N12 MT2

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RESPONSIBILITIES OF PRE-OP
NURSE

-Accurate Identification of Pt
-2 patient identifiers
-Known last meal for patient
-Safe transport to OR via stretcher with side rails up
-Psychosocial support for Mr. Ball and his family
-Patent IV with Fluids infusing
-Mr. Ball voids before pre-operative medications
-Pre-operative dose of Ativan 0.5 mg IV given once on stretcher
-Signed consent form is in the chart
-OR Checklist completed and on the front of the chart
-Accurate identification of patient, surgical procedure & site. Done in holding room with
physician present
-All pertinent labs and diagnostics (CXR, ECG) are on the chart with appropriate interpretations.
-Review labs once more to make sure there are no abnormalities that will cause problems during
the intra operative and post operative periods.

Medical history that needs to be

assessed pre-op

-Previous surgery/ anesthesia

-Serious illness or trauma
-Chronic illness
-Allergies
-Bleeding tendencies
-Cortisone/ steroid use
-Immune system
-Drugs, alcohol, nicotine

Diagnostics that could/should be

done pre-op

Chest x-ray : to rule out any pulmonary disease that predispose pt to pneumonia or respiratory
difficulties after surgery.
Electrocardiography for > 40 yrs: Anesthesia will want to know that the heart is healthy enough
for anesthesia and that he is not likely to have a peri-operative heart attack.
Complete blood count: Again the anesthesiologist is looking for elevated WBC that might tip us off
to infection or a low hemoglobin and hematocrit that might make his recovery from anesthesia
complicated. Also a low hemoglobin could cause pt to have a peri operative heart attack.
Electrolyte levels:
Urinalysis: UTI
X-ray: Limbs that are poorly perfused often get severe infections that do not respond to antibiotics.

appropriate monitoring
parameters for the patient
recovering from general or spinal
anesthesia

Vital signs: Are they stable?

Continuous Pulse ox:
Cardiac monitoring
Color and temperature of skin
Level of consciousness
Intravenous fluids
Surgical site management
Other tubes/drains
Comfort: pain, nausea, positioning
Position and safety: elevate operative leg on a pillow
Report on Fluid intake, output and estimated blood loss (EBL)
Monitor lab values
NPO until bowel sounds return

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appropriate safety standards during peri-operative

period to control the environment to prevent
accidents or injury to client or the healthcare team

Maintenance of sterile technique

Continuous patient monitoring and reaction to anesthesia
Instrument count/sponge count
Safety and prevention of injury: lots of electrical equipment, make sure
patient does not get electrocuted, shocked or burned.
Careful positioning to prevent pressure ulcers or nerve damage
Monitoring for changes in blood pressure, respiratory status or
dysrhythmias
Myocardial ischemia
Drops in BP from drugs of blood loss
Dysrrhythmias from drugs, stress
Vasospasm
Nursing Diagnosis: Impaired tissue perfusion
Emergencies: reactions to medications, malignant hyperthermia, airway
emergencies, hemorrhaging
Documentation of intra operative care
Transporting

Meds okay and not okay to give pre and perioperatively

OKAY TO GIVE:
Tranquilizers
Sedatives
Analgesics
Anticholinergics: to dry up secretions
H2 Blockers: prevent allergic reaction
Ativan: benzodiazepine to decrease stress
NOT OKAY:
Insulin- if pt is NPO
Anti-inflammatory: Aspirin, Motrin, Advil, Aleve (d/c 2 weeks prior)
Blood Thinners/Anticoagulant: Pletal, Warfarin, Heparin- Bleeding risk

7.

3 Requirements of Informed consent:

-Adequate disclosure of diagnosis-purpose, risks, and consequences of

treatment, probability of success, prognosis if not instituted
-Understanding & comprehension -patient must be drug free prior to
signing consent
-Consent given voluntarily -patient must not be persuaded or coerced to
undergo the procedure

8.

Medical emergency and consent-

2 physicians is necessity in chart:

In a medical emergency such as a MVA, when there is no documentation
of a DPOA or living will, 2 physicians may have to provide consent for a
surgery. Usually this would be in the absence of family.

Define ethical and legal issues as they relate to the

adult surgical patient

No patient should go to surgery without

-the signed consent.
-an advance directive or Durable Power of Attorney for Healthcare.

10.

Living Wills

Written and signed by the patient. The patient can opt out of this at any
given time. Patients are given the right to change their mind up to the last
moment.
Patient is usually a full code for 24 hours following surgery
Allows family to know patient wishes in the event of serious intraoperative complication

11.

Durable power of attorney for healthcare

This is a document that gives specific decision making power to a family

member or loved one. The person with DPOA should have a good
understanding of the patient's desires in a given circumstance.

9.

-Protects patient, surgeon, hospital and its employees

-Nurses role: advocate, witness, appropriate person signs

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How do you
determine risk for
latex allergy?

Genetic predisposition
Children with spina bifida
Urogenital abnormalities
Spinal cord injuries
Hx of multiple surgeries
Health care professionals
Allergies to avocado, tomato, banana

Signs and symptoms

of allergic reaction.

Urticaria
Rhinorrhea
Bronchospasm
Compromised respiratory status
Circulatory collapse & Death

General vs Local
Anesthesia/Conscious
Sedation

Patients who undergo general anesthesia are more likely to face complications than those who have only local
anesthesia or conscious sedation.
The patient who requires general anesthesia usually has extensive surgery and requires close monitoring in
the PACU for phase I recovery. This lasts for a few hours. Ultimately the patient returns to the acute care unit
for postoperative convalescence, which may last overnight or for several days.
In contrast, an ambulatory surgical patient who has had local anesthesia with no sedation or conscious
sedation most often only undergoes phase II recovery for a brief time (i.e., 1 to 2 hours). In phase II recovery
nursing staff prepare the patient for care in the home or extended care setting

15.

Surgical
considerations for
elderly pt's

Age alone is no longer a factor for determining the benefit that an individual can achieve from a surgical
procedure. Consequently nurses are caring for many more surgical patients of advanced age and are required
to know the age-related factors that affect a surgical procedure
A smaller margin of physiological reserve makes the older adult less able to compensate during the
perioperative period for changes that occur as a result of infection, hemorrhage, alterations in blood pressure,
and fluid/electrolyte abnormalities. Ongoing, focused assessments are necessary.
Older patients are at greater risk for postoperative delirium associated with an acute onset. Reduced level of
consciousness, reduced ability to maintain attention, perceptual disturbances, and memory impairment
characterize the typical presentation
Implement individualized measures to help the older-adult surgical patient achieve rest, sleep, and
orientation in the postoperative period to reduce the risk of delirium development.
Altered and unexpected drug responses are often related to different pharmacokinetics in the older adult.
Thus the nurse caring for the perioperative older patient needs to be alert to the possibility of a high risk for
adverse medication events with the administration of anesthetic agents and postoperative analgesics,
especially narcotics. "Start low and go slow" is the guiding principle when medicating older adults because of
their slow drug-clearance capability.

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Surgical
considerations for
bariatric pt's

Obesity increases surgical risk by reducing ventilatory and cardiac function. Obstructive sleep apnea,
hypertension, coronary artery disease, diabetes mellitus, and heart failure are common in the bariatric (obese)
population.
-Embolus, atelectasis, and pneumonia are common postoperative complications
-difficulty resuming normal physical activity after surgery and is susceptible to poor wound healing and wound
infection because of the structure of fatty tissue, which contains a poor blood supply.
-poor perfusion slows delivery of essential nutrients, antibodies, and enzymes needed for wound healing.
-It is often difficult to close the surgical wound of a patient who is obese because of the thick adipose layer;
thus he or she is at risk for dehiscence (opening of the suture line) and evisceration (abdominal contents
protruding through surgical incision)

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Surgical Considerations
for
Immunocompromised
pt's

Altered immune function are more at risk for developing infection after surgery.

Surgical Pain
Management

Before surgery conduct a comprehensive pain assessment, including the patient's and family's
expectations for pain management following surgery. Ask patients to describe their perceived tolerance to
pain, past experiences, and prior successful interventions used.
-Teach pt's how to score their pain before surgery
-Frequent pain assessments to alert nurses to treat pain and assess adequacy of pain interventions.
-Encourage the patient to use analgesics as ordered because, unless the pain is controlled, it is difficult for
the patient to participate in postoperative therapy.
-Pain relief has been shown to be more effective when analgesics are given around-the-clock (ATC) rather
than as needed (prn)
-Closely assess the patient's pain level, tolerance to activity, and response to pain-relieving interventions.

Spinal Block

The method of induction such as spinal, epidural, or a peripheral nerve block influences the portion of
sensory pathways that are anesthetized. No loss of consciousness occurs with regional anesthesia, but the
patient is often sedated.

Examples include patients with cancer, bone marrow alterations, and those who undergo radiation
therapy. Radiation is sometimes given before surgery to reduce the size of a cancerous tumor so it can be
removed surgically. It has some unavoidable effects on normal tissue such as excess thinning of skin
layers, destruction of collagen, and impaired vascularization of tissue. Ideally the surgeon waits to perform
surgery 4 to 6 weeks after completion of radiation treatments. Otherwise the patient may face serious
wound-healing problems.
The use of chemotherapeutic drugs for cancer treatment, immunosuppressive medications for preventing
rejection after organ transplantation, and steroids for treating a variety of inflammatory or autoimmune
conditions increases the risk for infection.

-the level of anesthesia can rise, which means that the anesthetic agent moves upward in the spinal cord
and affect breathing.
-migration of anesthetic depends on the drug type and amount and patient position.
-If level of anesthesia rises, respiratory paralysis can develop, requiring resuscitation. Elevation of the
upper body prevents respiratory paralysis.
-pt may have a sudden fall in blood pressure, which results from extensive vasodilation caused by the
anesthetic block to sympathetic vasomotor nerves and pain and motor nerve fibers.
-The patient requires careful monitoring during and immediately after surgery.
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General Anesthesia

General anesthesia results in an immobile, quiet patient who does not recall the surgical procedure.
-given by IV infusion and inhalation routes through the three phases of anesthesia: induction,
maintenance, and emergence.
-Surgery requiring general anesthesia involves major procedures with extensive tissue manipulation.
- The greatest risks from general anesthesia are the side effects of anesthetic agents, including
cardiovascular depression or irritability, respiratory depression, and liver and kidney damage.

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Differentiate between
these three aspects of the
immune response:
1st Line Anatomical
Barriers (Natural
Defense)
2nd Line Inflammation
3rd Line Active Immune
Defense

Skin and mucous membranes are first line of defense- stop it from getting in

Compare anatomical
defense mechanisms and
the nursing interventions
that promote/maintain
these natural defense
mechanisms.

The skin & membranes are anatomical defenses, which nurses must monitor and support to keep integrity
and prevent injury

Inflammation- Kills invaders by localized or systemic response

Active Immune System- Immune system kills antigen. Lymphocytes remember antigen and how to launch
attack

Respiratory, urinary, GI, reproductive systems all have normal flora and defense mechanisms that nurses
must keep healthy or keep in an environment where healing can take place.

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Differentiate the function of T cells, B-cells, and

significance of antibody formation in providing
immune protection.

...

Explain the physiology of inflammation

Acute inflammation is an immediate response to cellular injury. Rapid

vasodilation occurs, allowing more blood near the location of the
injury which causes localized warmth and redness
Injury causes tissue damage and possibly necrosis. The body releases
chemical mediators that increase the permeability of small blood
vessels and causes edema.
The swelling of inflamed tissues increases pressure on nerve endings,
causing pain. As a result of physiological changes occurring with
inflammation, the involved body part may have a temporary loss of
function.
Fever is caused by phagocytic release of pyrogens from bacterial cells,
which causes a rise in the hypothalamic set point.

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Explain effect of inflammatory mediators

The cellular response of inflammation:

-WBCs pass through blood vessels and into the tissues.
-Through the process of phagocytosis, specialized WBCs, called
neutrophils and monocytes, ingest and destroy microorganisms or
other small particles.
-Leukocytosis, or an increase in the number of circulating WBCs, is the
response of the body to WBCs leaving blood vessels.
WBC's >10,000

clinical symptoms associated with a localized

inflammatory response.

Signs of localized inflammation include swelling, redness, heat, pain

or tenderness, and loss of function in the affected body part.

clinical symptoms associated with a systemic

inflammatory response.

When inflammation becomes systemic, other signs and symptoms

develop, including fever, leukocytosis, malaise, anorexia, nausea,
vomiting, lymph node enlargement, or organ failure.

Analyze vital sign and physical assessment patient data

for clinical signs and symptoms of infection

Fever
Tachypnea
Tachycardia
Hypotension
Changes in LOC & activity
High WBC
Oozing, drainage
swelling
warm site

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Explain the significance of abnormal lab values on the

Complete Blood Count (CBC), urinalysis, PT, PTT, blood
cultures, sputum cultures, wound cultures, lactate levels

Elevation or low values could be signs of sepsis or

inflammation/infection/sepsis

Differentiate between Systemic Inflammatory Response

(SIRs) and Sepsis

Infection/Trauma leads to SIRS. SIRS is a clinical response arising

from a nonspecific insult.
Manifests 2 or more of the following:
Temp>38C
HR>90
RR>20
PaCO2<32 mmHg
WBC >12,000 or <4,000
Bands>10%
Lactate >4
Sepsis is SIRS with a presumed or confirmed infectious process

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Explain the physiology of sepsis.

Body launches a systemic response to infection including clotting cascade & fibrin.
In sepsis, the reaction does not stay local, it goes systemic. Body starts throwing clots
with thrombin and fibrin. Blocks perfusion, tissue oxygenation and can cause tissue
necrosis, organ failure and lead to severe sepsis.

Differentiate between the sepsis, severe

sepsis, and septic shock.

Sepsis is SIRS with a presumed or confirmed infectious process

Sever sepsis is Sepsis with at least one sign of organ failure
Shock is Cardiovascular, refractory hypotension

Summarize the effect of aging on the

immune system

Lowers immune response, so they don't always show typical signs of infection.
They have a harder time launching immune response like fever.

Create a care plan for a Sepsis pt that

includes 2 nursing diagnosis, measureable
outcomes, and interventions

Impaired tissue perfusion

Hypovolemia
Organ Dysfunction

Outcomes:
Stable BP
RR 12-20
T 36.5-37.5
Lactate Lowered
CVP 8-12 mmHg
MAP >65 mmHg
Urine Output >0.5 mL/hr
Interventions:
Fluids
Antibiotics
Vasopressor & Dobutamine
Steroids?
Insulin to keep BG 70-110
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What can initiate Sepsis?

Systemic Infection
Ischemia
Trauma
Shock
Surgery (esp abdominal)
Burns
Chem. Aspiration
Cirrhosis
Pancreatitis
Immunodeficiency
Immunodeficiency
Transfusion reaction

Signs of Organ
Dysfunction
(Marker o Severe Sepsis)

-Altered consciousness,
Confusion,
Psychosis
-Tachypnea >20,
Sao2 <90%
PaO2/FiO2>300
-Jaundice,
High enzymes,
low albumin,
high PT
-Tachycardia >90
Hypotension
low perfusion
-Oliguria
Anuria
Increased creatinine

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Physio of SIRS

Vasodilation leads to hypotension, capillary permeability and edema. Leads to clotting, decreased
perfusion, refractory hypoxia

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Goals of Treatment

MAP>65 mmHg
CVP of 8-12 mmHg
Load up with fluid to flush out microclots in blood and kidneys, and antibiotics within one hour

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SIRS Criteria

Temp>38C
HR>90
RR>20
PaCO2<32 mmHg
WBC >12,000 or <4,000
Bands>10%

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Lactate

Lactate-identifies the amount of disruption to the inflammatory system

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Not specific marker of sepsis

Can be mark if >4
Can be elevated in trauma, metabolic impairment at the mitochondrial level (seizure, found down, liver)
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Onset of Parkinson's
Disease

-Onset usually over the age of 50.

1% of people over 50 have PD
-Approximately 10 percent of Parkinson's cases young-onset (< 40 years)

Pathophysiology of
Parkinson's

Loss of neuro transmitter dopamine which is produced by substantia nigra is considered responsible for the
primary disease symptoms
By the time symptoms develop, 80-90% of the dopamine producing cells have been lost.
Dopamine governs movement, balance and walking

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Etiology of PD

Exact cause is unknown.

-may develop from long term use of anti psychotic medications.
-can also develop from carbon monoxide and mercury poisoning.
-In rare instances it can occur as a result from traumatic injury to the mid brain.

Clinical manifestations
of PD

Hand tremor (usually at rest)

Slow movements (Bradykinesia)
Rigidity (limb stiffness)
Posture change
Shuffling gait
Loss of habitual arm swing (akinesia)
Pill rolling

Early Signs of PD

Slowing in ability to perform ADL's

General feeling of stiffness
Mild diffuse muscular pain
Tremor to upper limbs at rest

How can you stop a pt's

hand with tremor from
shaking?

Use the hand to do something

Severe Manifestations

Akinesia (rigidity)
Shuffling gait with short steps
Lack of swinging arms (akinesia)
Stooped posture
Mask like facial expression
Speech difficulty (volume low with dysarthria)
Lack of spontaneous swallowing
"Droopy eyes" or eyelid closure
Swallowing difficulty (50%)
Majority have NO intellectual compromise

Other medical concerns

with PD

Depression
Constipation
Weight loss
Sleep disturbances
Drooling
Urinary tract infections
Excessive sweating
Problems with sexual performance

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Treatment of PD

No cure
-Symptoms managed with medications:
levodopa & carbidopa most common
-surgical procedures where part of the brain is destroyed or stimulated.
-Transplantation of fetal dopamine producing cells is promising but ethically controversial.

50.

Sinemet

Combo of L-Dopa and Carbidopa

-Treats the bradykinesia and rigidity
-Benefit declines with prolonged use

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The tremor in Parkinson's is an essential resting tremor. It may be reduced with voluntary movement like
grasping the arm rest of a chair or rolling coins together.

Dopamine cannot cross the blood-brain barrier. The dopamine precursor Levodopa is able to cross the
blood brain barrier and is converted to dopamine in the basal ganglia, where it acts as naturally
occurring dopamine.
Levodopa is rapidly metabolized so only a small fraction of the drug is available to the CNS, so we give an
inhibitor to the metabolism, carbidopa.
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Selegiline (ELDEPRYL)

Anti-cholinergic
-used to inhibit re uptake and storage of dopamine in the CNS, thus prolonging action of dopamine.
This reduces the incidence and severity of akinesia, rigidity, tremor by about 20% and reduces drooling
because it reduces salivary production. (side effect it gives the patient a dry mouth).
Elderly patients may show an increased sensitivity to anti cholinergics thus requiring strict dosage
adjustment and monitoring.

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On Off effect of PD drugs

An on-off phenomenon may occur where the patient suddenly loses therapeutic value or oscillates
between therapeutic effect and no effect. 15 - 40% of patients experience this after 2 - 3 years.

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MAO Inhibitor

MAO inhibitor may be started at the time of diagnosis. It blocks the breakdown of dopamine.

54.

Thalamotomy

surgically destroys cells in the brain's thalamus

No longer common course of treatment.
Reserved for younger group who have Parkinson's with one or two diabling tremors on one side of the body, so
someone with severe left side tremor would have cells on the right brain portion of the Thalmus destroyed with
liquid nitrogen through a small hole drilled into the skull above the target area.
This is all done with guided MRI and CT scan imaging.

55.

Stimulator
implantation

Implantation of electrode with tip in target site in the brain. This is connected to wire run beneath the skin to a
stimulator (brain pacemaker) placed in the chest wall.
When electrical current is activated it modifies the function of the target site.
-used to address tremors.
-Can't be left on because when they control symptoms in one part of the brain, they often make other things
worse, like further weakening the throat muscles that effect ability to swallow or speak, so that is why the device
is activated and deactivated for specific activities and time.

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Goals for PD pt

Promote independent self care

Access resources for optimal mobility/speech/social function
Provide Care Giver support
Client Safety

Nursing
considerations for
pt with PD

Dysarthria (diff. speaking) make it hard for pt to communicate, causes frustration

Why would you

refer PD pt to
speech therapist?

Swallow evaluation
Work to improve voice volume, quality, and articulation.
Therapeutic exercises: verbalizations and tongue movements
For severely impaired speech: bring in resources (machine or computer-generated voice set up)
Teach families new communication strategies: verbal cuing and signals to understand or assist.
(Limited data about which techniques are most successful)

Why would you

send PD pt to
physical therapist

Develop and monitor a home exercise program:

strengthening and flexing all limbs
stretching legs and feet,
Walking
facial and breathing exercises
Swallowing exercises

Why would you

send PD pt to
occupational
therapist

Strategies for ADLs

Assist devices for eating, drinking, teeth brushing

Etiology of MS

The cause of MS is unknown

-research findings suggest that MS is related to infectious (viral), immunologic, and genetic factors and is
perpetuated as a result of intrinsic factors (e.g., faulty immunoregulation).

Dysphagia can make it hard for pt to swallow, can cause aspiration

-susceptibility to MS appears to be inherited. First-, second-, and third-degree relatives of patients with MS are at
a slightly increased risk. Multiple genes confer susceptibility to MS.
Possible precipitating factors include infection, physical injury, emotional stress, excessive fatigue, pregnancy,
and a poorer state of health.

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Pathophysiology
of MS

Chronic inflammation, demyelination, and scarring in the CNS

-Autoimmune disease caused by overreactive T cells (lymphocytes)
-T cells activated and migrate to CNS, causes inflammation and and demyelination of axons.
-Plaques, or sclerosis, result
-Initially myelin sheath is damaged leading to slow nerve impulses, can lead to destruction of nerve axons, blocked
impulses, and loss of nerve function.
-Myelin sheath can regenerate and symptoms will disappear and experience remission

MS and
pregnancy

Some women with MS who become pregnant experience remission or an improvement in their symptoms during the
gestation period. -hormonal changes associated with pregnancy appear to affect the immune system.
-during the postpartum period, women are at greater risk for exacerbation of the disease.

Signs and
Symptoms of MS

Common signs and symptoms of MS include motor, sensory, cerebellar, and emotional problems.
Motor symptoms include weakness or paralysis of the limbs, trunk, or head; diplopia; scanning speech; and
spasticity of the muscles that are chronically affected.
Patients with MS experience a variety of sensory abnormalities, including numbness and tingling and other
paresthesias, patchy blindness (scotomas), blurred vision, vertigo, tinnitus, decreased hearing, and chronic
neuropathic pain. Radicular (nerve root) pains may be present, particularly in the low thoracic and abdominal
regions.
Lhermitte's sign is a transient sensory symptom described as an electric shock radiating down the spine or into the
limbs with flexion of the neck. Cerebellar signs include nystagmus, ataxia, dysarthria, and dysphagia.
Severe fatigue

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Diagnosis of MS

-no definitive diagnostic test for MS

-diagnosis is based primarily on history, clinical manifestations, and the presence of multiple lesions over time as
measured by MRI
-cerebrospinal fluid (CSF) analysis may show an increase in immunoglobulin G.
-CSF may also contain a high number of lymphocytes and monocytes.

66.

Interferon

Immunomodulator drugs are used to modify the disease progression and prevent relapses.

Drugs used to
treat acute
exacerbations

-Adrenocorticotropic hormone (ACTH)

-methylprednisolone
-prednisone
-muscle relaxers
-immunomodulators
-anticholinergics (bladder)

67.

helpful in treating acute exacerbations of the disease, probably by reducing edema and acute inflammation at the site
of demyelination.
These drugs do not affect the ultimate outcome or degree of residual neurologic impairment from the exacerbation.
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What triggers
MS
exacerbations?

triggered by infection (especially upper respiratory and urinary tract infections), trauma, immunization, delivery after
pregnancy, stress, and change in climate. Each person responds differently to these triggers

Why are TIA's

worrisome?

TIA- 50% of tia pt's end up having full blown stroke

70.

Describe the major nursing care

concerns associated with all types of
neurologic dysfunction.

Airway: Are the pulmonary muscles weak? (atelectasis, respiratory distress)

Are the esophageal muscles weak? (aspiration)
Safety: Is there brain dysfunction effecting judgment or control of movement? (injury, falls,
entrapment)
Elimination: Is innervations to bowel/bladder compromised? (constipation, urinary
retention)
Mobility: Are skeletal muscles effected? (immobility/contractures/DVT risk).
Medications: Are the medications to treat/prevent exacerbation of disorder prescribed? Is
the patient compliant with medications?
Care giver support: respite care, community resources, healthcare referrals
End of life decision making: Code status. Palliative Care vs Comfort Care

71.

Differentiate between an ischemic and

a hemorrhagic CVA

NEED STAT CT SCAN TO DIFFERENTIATE ISCHEMIC AND HEMORRHAGIC CVA

An ischemic stroke results from occlusion of an artery, or a CLOT.
-accounts for nearly 80% of strokes.
-Ischemic strokes are further divided into thrombotic and embolic strokes.
-HIGH RISK: SMOKER, HYPERLIPIDEMIA
Hemorrhagic strokes result from bleeding into the brain tissue itself (intracerebral or
intraparenchymal hemorrhage) or into the subarachnoid space or ventricles (subarachnoid
hemorrhage or intraventricular hemorrhage).
-account for 15% of all strokes
-DEADLIEST STROKES.
-Intracerebral hemorrhage
-HIGH RISK: DIABETES HYPERTENSION

72.

Cerebral thrombosis

A thrombotic stroke occurs from injury to a blood vessel wall and formation of a blood clot.

73.

Cerebral embolism

Embolic stroke occurs when an embolus lodges in and occludes a cerebral artery, resulting
in infarction and edema of the area supplied by the involved vessel.
- LEFT ATRIAL FIB CAUSES CLOTS TO LEAVE HEART

74.

Intracerebral hemorrhage

bleeding within the brain caused by a rupture of a vessel.

Hypertension is the most important cause of intracerebral hemorrhage.
Other causes include vascular malformations, coagulation disorders, anticoagulant and
thrombolytic drugs, trauma, brain tumors, and ruptured aneurysms.

75.

Subarachnoid hemorrhage

occurs when there is intracranial bleeding into CSF-filled space between the arachnoid and
pia mater membranes on the surface of the brain.
Subarachnoid hemorrhage is commonly caused by rupture of a cerebral aneurysm
(congenital or acquired weakness and ballooning of vessels).

76.

SYMPTOMS OF HEMORRHAGE

Usually have a severe headache

LOC changes common
Nausea a vomiting common
Patients appear generally sicker
Onset rapid, deterioration rapid
Can occur in younger patients
NO TPA MEDS FOR HEMORRHAGIC PT

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BP and Stroke, when do we

treat?

Blood pressure will be elevated

Too low a pressure will adversely affect brain perfusion
BP not treated unless > 200/100 in ischemic stroke non-thrombolytic candidates
If giving TPA must treat >185/110
With hemorrhage treat >160/90
If hemorrahage vessel is "fixed" in Intervention Radiology or surgically treat if >180/100
NEURO PT- WANT BP MINIMUM OF 120 SYSTOLIC TO PERFUSE BRAIN TISSUES

What tissue are we trying

to save in stroke?

Penumbra - Zone of compromised neuronal cells that are unable to function but remain viable, swelling
could be reversed
(healthy -> penumbra -> ischemic core)

TX OF ISCHEMIC STROKE

Intravenous tPA (tissue plasminogen activator) to dissolve clot.

Mechanical Thrombectomy
3 hour treatment window
Must know when patient was last seen "normal"
No recent major surgery or trauma, no seizures
No recent hemorrhage or coagulopathy (warfarin therapy with INR >1.7, platelets <100,000)
Can't be very hypertensive (>185/110)
CAN GIVE MEDS, TAKE 2 GOOD BP READINGS TO QUALIFY for tPA

Clinical Presentation of
Stroke

RIGHT SIDE OF BRAIN- SAD, FLAT AFFECT

LEFT SIDE- SPEECH, ETC, WILL BE MISSED
Clinical Presentation of Ischemic Stroke
Based on location, location, location
Size of stroke
Patient usually does not experience pain, other than headache
Usually does not have altered level of consciousness (LOC) unless stroke causes mass effect due to
swelling or involves the brainstem or thalamic regions bilaterally
Acute hemispheric infarction, B/P elevation and maybe drowsy without cerebral swelling
Thrombotic stroke - evolves over several hours to days
Embolic stroke - maximal at onset

Cerebellar stroke signs and

symptoms

FALL RISK, WEAKNESS

Truncal and gait ataxia,
ipsilateral limb ataxia,
ipsilateral facial weakness and sensory loss,
ipsilateral gaze paresis,
small reactive pupils

Brain Stem stroke

Quadriparesis or contralateral hemiparsesis, locked in syndrome, coma, horizontal gaze paresis,

hyperthermia and hyperventilation

HOW TO CARE FOR PT

AFTER STROKE

VS and neuro ck every hour

(ICU 1-2 hour check, floor- 4 hour ck)
oxygen,
ekg,
pulse ox
swallow eval by speech therapist
BM, I&O
CT if any neuro change
History
Neuro assessment: GC scale, NIH, alert, improvement? worsening? tPA received?
Resp
Ck labs, blood sugar, clotting, wbc, electrolytes, bun, creatinine
Labs
-sodium want higher (pull swelling from brain) if low can cause seizure
-blood glucose
-insulin
-High WBC can be sign of infection

84.

85.

86.

referrals for rehabilitation

services for the patient with
CVA

PT, OT, MSW, Speech Therapist

Glasgow comma scale

Universal tool for neuro documentation

3 categories
Eye opening 1-4
Verbal Response 1-5
Motor Response 1-6
Total possible score = 15
"Less then 8- EVALUATE need to Intubate"
Note: Patient can be dead and have a 3

Accurately assess a patient

with a neurological injury
using the Glasgow comma
scale.

EYE open
Spontaneously 4
To Speech 3
To pain 2
None 1
Best Verbal Response:
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
Best motor response:
Obeys commands 6
Localizes Pain 5
Flexion withdrawal 4
Abnormal Flexion 3
Abnormal Extension 2
Flaccid 1

87.

NIH STROKE SCALE:

15-item neurologic examination stroke scale used to evaluate the effect of stroke
Procedure for Use
A trained observer rates the patent's ability to answer questions and perform activities. Ratings for
each item are scored with 3 to 5 grades with 0 as normal, and there is an allowance for untestable
(UN) items. If an item is left untested, a detailed explanation must be clearly written on the form.
-measure the level of impairment caused by a stroke
-main use in clinical medicine is during the assessment of whether or not the degree of disability
caused by a given stroke merits treatment with tPA.

88.

NIH evaluations

Facial Droop:
1. Uneven smile
2. Flattening of the nasal fold
3. Drooping eye lid
4. Flattening of the brow furrow
Arm drift- Have patient hold arms up for 10 seconds, watch for drifting down of one side.
MORE ACCURATE WITH PALMS UP BECAUSE YOU CAN SEE HAND ROTATE EARLY
LEG- HOLD ONE AT A TIME FOR 5 SECONDS
TOUCH PT AND CK SENSATION, AND DON'T TOUCH A FEW TIMES
-USE ALCOHOL SWAB DIPPED IN ALCOHOL TO TEST SENSATION

89.

90.

What happens during stroke alert?

A "Stroke Alert" is paged overhead when a patient exhibiting

stroke symptoms of less than 6 hours arrives in the ED or for
an inpatient experiencing stroke symptoms
This alerts radiology of the need to quickly scan patient, this
may mean delaying a scheduled scan
Lab is notified to come to bedside to draw and process labs
ECG technician arrives at bedside to obtain 12-lead
House supervisor is alerted that ICU bed is needed
The Stroke team includes a neuroscience RN who acts as a
coordinator

Describe the different medications that can be used during the

treatment of ischemic stroke including drug class, reason for
administration, complications, required monitoring, and
exclusion criteria.

The use of anticoagulants (e.g., heparin) in the emergency

phase following an ischemic stroke is generally not
recommended because of the risk for intracranial
hemorrhage.
Acetylsalicylic acid (aspirin) at a dose of 325 mg may be
initiated within 24 to 48 hours after the onset of an ischemic
stroke.
-Complications of aspirin include gastrointestinal bleeding
with higher doses.
-Aspirin administration should be done cautiously if the
patient has a history of peptic ulcer disease.20
After pt has stabilized and to prevent further clot formation,
patients with strokes caused by thrombi and emboli may be
treated with platelet inhibitors and anticoagulants
-Platelet inhibitors: aspirin, ticlopidine (Ticlid), clopidogrel
(Plavix), and dipyridamole (Persantine).
-anticoagulants: warfarin (Coumadin) Additionally, the use
of statins has been shown to be effective for the patient with
an ischemic stroke.

91.

Left Sided Stroke

Broca: responsible for the motor aspects of speech and is

involved in coordination of activities for the formation of
verbal speech. Damage to this area results in expressive or
nonfluential aphasia.
and
Wornicke's area: speech and language processing
Injury to the left side of the brain is more difficult for patients
because it can involve these speech and language centers.

92.

Effects of Cerebellar stroke

Truncal and gait ataxia, ipsilateral limb ataxia, ipsilateral

facial weakness and sensory loss, ipsilateral gaze paresis,
small reactive pupils

93.

Effects of Brain Stem stroke

Quadriparesis or contralateral hemiparsesis, locked in

syndrome, coma, horizontal gaze paresis, hyperthermia and
hyperventilation

2 most common physiological findings associated with

Alzheimer's disease.

Amyloid Plaques and Tangles in hippocampus and cerebral

cortex, decreased acetylcholine and nourishment which leads
to destruction on these tracts
(DAILY AEROBIC EXERCISE IS WHAT STOPS BRAIN
DEGENERATION)

94.

95.

Early Stages of AD

Memory disturbance progresses

Poor judgment
Impaired problem solving skills
Careless work and household habits
Gets lost easily
Routine activities take increased time
Lacks ability to adapt
Irritability, suspicion, agitation
Dysphoria - aberrant behavior- ERRATIC

96.

Mid Stages of AD Language disturbance

Impaired word finding

Circumlocution- USING SAME WORDS
Paraphasias- SAME WORD/WRONG WORD
Repetitive speech
Indifference/quiet/staring off
Apraxia
Restlessness, pacing- CIRCULAR PATTERN
Depression, irritability
Delusions and psychosis

97.

Severe AD

Non recognition of family and friends

Rigid Limbs
Spastic Contractures
Urinary incontinence
Aspiration risk so patient's require assistance with feeding or feeding
tubes ROUTINE CARE OR MED TX?
Extremes of silence and agitation in different patients.

Discuss client/family teaching regarding safety

factors for the client with Alzheimer's Disease

Home environment safety evaluation

Busy street
Appliances
Computer access/fraud
DOOR ALARM
WANDER BRACELET TO LOCATE PT
APPLIANCES, KITCHEN, SWITCH FROM GAS TO ELECTRIC
REMOVE COMPUTER
ABUSE FROM CAREGIVER BECAUSE THEY ARE EXHAUSTEDRESPITE CARE
COMMUNITY HELP FROM CHURCH, TO TAKE THEM TO COFFEE,
ETC

Discuss client/family teaching regarding

medications for the client with Alzheimer's Disease

Several medications can help with retention of acetylcholine at the neuro

junction, slowing the degenerative effects of the disease
-acetylcholinesterase inhibitors
- glutamine blockers

98.

99.

These meds will decrease wandering, agitation and socially

inappropriate behaviors.
Also many physicians will give Vitamin E and Ginko Biloba to enhance
memory.
100.

Acetylcholinesterase inhibitors

Acetylcholinesterase inhibitors increase acetylcholine levels in synapse.

Improve symptoms but not disease:
-Rivastigmine (EXELON) brain-selective, WORKS ON AXONS
-Donepezil (ARICEPT) CAUSES NAUSEA, BAD SIDE EFFECTS, STOPS
PROGRESSION ONLY HELPS SHORT TERM
-Galanthamine (RAZADYNE, REMINYL)
- Tacrine (COGNEX) too many SE

101.

Acetylcholinesterase inhibitors

Acetylcholinesterase inhibitors increase acetylcholine levels in synapse.

Improve symptoms but not disease:
-Rivastigmine (EXELON) brain-selective, WORKS ON AXONS
-Donepezil (ARICEPT) CAUSES NAUSEA, BAD SIDE EFFECTS, STOPS
PROGRESSION ONLY HELPS SHORT TERM
-Galanthamine (RAZADYNE, REMINYL)
Tacrine (COGNEX) too many side effects

102.

Glutamine blockers

Memantine blocks glutamine.

OK for later stages of AD.
May allow combo therapy.

103.

Additional Meds for AD

Ginkgo biloba extract better than placebo.

Vitamin E slows progress by 7 months.
NSAID naproxen being studied.
Estrogen not helpful.
Given anxiolytics and anti depressants as well as neuroleptics and anti
psychotics:
Resperdol, zyprexa, seroquel, zoloft and celexa.

Explain the concept of "care giver stress" and the

impact this can have on a family system for
patients with chronic neurological disease.

CAREGIVER HAS 60% INCREASED MORTALITY,

DIE PRIOR TO PERSON THEY CARE FOR
DECLINE CAN HAPPEN RAPIDLY OR OVER 5-10 YEARS
(Hypertension)

How much of the cardiac output goes to the

kidneys?

25% goes to the kidneys, when they don't get that, they trigger mechanisms
to improve perfusion. (increase bp!)

106.

Aldosterone

Adrenal glands secrete aldosterone which signal the kidneys to retain

sodium and water, but also triggers thirst in the person.
With each of these mechanisms, blood volume and blood pressure rises and
the kidneys enjoy improved perfusion

107.

What regulates aterial pressure, and how?

Baroreceptor reflex. Baroreceptors in the carotid can perceive low blood

pressure and trigger sympathetic response that increases venous tone and
raises the blood pressure. Basically is causes vasoconstriction.

108.

Local regulation of tissue blood flow

- Angiotensin, ADH, Norepinephrine

109.

What is now considered hypertensive?

120/80, must be below that

110.

Primary hypertension

aka essential or idiopathic htn.

No etiology.
Many cases of combined systolic and diastolic elevation fall into this
category.

111.

Secondary hypertension

results from an identifiable cause.

Various specific disease states or problems are responsible the elevation in
BP.

104.

105.

causes:
Chronic renal disease,
Glomerulonephritis,
Renal artery stenosis,
Adrenal gland dysfunction

112.

White coat
hypertension:

htn in people who are actually normotensive except when their blood pressure is measured by a health care
professional.
Intermittent vasovagal response accounts for the transient elevations in blood pressure.
Tx of this is controversial
Treating produces hypotension.
However, essential or secondary htn disguised as white coat htn and left undiagnosed & untreated has
consequences over time.

113.

Isolated systolic
htn:

systolic BP is 140mm or higher but the diastolic BP remains less than 90.
Etiology: increased cardiac output or atherosclerosis induced changes in blood vessel compliance or both in
older adults.
Chances of developing of ISH increases with advancing age as does the severity.
Common in females

Persistent severe
hypertension

diastolic BP above 110 to 120 mm.

Etiology: results when hypertension is left untreated or is unresponsive to treatment and becomes a truly severe
emergency condition as the pressure continues to rise unchecked.

115.

Symptoms of HTN:

Persistent headaches(vertex, top of head)

Fatigue
Dizziness
Palpitations
Flushing
Blurred or double vision
epistaxis (nosebleed)

116.

BETA BLOCKERS

Beta blockers often end in lol. Metoprolol, Labetalol

keeps HR low even in case of car crash and drop in blood pressure
Atenolol: usually 50 - 100mg daily
Slows heart rate and dilates peripheral vasculature
Blocks the actions of the sympathetic nervous system
Specifically the Beta Receptors
Contractility
Bronchoconstriction (asthma)

117.

DIURETICS

-drops HR, vasodilate, can cause gout, dehydration

114.

Furosemide (Lasix)
20 - 40 mg per day
Given early in the day
Used for the CHF that can occur with longstanding HTN
Watch Potassium!
Hydrochlorothiazide (Dyazide)
HCTZ 12.5 - 25 mg per day
Used in combinations
118.

ACE INHIBITORS

-pril ending
stops RAA1 from working
good for hypertension and diabetics with HTN, protects kidneys
prevents heart remodeling
can cause swelling and airway ostruction
Lisinopril, enalopril, benazapril
Inhibits the conversion of Angiotension I to Angiotension II in the lungs
Stimulates bradykinins that can cause a chronic cough
Inhibits the CHF that can develop from HTN
Protects the kidneys from DM II and HTN

119.

Angiotensin Receptor Blockers

-artan endings
expensive
Diovan
AKA - ARBs
Losartan, Candasartan, Irbesartan
Blocks the receptors sites of Angiotensin II
Lowering Blood pressure
Similar effects of ACEIs
No cough!
Fewer allergies than ACEIs
Used in combinations

120.

Alpha Blockers

Clonodine, Cozaar,
Simply blocks the alpha receptors that stimulate vasoconstriction
Not used as often as beta blockers, ACEIs and ARBs

121.

Calcium Channel Blockers

Amlodipine, Nifedipine(procardia), Verapamil, Cardiezem

Vasodialate
Card- lowers HR
Amlod- good for lowering bp Slow tachycardias
Used especially in patients with HTN and CAD
Also used extensively in smokers
Seem to work very well for African Americans with HTN

122.

Complications of HTN

Renal failure
Congestive heart failure
Cerebral vascular accident
Aortic aneurysm / dissection
Acute myocardial infarction
Peripheral vascular disease

123.

Causes of Heart Failure

Increased cardiac workloadHypertension,

Valve disorders,
Anemia,
Congenital heart defects
Acute, non cardiac causesVolume overload,
Hyperthyroidism, Fever,
infection,
Massive pulmonary embolus

The volume of blood ejected with each

heart beat determined by

Preload: volume of blood in the ventricles at end diastole

Afterload: force needed to eject blood into the circulation

125.

Myocardial contractility:

the natural ability of cardiac muscle fibers to shorten during systole

Contractility is measured by the ejection fraction, which is the percentage of blood in
ventricle ejected during systole.
A normal ejection fraciton is approx. 60%.

126.

Frank Starling mechanism:

The greater the stretch of cardiac muscle fibers, the greater the force of contraction.
Increases contractile force leading to increased CO complication: increased myocardial
oxygen demand and is limited by overstretching.

127.

Neuroendocrine responses

Decreased cardiac output stimulates aortic baroreceptors which in turn stimulate SNS.
SNS causes release of catecholamines, causing increase in HR, BP and contractility.
Also causes increased vascular resistance and increased venous return.
Complication:
tachycardia with decreased filling times and decreased CO. Also causes increased vascular
resistance and increased myocardial work and oxygen demand.

124.

128.

Decreased renal perfusion from

heart failure

Release of Renin from Kidneys

Adrenal cortex produces Aldosterone
Posterior pituitary releases ADH
Mass effect of these hormones is significant vasoconstriction and salt and water retention,
with a resulting increase in vascular volume

What does the body do to compensate

for heart failure?

Increased vascular volume and venous return increases atrial pressures

Stimulates the release of Atrial Natriuretic factor and Ventricular remodeling occurs
Compensatory mechanisms actually begin to cause the failure of the heart.
A vicious cycle ensues

130.

Atrial natriuretic factor-

balances the effects of the other hormones to a certain extent,

promotes sodium and water excretion and inhibits the release of norepinephrine, renin, and
ADH.
Natural preventive that delays severe cardiac decompensation.

131.

Ventricular remodeling

occurs as the heart chambers and myocardium adapt to fluid volume and pressure increases.

129.

chambers dilate to accommodate excess fluid resulting from increased vascular volume and
incomplete emptying.
Initially, this additional stretch causes more effective contractions.
Ventricular hypertrophy occurs as existing cardiac muscle cells enlarge, increasing their
contractile elements and force of contraction.
132.

Left vs Right sided HF

Left sided:
Blood backs into lungs, can't fill, CAD and HTN
Side effects:
Fatigue, activity intolerance, dyspnea, SOB, cough, orthopnea, inspiratory crackles,
wheezes, S3 gallop.
Right sided:
Blood backs in the periphery. Third spacing.
Side effects:
COPD, Peripheral edema, JVD, hepatomegaly, anorexia

133.

Heart Failure Classifications

Class I No limitations in physical activity

ClassII Symptoms with strenuous activity
Class III Symptoms with mild activity
Class IV Symptoms at rest

134.

How to test for CHF:

History and physical

Beta Natiuretic peptide
Electrolytes
Urinalysis, BUN, Serum Cr
LFT- liver fn test
Thyroid function tests- hyperthyroid raises BMR and tachycardia
ABGs in acute HF
CXR- look for fluid and enlarged <3
ECG, Echocardiogram- abnormality

135.

Drugs used for HF

Angiotensin Converting Enzyme Inhibitors

Lisinopril, enalapril, benazapril
Angiotensin II receptor Blockers
Losartan, Cozaar, Diovan
Beta Blockers
Atenolol, Metoprolol, Labetalol
Diuretics
Lasix, Bumex, Demadex, Thiazide
Nitrates
Isorbide or NTG
IV nitroglycerine to dilate veins, Decrease preload coming back to <3
Positive Inotropic agents- Dig

136.

Digitalis glycosides

used judiciously in symptomatic HF.

-Digitalis has a positive inotropic effect on the heart, increases the strength of
myocardial contraction.
-decreases SA node automaticity ans slows conduction across the AV node
increasing ventricular filling time
-very narrow therapeutic window and dig toxicity can be problematic.
-S and Symptoms of toxicity can include anorexia, nausea and vomiting. Altered
vision and confusion can also occur. A number of dysrhythmias can also occur.
!!!!!Digitalis is often administered concurrently with diuretics. Diuretics often
cause hypokalemia. Hypokalemia can potentiate the risk of dig toxicity, so
beware!!!!!

137.

New Drug: BiDil

Specifically for African Americans

Fixed dose combination of two vasodilators (hydralazine and isorbide)
Dose: 1 - 2 tablets TID

138.

Care of HF pt

Monitor vital signs and oxygen saturation as indicated

Auscultate heart and breath sounds Q 4 hours
Administer supplemental oxygen as needed
Monitor intake and output, min. fluid
Record weight and abdominal girth Q 24 hr. Weight gain of more than 2 lbs
requires call to MD
Administer prescribed medications
Encourage rest

139.

Pt teaching in HF

Rationale for sodium restrictions

Encourage small frequent meals
Weight monitoring: weight gain of 2 lbs in 24 hours requires call to provider
Specialized information on medications
Provide a list of foods to avoid
High sodium
High fat
High cholesterol

What would you do if a HF pt shows signs of

air hunger, cough with pink, frothy sputum?

GET RRT
lung sounds, RR, O2 sats, HR, VS, EKG, CXR
Raise HOB,
!!!!!!!urine output!!!!!!!!! tells us about kidney failure
Acute Pulmonary Edema is a medical emergency and develops rapidly

Peripheral Vascular Disease Risk Factors

Atherosclerosis
Diabetes
Smoking
Elevated lipid levels
Phlebitis
Autoimmune disease

140.

141.

142.

Most common locations of

occlusion & stenosis

The lower limbs are more susceptible to arterial occlusive disorders and atherosclerosis than are
the upper limbs.
lower extremity:
aorto-iliac bifurcation and the femoral bifurcation.
Arteries can be occluded acutely from embolism, thrombosis, trauma, vasospasm or edema.
Emboli of a cardiac origin are usually due to atrial fibrillation.
Emboli tend to lodge at artery bifurcations or in areas where vessels abruptly narrow such as the
femoral artery bifurcation.

Peripheral Vascular Disease

Pathophysiology

Progressive nature
Starves tissues of oxygenated blood
Collateral circulation can develop
Vasodialation : limited effect
Cellular anaerobic metabolism-lactic acid, pain, tissue pain
Sustained lack of arterial blood flow results in pain
Intermittent Claudication (muscle is forced to work without an adequate blood supply to meet its
metabolic demands.)

144.

Venous Disorders

Lower extremity edema: can't pump blood back up

Erythema- redness
Skin dry and flaky, itching
Continued irritation results in Stasis Dermatitis- lower legs swell, skin is tight & shiny red/purple
Ulcers develop in the lower third of leg

145.

DVT

DVT- will still have pulse because clot is in the vein, so it will not block arterial pulse
Causes:
Prolonged position of hip flexion
Venous stasis
Previous DVT
Cardiac disease
Pregnancy
Trauma, especially of the lower extremities
Estrogen therapy or oral contraceptives
Malignancy
Obesity
Family history of clotting disorders.
Hypercoagulabiliy often accompanies malignant neoplasms, Cancer pt's more coagulable.
age over 75 in women, smoking & BC.
Dehydration and blood dyscrasias may raise the platelet count, decrease fibrinolysis, increase the
clotting factors or increase the viscosity fo the blood.

146.

Prevention of DVT

Activity
Passive or active contraction of leg muscles
Sequential compression devices (SCD's)
Applied after surgery until ambulation
Anticoagulation
Assessment
Homan's
Edema
Pain

143.

147.

Anticoagulant therapy

Designed to prevent initiation or extension of thrombi

Inhibits synthesis of clotting factors
Agents don't break up or dissolve clot once they are formed
Close monitoring of anticoagulant
Dosage is adjusted according to PTT or INR
Heparin - aptt
Coumadin and lovenox - PT/INR
Lovenox is safer that Heparin

148.

How to differentiate DVT from AVT

DVT- PAIN WITH RAISING LEGS

AVT- FEELS BETTER WITH LEGS RAISED

149.

Clinical manifestations of arterial disorders

Leg pain
Decreased exercise tolerance
Paresthesias
May occur any where along the arterial system
Dependent rubor
Impotence
Ulcers

150.

Arterial disorders signs and symptoms

Decrease or absence of arterial pulses

Thin shiny hairless skin
Thick ridged toenails
Cool skin temperature
Pain with ambulation
Pain with leg elevation

151.

Medical MGMT of Arterial Disorders

Smoking Cessation
Skin care
Exercise
Dietary changes
Promotion of arterial flow
Platelet inhibitors: Trental, Plavix
ASA

152.

Surgical Interventions

Endovascular Interventions
Angioplasty
Atherectomy
Stent Placement
Arterial Bypass
Revascularization of limbs
Arteriography to determine level of obstruction
Amputation

153.

Prevention of Complications

Fluid volume deficit

Hemorrhage
Hematoma
Fluids shifts
Compartment syndrome
Infection
Graft Thrombosis

154.

Signs of problems

Pallor
Pulselessness
Pain
Paresthesias
Temperature Change

155.

Aneurysm Pathophysiology

Caused by HTN and atherosclerosis

Leads to weakening of arterial wall, ballooning of wall of artery
Can rupture with elevated blood pressure

156.

Abdominal Aortic
Aneurysm

The most common type of aneurysm

Most often in men 40 -70 years of age.
Many are asymptomatic
Discovery is incidental
When greater than 5 cm it can be palpated
Patient awareness of a pulsating mass in abdomen
As the aneurysm expands, there may be groin or flank pain due to increasing pressure on other structures.
Sometimes mottling of the extremities or distal emboli in the feet alert the clinician to a source in the abdomen.
Requires endovascular procedures to repair.

157.

158.

Complications of
aneurysm repair

Caused by underlying CAD and COPD

Client at risk for myocardial infarction
Pre renal failure can develop
Emboli can develop
Spinal cord can become ischemic
Changes in sexual function
Rupture of AAA

Aneurysm Rupture

Surgery is the only intervention for clients with rupture.

Pt will have significant hemodynamic instability due to preoperative blood loss and ishemic organ disease.
Abrupt excruciating pain is the most common presenting manifestation in clients with aortic dissection.
-ripping or knifelike, tearing sensations that radiate to the back, abdomen, extremities or anterior part of the
chest.
-looks "shocky" and is sweating profusely, is severely apprehensive and has diminished peripheral pulses.
-unequal pulses.
-Different blood pressures in the arms,
-paraplegia or hemiplegia,
-decreased uring output or hematuria,
-mental status changes
-chest pain.

159.

Raynauds

Small arteries and arterioles constrict in response to various stimuli

Vasospastic
Obstructive
Often induced by cold, nicotine, caffeine and stress
Often found in association with autoimmune disorders

160.

s/s of Raynauds

-pallor
-cyanosis
-cold extremity

Criteria for
diagnosing
Raynaud's disease

1. manifestations of at least 2 years

2. intermittent attacks of pallor or cyanosis of the digits by exposure to cold or from emotional stimuli,
3. bilateral or symmetrical involvement,
4. no evidence of occlusive disease in the digital arteries
5. gangrene

Burger's Disease

AKA Thromboangiitis Obliterans

Inflammatory disease of the small and medium sized arteries and veins of extremities
Seen in men
Related to smoking
Ulcers
Pain

161.

162.

163.

164.

Clinical
Manifestations of
Burger's Disease

Pain is the outstanding clinical manifestation.

Pain from ischemia
-accompanied by manifestations of ischemia such as color or tem changes in the fingers.
Cold sensitivity.
Lower extremity paresthesia
Claudication type pain is common
Ulceration and gangrene are frequent complications and may occur early in the course of the disease Edema of
the legs if common in advanced cases Segmental thrombophlebitis affects the smaller veins in 40% of clients.

Treatment of
Burger's Disease

Use of well-fitting protective footwear to prevent foot trauma and thermal or chemical injury
Early and aggressive treatment of extremity injuries to protect against infections
Avoidance of cold environments
Avoidance of drugs that lead to vasoconstriction
NO SMOKING!
Amputation if it does not resolve, turns gangrenous