sign)

Pulse may be normal, rapid, or irregularly regular

*have an abnormal but predictable rhythm-Like A fib
Any new atrial fibrillation means pt may be decompensating
Report changes to Dr.
A rumbling apical diastolic murmur may be noted on auscultation
(Review) Chart 35-6 Key Features of Mitral Stenosis:
Fatigue
Dyspnea on exertion
Orthopnea (lying down w/SOB)
Paroxysmal nocturnal dyspnea (severe SOB and coughing at night; awakens person sleeping)
Hemoptysis (coughing up blood)
Hepatomegaly (abnormal enlargement of liver)
Neck vein distention
Pitting edema
Atrial fibrillation
Rumbling, apical diastolic murmur (atrium rest/filling up)

Mitral regurgitation (leaky) pg 693

Primary cause is degenerative r/t aging, and infective endocarditis.
Other causes are papillary muscle dysfunction, rupture from ischemic heart disease,
congenital anomalies.
Also Rheumatic fever- usually has some mitral stenosis with regurgitation when it is
rheumatic fever.
Affects women more often than men

What happens:
 Fibrotic and calcification changes prevent mitral valve from closing during systole.
Incomplete closure causes backflow of blood into left atrium when left ventricle
Contracts.
During systole the extra blood that flowed into left atrium moves with normal
blood flow into left ventricle. But there is now a larger volume.
Larger volume causes left atrium and ventricle to dilate and hypertrophy.
Symptoms start when left ventricle fails r/t chronic volume overload.

What it looks like:

Progresses slowly. Symptom free for decades.
When left ventricle fails- fatigue, chronic weakness (think reduced cardiac output)
anxiety, atypical chest pain.
Later: dyspnea on exertion and orthopnea
Assessment may show normal B/P, Afib, and respiratory changes.

Right sided heart failure - distended neck veins, enlarged liver, pitting edema.
High pitched systolic murmur at apex with radiation to left axilla heard on
auscultation. Severe regurgitation exhibits a third heart sound at S3.

Chart 35-6 Key Features Mitral Regurgitation:

Fatigue
Dyspnea on exertion
Orthopnea
Palpitations
Atrial fibrillation
Neck vein distention
Pitting edema
High-pitched holosystolic murmur

Mitral Valve prolapse

Etiology is variable. Associated with marfan syndrome and other congenital
heart defects. Can be hereditary. Usually no other cardiac abnormality is found.
Note Marfan syndrome-rare disorder t/causes connective tissue in body to be weaker than it
should be. CT is the material that holds together many structures in your body including heart valves.
What happens:
Mitral valve leaflets enlarge and prolapse into left left atrium during systole
What it looks like:
Mostly benign- can progress to mitral regurgitation in some
Most are asymptomatic
May report chest pain, palpitations, exercise intolerance,
Chest pain usually atypical, described as sharp and on left side of chest.
Normal HR and B/P
Mid systolic click and late systolic murmur heard at apex of heart.
*intensity of murmur not related to severity of prolapse.

Chart 35-6 Key Features Mitral Valve Prolapse

Atypical chest pain
Dizziness, syncope
 Palpitations
Atrial tachycardia
Ventricular tachycardia
Systolic click

Aortic Stenosis
Most common valve dysfunction
Disease of wear and tear in aging population
Congenital bicuspid or unicuspid aortic valves are primary cause for many
Rheumatic aortic stenosis occurs with mitral stenosis following rheumatic fever.
Atherosclerosis and degenerative calcification of aortic valve are major causative
factors in older adults.

What happens:
Aortic valve orifice narrows, obstructs left ventricular outflow during systole
Increased resistance to ejection or afterload L/T ventricular hypertrophy
Cardiac output becomes fixed and cannot increase to meet the demands of the
body with exertion.
Eventually left ventricle fails, blood backs up in left atrium.
Pulmonary system becomes congested and Right sided heart failure occurs.
When surface area of valve becomes 1 cm or less, surgery indicated/urgent!
What is looks like:
Fixed cardiac output creates dyspnea, angina, syncope upon exertion.
When cardiac output falls in later stages marked fatigue, debilitation and
peripheral cyanosis.
Narrow pulse pressure when BP measured..
Diamond shaped systolic crescendo decrescendo murmur is usually noted on
auscultation

Chart 35-6 Key Features Aortic Stenosis

Dyspnea on exertion
Angina
Syncope on exertion
Fatigue
Orthopnea
Paroxysmal nocturnal dyspnea
Harsh, systolic crescendo-decrescendo murmur

Aortic regurgitation
Usually non rheumatic causes
Infective endocarditis, congenital anatomic aortic valvular abnormalities, HTN, marfan
syndrome.
What happens:
Aortic leaflets do not close properly during diastole
Annulus (valve ring that leaflets attach to) is usually dilated, loose or deformed
This allows backflow of blood from aorta to left ventricle in diastole.
Left ventricle to compensate dilates, and eventually hypertrophies.
What it looks like:
 Most asymptomatic due to compensatory mechanism of left ventricle
When left ventricle failure happens- dyspnea, orthopnea, paroxysmal nocturnal dyspnea.
Palpitations may be noted with severe disease, worse when lying on left side
Nocturnal angina with diaphoresis.
Bounding arterial pulse
Widened pulse pressure
Elevated systolic pressure and diminished diastolic pressure
High pitched blowing decrescendo diastolic murmur

Chart 35-6 Key Features Aortic Regurgitation

Palpitations
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue
Angina
Sinus tachycardia
Blowing, decrescendo diastolic murmur

Correlate common signs and symptoms with the pathophysiology of following inflammatory or genetic
cardiac disorders:

Infective endocarditis
Pathophys: A microbial infection of the endocardium (innermost layer). Typically in patients that abuse drugs,
have had valve replacements, have a systemic infection, or structural cardiac defects,
Structural defect side note: Blood flow may go from a high pressure to a low pressure zone eroding a
section of endocardium, allows a perfect area for bacteria and deposited vegetation to thrive more platelets and
fibrin will come which allows the area to grow leaving the endocardium and valve to be destroyed. It also may
cause emboli to be released into the general circulation
Portals of entry: Oral cavity (think dental procedures abscessed teeth, ect. Needs to be on antibiotics a
week before procedures), Skin rashes, lesions, Infections or invasives surgeries.
s/s: Clinical manifestations typically occur within two weeks of bacteremia.
Fever associated with chills, night sweats, malaise (feeling ill or not right), fatigue
Recurrent( 99-103)
Cardiac murmur (newly developed or change in existing)
Really common! May even hear and S3 orS4 murmur.
Most common complication is heart failure
Right sided HF Via peripheral edema, weight gain and anorexia
L sided HF via Fatigue, SOB, crackles upon auscultation
Evidence of systemic embolization
Arterial immobilization is a BIG deal!
Fragments of vegetation may just randomly fall off and go into circulation
L side of the heart? Travels to spleen, kidneys, GI, brain, extremities
R side? Its going to the lungs bro!
Petechiae (pinpoint red spots)
Look on mucous membranes! Palate, conjunctivae, and the skin above the clavicles may have small, red, flat
lesions.
Splinter hemorrhages
 Look at the distal 3rd of nail beds presents as black longitudinal lines or small red streaks
Splenic infarction
Sudden abdominal pain maybe radiation to the shoulder, Look for rebound tenderness,
Renal infarction?: Flank pain radiating to groin accompanied with hematuria and/or pyuria (WBC in urine).
Neurologic changes occur in of patients, Others may present with pulmonary issues
TIA, stroke or pulmonary emboli
Look for confusion, reduced concentration, aphasia or dysphasia.
Pleuritic chest pain dyspnea and cough
Oslers nodes (On palms of hand and soles of feet)
Janeways lesions (flat reddened maculae on hands and feet)
Positive blood cultures
Pericarditis
Acute pericarditis is inflammation or alteration of pericardium (membranous sac enclosing the heart)
Most commonly associated with: Infective organisms, post-myocardial infarction (MI) syndrome,
postpericardiotomy syndrome, acute exacerbations of systemic CT disease
Chronic pericarditis is the chronic inflammatory causes fibrous thickening of the pericardium, pericardium
becomes rigid, prevents adequate filling of ventricles therefore constricting the heart causing compression
Causes: tuberculosis, radiation therapy, trauma, renal failure, metastatic cancer
Can result in loss of pericardial elasticity or an accumulation of fluid within the sac
HF or cardiac tamponade may result
Assessment:
Pain in anterior chest that radiates to L side of neck, shoulder, or back
Pain is grating and is aggravated by breathing, coughing, and swallowing
Pain is worse when in supine position; may be relieved by leaning forward
Auscultation: pericardial friction rub at left lower sternal border (scratchy, high-pitched sound)
Fever and chills, fatigue and malaise, elevated WBC, ST segment elevation w/ onset of inflammation, a-fib
common, signs of ventricular failure in clients with chronic constrictive pericarditis.
Interventions:
Assess nature of pain
Position in high fowler's or upright and leaning forward
Admin analgesics, NSAIDs or corticosteroids
Check results of blood culture to identify causative organism
Administer antibiotics and digoxin as prescribed with chronic constrictive pericarditis---SURGICAL INCISION
may be necessary (pericardiocentesis 8 in, 16-18 gauge needle into pericardial sac)
Monitor of signs of cardiac tamponade, including pulsus paradoxus, jugular vein distension w/ clear lung sounds,
muffled heart sounds, narrowed pulse pressure, tachycardia, and decreased CO

Myocarditis
Description
Acute or chronic inflammation of the myocardium as a result of pericarditis, systemic infection, or allergic
response
Assessment
Fever, pericardial friction rub, gallop rhythm murmur that sounds like fluid passing an obstruction, pulsus
alternans, signs of HF, fatigue, dyspnea, tachycardia, chest pain.
Interventions
Assist client to a position of comfort: such as sitting up and leaning forward.
Administer analgesics, salicylates, and NSAIDS as prescribed
Administer oxygen, provide adequate rest periods, limit activities to avoid overexertion, administer digoxin if
prescribed; monitor toxicity, administer antidysrhythmics, administer antibiotics to treat causative organism,
monitor for complications such as: thrombus, HF, and cardiomyopathy.

Rheumatic pericarditis
 Description:
A sensitivity response that develops after an infection with group A beta-hemolytic streptococci
Inflammation is evident in all layers of the heart and results in impaired contractile function of the myocardium,
thickening of the pericardium, and inflamed endocardium, leading to valvular damage
Common manifestations:
Symptoms of streptococcal infection, leading to endocarditis
Fever, sore throat, tachycardia, and elevated serum findings of antideoxyribonuclease B titer, antistreptolysin O
titer, complement assay, C reactive protein
New onset murmur, pericardial friction rub, precordial pain, and or extreme fatigue
Acute electrocardiogram changes indicating pericarditis
Symptoms of cardiac scarring and cardiac valve disease after acute infection or recurrent infection
Cardiomegaly
Development of new murmur or change in existing murmur
Symptoms of HF
Treatment:
Antibiotics: penicillin or erythromycin
Managing fever
Adequate rest
Teaching patient that antibiotic prophylaxis to prevent infective endocarditis is considered for dental and invasive
procedures throughout life
Cardiomyopathy
Description
Subacute or chronic disorder of the heart muscle
Treatment is palliative, not curative and client needs to deal with numerous lifestyle changes and shortened life
span
Different types: dilated, nonobstructed, obstructed, restrictive
Dilated Cardiomyopathy
Fibrosis of myocardium and endocardium, dilated chambers, mural wall thrombi present
Signs/Symptoms: fatigue, weakness, L sided HF, dysrhythmias or heart block, systemic or pulmonary emboli, S3
and S4 gallops, moderate to severe, cardiomegaly
Treatment: symptomatic treatment of HF, vasodilators, control of dysrhythmias, HEART TRANSPLANT
Nonobstructed:
Hypertrophy of walls and septum, small chamber size. Enlarged thickened muscle= smaller chamber
S/S: dyspnea, angina, fatigue, syncope, palpitations, mild cardiomegaly, S4 gallop, ventricular dysrhythmias,
sudden death, HF
Treatment: symptomatic,B blockers, conversion of a-fib, ventriculomyotomy or muscle resection with mitral
valve replacement, digoxin, nitrates, and other vasodilators contraindicated with obstructed form
Restrictive Cardiomyopathy
Mimics constrictive pericarditis, fibrosed walls cannot expand or contract, chambers narrowed; emboli common
S/S: dyspnea and fatigue, HF R side, mild to moderate cardiomegaly, S3 and S4 gallops, Heart block, emboli
Treatment: supportive treatment of symptoms, treatment of hypertension, conversion from dysrhythmias, exercise
restrictions, emergency treatment of acute pulmonary edema

Collaborative Management of Arterial Disorders

Describe the term PAD AKA Peripheral Artery Disease
This is a result of systemic atherosclerosis. Chronic condition where partial or total arterial occlusion decreases
perfusion to the extremities. The tissue below this occlusion cannot survive.
 Inflow: Distal ends of aorta and common, internal and external illiac arteries
Outflow: Femoral,popliteal tibial arteries.
Gradual inflow not as big of a deal as gradual outflow
Most common cause is atherosclerosis
Compare and contrast etiology, pathophysiology, assessment findings, and nursing interventions
PVD:
Disorders that alter the natural blood flow through arteries and veins of peripheral circulation. Tends to affect
lower extremities. A diagnosis of this typically implies an arterial rather than a venous involvement. Some patients
have both.
Three health problem result in PVD
1. Venous blood flow may be altered by thrombus formation and defective valves
a. Thrombus formation is associated with bed rest of more than 3 days, pitting edema. Endothelial injury, dilated
superficial veins and hypercoagulability from cancer and previous VTE
2. Venous insufficiency results from prolonged hypertension and phlebiti , which stretch the veins and damage
valves
3. Reduces skeletal muscle activity
peripheral arterial disease: Blood getting to extremities
Etiology: 10-12 million americans have PAD, most over 65. African americans are more affected than any other
group.
Pathophys: Atherosclerosis is the most common cause. Risk factors for both are: hypertension, hyperlipidemia,
diabetes mellitus, cigarette smoking, obesity high cholesterol and lipid levels and genetic factors
Can be classified as:
Inflow disease: Discomfort in lower back, buttock or thigh.
Mild: discomfort after two blocks. More of a pain but eases with rest and time
Severe: Severe pain after walking less than a block. Typically have rest pain as well
Outflow disease: Burning, cramping in calves, ankles and feet and toes. Indicates a block below the popliteal
artery.
Mild: Discomfort felt after walking 5 blocks, relieved by rest
Moderate: Discomfort after 2 blocks. Intermittent rest pain
Severe: Cannot walk more than block, tend to hang their feet for relief and sleep at night
Assessment findings: Stages and their clinical manifestations
Asymptomatic
No caludation (to limp)
Bruit or aneurysm may be present
Decreased or absend pedal pulse
Claudication
Muscle pain, cramping or burning occurring with exercise and relieved while at rest.
Symptoms are reproducible
Pain will stop at rest until rest pain occurs (stage 3)
Rest Pain
Pain while resting, may wake up to leg pain at night
Numbness,burning toothache-y type of pain
 Typically in the distal portion of extremities (toes, arch,forefoot, heel,) Rarely in calf or ankle
Pain relieved by playing in a dependant position
Necrosis.Gangrene
Ulcers/blackened tissue occurs on toes, forefoot and heel
Distinctive gangrenous odor is present

Things to look for:

Loss of hair on lower calf/ankle and foot
Dry, scaly, dusky, pale or mottled skin. Thickened toenails
Dependent Rubor (redness) may occur.
May be cyanotic, or pallor
ANY SIGN of ulcer formation!!! Prevention is key. ( see chard 36-4 on pg 721 had a nice picture of the
different kind of ulcers)
Nursing Intervention:
Non-surgical management:
Exercise and positioning:
Work toward Collateral circulation (the more you move, the more your blood moves) Encourage walking every
day
Positioning: if edema in legs, encourage them to raise them above heart level
Promoting vasodilation
Provide warmth to affected extremity, wear socks!
Avoid cold
Hydrate hydrate hydrate
Avoid emotional stress, caffeine and nicotine
Drug therapy
Aspirin
Clopidrogel (helps prevents MI, stroke but NO GRAPEFRUIT!
Satins
Phosphodiesterase inhibitors
Invasive procedure
Percutaneous vascular intervention or percutaneous transluminal coronary angioplasty
Dilated arteries with a balloon catheter
Usually have stents placed to ensure blood flow
WATCH FOR BLEEDING
Surgery
Arterial revascularization

Describe and prioritize post-procedure collaborative care for clients who have undergone peripheral
vascular procedures, including:
Angioplasty:
Assess neurological and cardiovascular status.
Before discharge after carotid stent placement, teach the patient to report these symptoms to the health care
provider as soon as possible:
Severe headache
Change in level of consciousness or cognition (e.g., drowsiness, new-onset confusion)
Muscle weakness or motor dysfunction
Severe neck pain
Neck swelling
Hoarseness or difficulty swallowing (due to nerve damage)
 Vascular bypass surgery (arterial revascularization):
Patients should limit activity
Usually need temporary help with daily activities by the family or other caregiver.
Home health is usually Rxd in these cases
Thrombolytic therapy:
Observe the affected extremity for improvement in color, temperature, and pulse every hour for the first 24 hours
or according to the postoperative surgical protocol.
Monitor patients for manifestations of new thrombi or emboli, especially pulmonary emboli (PE). Chest pain,
dyspnea, and acute confusion (older adults) typically occur in patients with PE.
Notify the health care provider or Rapid Response Team immediately if these symptoms occur.

Describe the nursing management of the client undergoing the following diagnostic procedures:
Arteriography:
Client recovers in a specialty area. Must be restricted to bed rest and keep catheter site straight. Must stay in bed
for 2-6 hours.
Monitor vital signs q15 min for first hour, then every 30 min for the next two, then as often as facility policy.
Assess insertion site for bloody drainage or hematoma formation. Assess peripheral pulses as well as skin temp
and color with every vital sign check
QSEN: Any s/s of cardiac ischemia (chest pain, dysrhythmia, bleeding, hematoma, change in peripheral pulses
ect) Contact Rapid Response Team to provide prompt intervention. Watch for Neuro changes as well! (visual
disturbances, slurred speech, swallowing difficulties, extremity weakness)
Monitor urine output and provide sufficient liquids to help promote the excretion of the dye.
Home teaching: Limit activity for several days, leave dressing in place, observe insertion site for any
redness/swelling/pain ect.
CT Scan
Ankle-Brachial Index (ABI): (pg 720)
Used to evaluate outflow disease!
Derived by dividing the ankle blood pressure by the brachial blood pressure.
An ABI of 0.90 in either leg indicates PAD, people with diabetes are known to have a falsely elevated
ABI.

Discuss the following conditions and/or undergoing the following procedures or treatments
Aneurysm
Definition:
 Permanent, localized dilation of an artery accompanied by weakening of the vessel wall
Forms when the media, or middle layer of the artery is weakened producing a stretching effect in the intima (inner
layer) and adventitia (the outer layer)
High BP can enlarge aneurysm
Can thrombose, embolize, or rupture
Most common cause:
atherosclerosis or atheromatous plaque that weakens the intimal surface
Can be described as true: meaning arterial wall is weakened by congenital or acquired problems
False aneurysms occur as a result of injury or trauma
Contributing factors:
smoking, hypertension, hyperlipidemia
Other causes:
Syphilis, marfan syndrome, Ehlerstion Danlos syndrome (rare genetic disorder), chronic inflammation, blunt
trauma, usually from motor vehicle crashes
Classified as:
Saccular: outpouching from a distinct portion of artery wall
Fusiform: a diffuse dilation involving the total circumference of the artery
Assessment:
Most patients with abdominal or thoracic aneurysm are asymptomatic
Abdominal aortic aneurysms:
Abdominal, flank, or back pain that is usually steady, with a gnawing quality, is unaffected by movement, and
may last for hours or days
Prominent pulsation in the upper abdomen DO NOT PALPATE
Abdominal or femoral bruit
Thoracic aortic aneurysms:
Back pain, SOB, hoarseness, difficulty swallowing, visible mass above the suprasternal notch
Abdominal or thoracic rupture:
Pain: tearing, ripping, stabbing
Pain located in chest, back, and abdomen
Symptoms of hypovolemic shock: hypotension, tachycardia, diaphoresis, and decreased mentation
N, V, faintness, apprehension, decreased or absent peripheral pulses
Xray, CT, ultrasound
Nonsurgical management:
Abdominal aneurysm that is smaller than 2 or 3 inches or when surgery is not feasible:
Antihypertensive drugs
Teach importance of keeping scheduled CT scans appts
Review with patient clinical manifestations that need to be promptly reported
Avoid lifting and certain activities
Endovascular stent
Surgical management:
Endovascular stent placement via an intra aortic catheter
Watch for complications: bleeding, aneurysm rupture, peripheral embolization, mis-deployment of the stent graft
Symptomatic lesions or aneurysm greater than 3 inches: SURGICAL REMOVAL!
Replaced with a graft
Post op care: maintain MAP and assess peripheral pulses
More postoperative care:
Assess vital signs every hour to detect early signs of hypotension from graft leak
Assess circulation by checking pulses distal to graft site when checking vitals
 Report signs of leak or occlusion immediately: pulse changes, severe pain, cool to cold extremities below graft,
white or blue extremities or flanks, abdominal distention, decreased urinary output
Assess renal function and spinal cord when abdominal aneurysm b/c of clamping aorta during repair
Instruct patient with thoracic aneurysm repair to report back pain, SOB, difficulty swallowing and/or hoarseness
Community based care:
Compliance to CT schedule!
Control BP
If surgery was performed:
Avoid lifting heavy objects 6-12 weeks post op
Be aware in activities that involve pulling, pushing, straining
Avoid certain hobbies such as: tennis, horseback riding, golf
Defer from driving car for several weeks
Pain management
Wound care instructions

Aortic Dissection
Thought to be a sudden tear in the aortic intima, opening the way for blood to enter the wall
Causes/Location
Degeneration of the aortic media may be primary cause: with hypertension being a contributing factor
Often associated with CT disorders; for example; Marfans syndrome
Ascending aorta and descending thoracic aortic more common areas, but can also occur in abdominal aorta and
other arteries
CIRCULATION IS IMPAIRED THIS IS AN EMERGENCY SITUATION
When it can occur:
More prevalent in 50s and 60s
Men are more commonly effective than woman
Assessment/symptoms:
Pain: sharp, tearing, ripping, stabbing: tends to move from point of origin
May feel pain in anterior chest, back, neck, throat, jaw, or teeth
Diaphoresis, nausea, vomiting, faintness, apprehension
BP elevated unless cardiac tamponade or rupture has occurred.
Cardiac tamponade situations: pt will become rapidly hypotensive, and these other things can also occur: decrease
in peripheral pulses, aortic regurgitation (musical murmur), Altered LOC, paraparesis, strokes
Confirming diagnosis:
Chest xray, CT, MRI, aortic angiography
MRI is not test of choice b/c it's time consuming
If pt cannot be moved from bed: transthoracic echocardiography or transesophageal echocardiography
Interventions:
Elimination of pain and reduction of systolic BP to 100 to 120mm Hg
2 large bore catheters to infuse 0.9% sodium chloride and give medications
Indwelling urinary catheter
IV morphine sulfate and IV beta blocker
If not effective give nicardipine hydrochloride or other antihypertensive may be used
Proximal dissection: surgical treatment
Typically require cardiopulmonary bypass (removes the intimal tear and sutures the edges of dissected aorta.
Uncomplicated Distal dissection: continued medical treatment
Long term medical treatment:
Systolic BP must be maintained or at/below 130 to 140 mm Hg
Beta blockers and Calcium channel antagonists are prescribed to help maintain goal once pt is stabilized
 Collaborative Management of Venous Disorders

Describe nursing interventions used to help prevent venous thromboembolism (VTE).<< Geana :)
Anticoagulants are the drugs of choice for actual DVT and for patients at risk for DVT.

The Patient Receiving Anticoagulant Therapy

Carefully check the dosage of anticoagulant to be administered, even if the pharmacy prepared the drug.
Monitor the patient for signs and symptoms of bleeding, including hematuria, frank or occult blood in the
stool, ecchymosis, petechiae, altered mental status (indicating possible cranial bleeding), or pain (especially
abdominal pain, which could indicate abdominal bleeding).
Monitor vital signs frequently for decreased blood pressure and increased pulse (indicating possible internal
bleeding).
Have antidotes available as needed (e.g., protamine sulfate for heparin; vitamin K for warfarin [Coumadin,
Warfilone]).
Monitor activated partial thromboplastin time (aPTT) for patients receiving unfractionated heparin.
NOTIFY DOC IF > 70 SEC. Monitor prothrombin time (PT)/ international normalized ratio (INR) for
patients receiving warfarin or lowmolecular-weight heparin (LMWH).
Apply prolonged pressure over venipuncture sites and injection sites.
When administering subcutaneous heparin, apply pressure over the site and do not massage.
Teach the patient going home while taking an anticoagulant to:

Use only an electric razor

Take precautions to avoid injury; for example, do not use tools such as hammers or saws, where
accidents commonly occur

Report signs and symptoms of bleeding, such as blood in the urine or stool, nosebleeds, ecchymosis, or
altered mental status

Take the prescribed dosage of drug at the precise time that it was prescribed to be taken

Not stop taking the drug abruptly; the physician usually tapers the anticoagulant gradually

Describe the nurse's role in monitoring clients who are receiving anticoagulants.
 Avoid oral contraceptives.
Drink adequate fluids to avoid dehydration.
Exercise legs during long periods of bedrest or sitting.
Patient education
Leg exercises
Early ambulation
Adequate hydration
Graduated compression stockings
Intermittent pneumatic compression, such as sequential compression devices (SCDs)
Venous plexus foot pump
Anticoagulant therapy

Determine the collaborative management for a client with the following conditions:
(what is it, what do you do about it?)

Venous thrombosis:
A blood clot believed to result from an endothelial injury, venous stasis, or hypercoagulability
May include all 3 elements, or just one
Often associated with inflammatory process
When a thrombus develops, inflammation occurs around the clot, thickening the vein wall and possibly leading to
an embolization

Venous insufficiency:
Etiology: Typically due to a valvular dysfunction. It typically occurs from prolonged venous hypertension. Things
that are risk factors include:
People who stand or sit for long times, obesity, thrombus formation, those who have chronic thrombophlebitis.
Pathophys: Prolonged venous hypertension eventually causes the veins to stretch and damages the valves. Can
lead to a back up of blood and further the venous hypertension. Results in edema, and decreased tissue perfusion,
venous stasis ulcers swelling and cellulitis.
Assessment: Some things you may see are..
Varicose veins, engorged veins
Edema
Reddish/brown discoloration of the legs (stasis dermatitis)
Stasis ulcer formation
Typically occur over the malleolus and more medially of the ankle
Typically chronic, hard to heal
Nursing Intervention: Decrease edema and promote venous return!
Ted hose! SCDs! (Una boot if ulcer is present)
Talk with wound care and dietician to help heal if ulcer is present
 Elevate lower extremities, Weight reduction, Long term emotional support will most likely have this for rest of
their life.

Phlebitis
Vein inflammation
Associated with invasive procedures such as IV therapy
Can also predispose patient to thrombosis

Varicose veins
Definition: distended, protruding veins that appear darkened and tortuous
Vein walls weaken and dilate. Venous pressure increases and valves become incompetent. Incompetent valves
enhance vessel dilation and veins become tortuous and distended
Can occur in anyone, but they are common in adults older than 30 yrs whose occupations require prolonged
standing activity, pregant women are also at risk, inquire family history
Telangiectasias aka spider veins: are dilated intradermal veins less than 1 to 3 mm in diameter that are visible on
skin surface
Most patients are not bothered by these
Most do not develop the severe varicose vein disease
More advanced disease:
Venous distension, edema, feeling of fullness in the legs, and pruritus
As a result: venous stasis ulcers, brown pigmentation from extravasated RBCs and pain
Diagnosed by: simple ultrasonography or duplex ultrasonography
ELASTIC EXERCISE ELEVATION
Avoid high impact exercises
Different procedures/options:
Sclerotherapy: HCP injects a chemical to sclerose the vein, performed on small or a limited number of varicosities
Laser treatment: uses heat and close main vessel that is contributing to the problem
Radiofrequency ablation: heating the vein from the inside and shrinking the vein. Surgical intervention entails
ligation and stripping the affected veins with the patient under general anesthesia

Arteriosclerosis and Hypertension

Discuss the role of diet therapy, lifestyle, and drug therapy in the management of clients with
atherosclerosis.
What is atherosclerosis?
*type of arteriosclerosis (thickening or hardening of arterial wall assoc w/ aging)
Involves formation of plaque w/in arterial wall
Leading risk factor for cardiovascular disease
Thought to occur from blood vessel: damage causes inflammation
Diet therapy
Lifestyle
 Drug therapy
Describe the differences between essential and secondary hypertension.
Hypertension is also classified into two categories based on the cause.

Essential(primary) is the most common and is not caused by a preexisting condition.

Family history of hypertension Excessive sodium and caffeine intake

African-American ethnicity Overweight/obesity
Hyperlipidemia Physical inactivity
Smoking Excessive alcohol intake
Older than 60 years or postmenopausal Low potassium, calcium, or magnesium intake
Excessive and continuous stress

Secondary Hypertension is caused by a preexisting health condition.

Kidney disease Pregnancy

Primary aldosteronism Drugs:
Pheochromocytoma Estrogen (e.g., oral contraceptives)
Cushing's disease Glucocorticoids
Coarctation of the aorta Mineralocorticoids0
Brain tumors Sympathomimetics
Encephalitis

Identify normal values for arterial blood pressure and discuss physiological mechanisms that regulate blood
pressure.
For people over 60:
Below 150/90
For people younger than 60:
Below 140/90
According to Joint National Committee 8 (JNC 8) guidelines, patients whose blood pressures are above these
goals should be treated with drug therapy

Stabilizing mechanisms exist in the body to exert an overall regulation of systemic arterial pressure and to prevent
circulatory collapse. Four control systems play a major role in maintaining blood pressure:
The arterial baroreceptor system: Monitors the level of arterial pressure and counteracts a rise in arterial
pressure through vagally mediated cardiac slowing and vasodilation with decreased sympathetic tone.
Regulation of body fluid volume: If there is an excess of sodium and/or water in a person's body, the blood
pressure rises through complex physiologic mechanisms that change the venous return to the heart, producing
a rise in cardiac output. If the kidneys are functioning adequately, a rise in systemic arterial pressure produces
diuresis (excessive voiding) and a fall in pressure.
The renin-angiotensin-aldosterone system: The kidney produces renin, an enzyme that acts on angiotensinogen
(a plasma protein substrate) to split off angiotensin I, which is converted by an enzyme in the lung to form
angiotensin II. Angiotensin II has strong vasoconstrictor action on blood vessels and is the controlling
mechanism for aldosterone release. Aldosterone then works on the collecting tubules in the kidneys to
reabsorb sodium. Sodium retention inhibits fluid loss, thus increasing blood volume and subsequent blood
pressure.
Vascular autoregulation: keeps perfusion of tissues in the body relatively constant, appears to be important in
causing hypertension. (Iggy, 710)

Identify cultural considerations that impact care for clients with hypertension.
 The prevalence of hypertension in African Americans in the United States is among the highest in the world and is
constantly increasing. When compared with Euro-Americans, they develop high BP earlier in life, making them
much more likely to die from strokes, heart disease, and kidney disease (Go etal., 2013). The exact reasons for
these differences are not known, but genetics and environmental factors may play a role. Efforts to raise
awareness of hypertension through education within African-American communities, including the importance of
receiving treatment and controlling blood pressure, have been somewhat successful. Geographic differences still
exist (Go etal., 2013).
A higher percentage of men than women have hypertension until age 45 years. From 45 to 54 years, women have
a slightly higher percentage of hypertension than men. After age 54 years, women have a much higher percentage
of the disease (Go etal., 2013). The causes for these differences are not known.
Many of the medication listed above under the heading of Heart Failure, are meds used in the control of
hypertension. Be able to recognize those meds that have the intended purpose of controlling hypertension.

Heart Failure

Compare and contrast the clinical findings for a patient with right-sided heart failure with a patient with
left-sided heart failure.

Right sided heart failure (edema, weight gain, anorexia)

Left sided heart failure (fatigue, shortness of breath, lung crackles)

Safe and Effective Care Environment

1. Collaborate with interdisciplinary healthcare team members when providing care for
patients with perfusion and clotting problems.
2. Prioritize care for patients with hypertension.

Health Promotion and Maintenance

1. Identify risk factors for vascular problems.

a. Smoking
b. HTN
c. Hyperlipidemia
d. High cholesterol
e. Familial pre-disposition
f. Sedentary lifestyle
g. Obesity/Overweight
h. Hx of diabetes mellitus, renal disease, anemia, high BP, stroke, bleeding disorders, connective tissue diseases,
chronic pulmonary diseases, heart disease, and thrombophlebitis.
2. Teach patients about lifestyle modifications to prevent vascular problems (Pretty much
common sense).
a. Nutrition/Diet
b. Activity/Exercise
c. Smoking cessation
d. Decrease alcohol consumption

Physiological Integrity

1. Explain the inflammation process that is associated with the development of

arteriosclerosis and atherosclerosis.
a. Arteriosclerosis
i. Reduced local tissue circulation, resulting in ischemia, impaired leukocytic response to wounds, and increased
susceptibility to wound infection.
b. Atherosclerosis
i. After the vessel becomes inflamed, a fatty streak appears on the intimal surface (inner lining) of the artery.
Through the process of cellular proliferation, collagen migrates over the fatty streak, forming a fibrous plaque.
The fibrous plaque is often elevated and protrudes into the vessel lumen, partially or completely obstructing blood
flow through the artery. Plaques are either stable or unstable. Unstable plaques are prone to rupture and are often
clinically silent until they rupture.
2. Interpret essential laboratory data related to risk for atherosclerosis.
a. Elevated lipids including cholesterol and triglycerides. Total serum cholesterol levels should be below 200mg/dL.
Elevated cholesterol levels are confirmed by HDL and LDL measurements (LDL=bad, HDL=good). High levels
of both indicate risk for atherosclerosis. Desirable LDL= <130 mg/dL for healthy, <70mg/dL for older adults
diagnosed with CVD or who are diabetic. Desirable HDL= >45mg/dL for men and >55mg/dL.
b. Triglycerides may be elevated with atherosclerosis and is emerging lipid risk factor.
>160mg/dL=hypertriglyceridemia in men, women should be below 135mg/dL. Elevated levels are considered a
marker for other lipoproteins, suggest metabolic syndrome (increases risk for coronary heart disease)
3. Discuss the role of nutrition therapy in the management of patients with arteriosclerosis
a. Higher intake of veggies, fruits, whole grains. Consume low fat dairy products, poultry, fish, legumes, nontropical
(canola) vegetable oils, and nuts. Limit intake of sweets, sugar sweetened beverages, red meats. Aim for dietary
pattern that includes 5%-6% of calories from saturated fat, reduce percent of calories from trans fat
4. Describe the differences between essential and secondary hypertension.
a. Essential hypertension is the most common type and is not caused a pre existing health problem. Secondary
hypertension is caused by specific disease states and drugs
5. Develop an evidence-based plan of care for a patient with essential hypertension.
a. Lifestyle changes: restrict sodium intake in the diet, reduce weight if overweight or obese, use alcohol sparingly
(no more than 1 drink/day), exercise 3 to 4 days a week for 40 minutes each time, use relaxation techniques to
decrease stress, avoid tobacco/caffine
b. Garlic and CoQ10, although discuss with provider before starting any herbal remedy with other medications
c. Drug therapy: individualized for each patient with consideration given to culture, age, other existing illnesses,
severity of blood pressure elevation, cost of drugs, and follow up. Many patients require more than 2 drugs a day
to control HTN. Best therapy is blood pressure med and diuretic.
6. Document a teaching plan for patients receiving drug therapy for hypertension.
a. Educate patient on sticking to drug adherence, even when asymptomatic
b. Provide oral and written info about the indications, dosage, times for administration, side effects, and drug
interactions for antihypertensives. Stress importance of taking as prescribed. Urge to report unpleasant side effects
 such as excessive fatigue, cough, sexual dysfunction. Monitor BP at home (obtain an ambulatory blood pressure
monitoring (ABPM) device), monitor weight on scale
c. Instruct on dietary and lifestyle changes
7. Compare common assessment findings present in patients with peripheral arterial and
peripheral venous disease.
a. A diagnosis of PVD implies arterial disease rather than venous involvement. Some patients have both arterial and
venous. Result of systemic atherosclerosis.
b. Inflow obstruction involve distal end of aorta and common/internal/external iliac arteries. Discomfort in lower
back, buttocks or thighs. Mild: walk 2 blocks before painful enough to stop, moderate: pain in 1-2 blocks, severe:
painful after walking < 1 block, rest pain.

Outflow involves femoral, popliteal, and tibial arteries and below superficial femoral artery.
Burning/cramping in calves, ankles, feet, and toes. Instep/foot pain=obstruction below popliteal
artery. Mild: painful after walking 5 blocks, moderate: pain after 2 blocks, intermittent rest pain,
severe: pain after block, rest pain

c. Intermittent claudication: Can walk certain distances then burning, cramping muscle discomfort and pain occurs.
Pain stops after rest, returns after walking again, distances get shorter and shorter. Eventually pain happens at rest
(numbness/burning sensation, described as toothache severe enough to wake patient up at night)
d. Observe for loss of hair on lower calf/ankle/foot, dry/scaly/dusky/pale/mottled skin, thickened toe nails. Extreme:
extremity is cold, cyanotic, darkened, pallor if elevated, muscle atrophy, rubor (redness) when extremity is
lowered. Palpate pulses (posterior tibial pulse best one), assess for ulcers (small, round, with punched out
appearance, well defined borders, usually develop on great toe. MRA used to assess blood flow, dopplers, BP
readings are usually higher in thigh than arm (readings lower than brachial show presence of PAD) inflow:
mild=difference of 10-30 mm HG pressure than brachial, severe= 40-50 difference. Outflow: ankle brachial index
(ABI), divide ankle pressure by brachial (ABI<0.90 in either leg is diagnostic of PAD, patients with diabetes
known to have falsely elevated ABI)
8. Identify when venous thromboembolism (VTE) and complications of VTE occur.
a. Active cancer, paralysis, casting of an extremity, bedridden for more than 3 days, major surgery w/ GA within last
3 months, localized tenderness along deep venous system, swelling of entire leg, calf swelling of greater than 3cm
larger when compared to other leg, pitting edema in one leg, dilated superficial veins in one leg, previous
documented DVT
b. Some patients asymptomatic. Classic signs: calf/groin tenderness, pain/sudden onset of swelling of leg, pain in
calf on dorsiflexion of foot (although unreliable, Homans sign).
c. Gently palpate, feel for induration (hardening) along blood vessel for warmth/edema, redness may be present
d. Complications: thrombophlebitis (thrombus w/ inflammation), phlebothrombosis (thrombus w/ no inflammation),
DVT.
e. Associated with PE, statis of blood flow, endothelial injury, hypercoagulability (Virchows triad)
f. Symptoms: SOB, chest pain, acute confusion (older patients)
9. Plan evidence-based nursing interventions to help prevent VTE.
a. Combination of rest and drug therapy. Preventative measures are best bet. Elevate, ambulation, SCDs,
compression stockings, intermittent or continuous warm soaks to the area, (DO NOT MASSAGE), drug therapy
 (IV unfractionated heparin followed by PO warfarin, usually. Each pt treatment is different and varies on pt
response)
b. Surgical removal is rare and only happens if occlusion is bad and cannot/will not respond to drug therapy.
Thrombectomy, or inferior vena cava filtration (umbrella placed in femoral that traps blood clots that could travel
to lungs, but still allows the flow of blood), teaching patients importance of anticoagulation therapy
10. Explain the nurse's role in monitoring patients who are receiving anticoagulants.
a. Safety
b. Patient teaching
i. Foods to eat/avoid (Vitamin K)
11. Compare assessment findings associated with Raynaud's phenomenon and Buerger's
disease.
a. Raynauds: painful vasoaspasms in extremities especially digits. Causes red/white/blue skin color on exposure to
cold temperatures or stress. Cause unknown, happens mainly in women, possible autoimmune (associated with
many rheumatic diseases such as lupus)
b. Buergers: claudication in feet and lower extremities, worse at night. Causes ischemia and fibrosis of vessels in
extremities with increased sensitivity to cold. Ulcerations/gangrene occur on digits, cause unknown but associated
with smoking

What happens in an ECG wave?

Disturbances in the conductivity of the heart too rapid de/repolarization/too slow de/repolarization/ pathway
blocked /impulse travels an abnormal pathway

P-Wave = originate in the SA node of R-atrium (Atrial depolarization) (Depolarization is when the normally (-)
charged cells in heart muscle develop a (+) charge)
Make sure: 1. P waves are present; 2. Make sure they are occurring regularly; 3. Is there ONE P-wave for each
QRS complex; 4. Are they smooth and rounded, and upright, or are the inverted; 5. Do they all look similar on the
strip you are reading?
PR interval = (Time required for the impulse to travel through AV node atrial depolarizationthru wbundle of
His, bundle branches and Purkinje fibers.just before ventricular depolarization. 1. Are PR intervals greater than
0.20 second? 2. Are PR interval less than 0.12 second? 3. Are PR intervals consistent across the ECG strip?
QRS interval = Ventricular depolarization. 1. Are QRS intervals less than or greater than 0.12 second? 2. Are
QRS complexes similar in appearance across the ECG strip?
(Normal = 0.04 0.10 second)
ST Segment = (Early ventricular repolarization). Abnormalities here: Elevated or depressed >1mm in 2 or more
leads (the electrodes placed on the body) ST elevation can indicate MI, Pericarditis, hyperkalemia. STEMI
ST depression can indicate MI, hypokalemia, ventricular hypertrophy NSTEMI
T wave = (Ventricular repolarization) Note shape and height of T-Wave. Tall-Ts - The T waves were wide in
ischemic heart disease and thin and peaked in uremia.
QT interval = (time required for ventricular depolarization and repolarization to occur) Normal QT should be
equal to or less than the distance of the R to R interval.

BASIC HEART PHYSIOLOGY

So, we have the heart right? It has two atria and two ventricles. The superior and inferior vena cava as well as the
coronary sinus all empty deoxygenated blood into the RIGHT atrium (Preload aka FILLING UP WITH BLOOD).
It then flows to the RIGHT ventricle. As the heart contracts, the force from the contraction pushes the
deoxygenated blood up from the ventricle into the Pulmonic valve (Afterload aka EJECTION of blood). The
blood then flows from the heart into the lungs where it becomes OXYGENATED. From there, this
OXYGENATED blood enters the heart from the pulmonary veins (Dont let this trick you! Veins return blood to
the heart!). It is then dumped into the LEFT atrium and flows into the LEFT ventricle (Preload aka FILLING
UP with blood). When the heart contracts, the blood is pushed out the aorta and into the circulatory system.
Systole:
Diastole: