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NURSING 440 FINAL EXAM

SHOCK

Shock: a condition in which the cardiovascular system fails to perfuse tissues adequately

An impaired cardiac pump, circulatory system, and or volume, can lead to

compromised blood flow to tisues

Inadequate tissue perfusion can result in:o Generalized cellular hypoxia (starvation)

o Widespread impairment of cellular metabolism

o Tissue damageorgan failure

o Death

Diagnosis

MAP

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1.HYPOVOLEMIC SHOCKa.DEFINITION

i. Acute blood loss from trauma, fluid shifts, loss from surgeryor burns, vomiting or diarrhea; Severe electrolyte imbalance

ii. Small children are more susceptible than adultsiii. Teens & young adult are high risk because trauma maindeath in MVAs

b.CAUSE

i. Decrease in clients circulating blood volume that leads toinadequate tissue perfusion. This can lead to organ damageand death.

ii. Most common cause- Acute blood loss from traumaiii. Burn (Massive evaporation of water from skin)iv. Vomiting/Diarrhea (Fluid & Electrolyte imbalance)v. Shock occurs when less of 20% of circulating blood volume

is lost and severe shock occurs when the patient has lostmore than 40% of the blood volume. Most adults have a totalblood volume of 5 liters, and do not show symptoms ofshock until at least 500 mL is lost.

c.S/S

i. Early Signs1.Mild tachy, mild hypotension (

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vi. Activity as tolerated; Reposition Q 1-2 hoursvii. Monitor I&O Q1-2 hrs (Foley)viii. Monitor EKGix. Monitor for signs of fluid overloadx. Adequate sleep

xi. *Monitor changes in mental status

2.CARDIOGENIC SHOCKa.DEFINITION

i. MI, Ventricular Rupture, Cardiac tamponadeb.CAUSE

i. Hypotension, cellular hypoxia & inadequate tissue perfusionresulting from decreased urine output

ii. Usually from MIiii. Occurs in 5-10% of clients with MIiv. Risk factors: Female, CAD, previous MI

c.S/S

i. Cool & clammy skin, weak thread pulses, tachy, increasedRR, decreased UO, lower extremity edema, EKG changes,decreased BP, anxiety, feelings of impending doom, chestpain, SOB, hypotension

d.DIAGNOSIS

i. ABGii. Cardiac catheterization (inserted into femoral artery and

threaded into the heart)iii. Chest xrayiv. Echocardiogram (ejection fraction 50-75%)v. Osmolarity (fluid status)vi. Troponin (indicates MI)vii. WBC

e.TREATMENT

i. Treatment centered at restoring pump function and easingworkload of heart

ii. *Medication is first line of treatment-1.Dopamine & Primacor

iii. Cardiac output will be less than 2.2L/min (normal 4-8L/min)

iv. Diet as tolerated (if critically ill NPO or TPN); May be on

ventilator; may need tube feedingsv. Patient placed in supine Trendelenburg position or passive

leg elevation unless patient is having respiratory distress andlower extremity edema

vi. Reposition Q1-2H; Bed Restvii. O2 if orderedviii. UO Q1-2 hrs

3.SEPTIC SHOCKa.DEFINITION

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i. Infection from sources including bone, blood, invasive lines,GI tract, GU tract, pulmonary, cardiac, skin & CNS

b.CAUSE

i. Bacteria releases endotoxins into the bloodstream andinflammatory cascade if triggered that causes inflammation

in the entire body, edema, hypotension, hypoxia, decreasedcellular perfusionii. *Sepsis has a 40-50% mortality rate

c.S/S

i. Warm, flushed skin, fever above 100.4F, tachy; elevated RRabove 20/minn, WBC count to low or to high Anxiety,hypotension, hypoxia, mental status change

ii. If tachy worsens metabolic acidosis can occuriii. Septic shock can lead to organ damage to the brain, heart,

lungs, liver, and kidneys. DEATH.d.DIAGNOSIS

i. **Risk increases with age

ii. ABGiii. Blood cultureiv. BUNv. CBCvi. Creatinevii. EKGviii. LDHix. PTT; PTx. Urinalysis with culture

e.TREATMENT

i. Finding and treating the cause is essentialii. 1stline of tx- IV ANTIBIOTICSiii. Fluid resuscitation, vasopressors, and O2iv. Usually a central line is used for multiple line accessv. Monitor BPvi. Glucocorticoids used as anti-inflammatory, Solu-medrol is

steroid of choice administeredvii. IV Q6-8 hrsviii. Bed restix. Proper Foley cath care

4.NEUROGENIC SHOCKa.DEFINITION

i. Spinal cord injury, or permanent paralysisb.CAUSE

i. Interruption of the sympathetic nervous system response;NS is more severe form of spinal shock

ii. Sympathetic innervation of the spinal cord is lost but theparasympathetic function continues

c.S/S

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i. Flaccidity and paralysis can result in loss of motor andsensory function

ii. Hypotension, brady, low BP, weak thready pulse, coolclammy skin, decreased UO, cyanosis, increased RR

iii. Symptoms can last 4-6 weeks

iv. Complication-organ failure, MI, stress ulcersd.DIAGNOSIS

i. ABGii. BUNiii. CBCiv. Creatinev. EKGvi. LDHvii. Urine specific gravity

e.TREATMENT

i. Correction of hypotensionii.

IV fluid

iii. Vasopressors** first line of treatmentiv. O2; Respiratory support PRNv. No dietary restrictionsvi. Maintain flat positionvii. Monitor EKG; Monitor Blood sugarviii. Assess level of anxiety

5.ANAPHYLACTIC SHOCKa.DEFINITION

i. Type I Hypersensitivity reaction caused when a allergencomes in contact with the body

b.CAUSE

i. Body reacts to a foreign substance with a misdirectedimmune response.

ii. IGE antibodiesiii. Common allergies: milk & eggs (especially infants); peanuts,

chocolate, strawberries, tomatoes, & seafood (common inadults)

iv. Physiological changes within the body in response toanaphylactic reactions include: bronchoconstriction,hypotension, tachy, hypovolemia, & febrile response

c.S/S

i. Can occur within mins-hours; itching, hives, nasalcongestion, HA, N/V, diarrhea. Hypotension, tachy,wheezing, tachypnea, cyanosis, chest pain, arrhythmias,seizures

ii. Rare symptoms: pelvic pain, vaginal bleeding, and urinaryincontinence

d.DIAGNOSIS

i. ABG

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ii. BUNiii. CBCiv. Creatine (renal function)v. LDH (tissue ischemia, necrosis, or acidosis), Urine specific

gravity (fluid status)

e.TREATMENTi. No dietary restrictions, except avoid food allergensii. EPINEPHRINE

1.Epi-pen; do not inject IV or into buttocksiii. Benedryl (antihistamine)iv. Corticosteroids (inflammatory mediators)v. Trendelenburg position or supinevi. O2 PRNvii. IV NS OR LR

viii. Most severe complication is death

ARTERIAL BLOOD GASES (ABGS)ARTERIAL BLOOD GASES ABGS):

PH: 7.35-7.45

o Amount of free hydrogen ions in arterial blood

Pac02: 80-100 mmhg

o Partial pressure of O2

PaCo2: 35-45 mmHg

o Partial Pressure of CO2

HCO3-: 22-26 mEq/L

o Concentration of Bicarbonate in arterial blood

SaO2: 95-100%

o

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Respiratory acidosis (retention of c02)o Depression of the respiratory center (head injury, anesthesia, narcotic

overdose), obstruction of respiratory passages (pneumonia, atelectasis), and

chronic respiratory problems (COPD) all prevent the normal excretion of

co2 through ventilation

o Compensatory mechanism: the kidneys compensating by retaining more

hco30 to compensate for the acidosis

o Common causes: secondardy to problems that cause hypoventilation:

CNS depression:head injury, sedatives, anesthesia

Increased resistance:aspiration, bronchospasm,laryngospasm, pronlonged narrowing of the airway (asthma,

airway edema)

Loss of lung surface:Atelectasis, COPD, Pneumonia,Pneumothorax, Chronic Pulmonary Diseases

Neuromuscular Diseasesaffecting respiratory muscles:Guilain-Barre syndrome and myasthenia gravis,

Mechanical Hypoventilationincreased retention of CO2,

Sedative or barbiturate overdose

o Signs/Symptoms Restlessnessprogressing to lethargy, Drowsiness,

Confusion, Coma, Tachycardia, Tachypnea, Dysrhythmias

associated with hypoxia and hyperkalemia, Seizures, Paleto

cyanoticand dry skin, Hypercapnia (elevated CO2level),

which will causecerebral vasodilation and increase problems

with increased intracranial pressure (ICP)

Urine pH is

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o Common Causes: DKA(most common), Lactic acidosis(shock, respiratory or

cardiac arrest), Renal failure, Severe diarrhea, Salicylate

toxicity, Starvation, Gastrointestinal (GI) fistulas

o Signs & Symptoms

Kussmaul respirations (deep, rapid), Confusion, Disorientationprogressing to coma, Headache and Lethargy, Hypotension,

Dysrhythmias secondary to hyperkalemia, Warm flushed skin

(peripheral vasodilation), Abdominal pain, Nausea/Vomiting

Urine pH 6

o Medical Management Assess the need for an antianxiety medication Decrease rateand tidal volume(if on a ventilator)

o Nursing Management

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Monitor ABGs, Presence of decreased K+, Monitor fordysrhythmias, Relax/Calm encourage slow, deep breathing,

guided imagery, Rebreathing Mask (paper sack) to increase

CO2retention, Reduce environmental noise and stimuli,

Encourage slowing down respirations, Analgesic Medications

(pain), Antipyretic Medications (fever) Metabolic Alkalosis (loss of acid)

o Excessive retention of HCO3- or a loss of acid, may occur if too muchHCO3- was given during resuscitation, gastric suctioning or prolonged

vomiting and diarrhea.

o Compensatory Mechanism: *The lungs retain more CO2to balance thepH

o Common Causes: Loss of acid through gastric suctioningor vomiting, Excess

alkaliintake antacids or sodium HCO3-,Adrenal disease

(hyperaldosteronism), Excessive intake of

mineralocorticoids, Diuretic therapyo Signs & Symptoms: Nervousness, Dizziness, Cardiac irritability

(Decreased K+, Ventricular Dysrhythmias, Atrial Tachycardia), N/V,

Paresthesiasin fingers/toes, Tetany and muscle cramps(late

signs), Hypoventilation(compensated by the lungs), Hydration

status(fluid volume deficit)

Urine pH >6

o Medical Management: Stop the intake of HCO3- Replace fluid loss

o Nursing Management History (precipitating cause GI suctioning or vomiting, K+

values (hypokalemia usually occurs, but levels will increase

with treatment of the alkalosis)

If taking digitalis, monitor pH, digitalis, and K+ levels.Digitalistoxicity may occur with hypokalemia.

Monitor repirations, lungs will compensate by retaining CO2.Antiemetic meds for N/V, assess for Paresthesias (numbness

and tingling) of toes and fingers.

Respiratory Acidosis(hypoventilation) Possible Causes:

o Over Sedationo Brainstem Traumao Immobility

o Respiratory muscle paralysis

K+ will go up

Lungs will compensate acidosis by decreasing the CO2

Diabetes, poor perfusion, poor ventilation, and real failure canall causeACIDOSIS.

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Respiratory Alkalosis(hyperventilation) Possible Causes:

o Hyperventilation with anxietyo Pulmonary Disease

o High Altitudes

o Ventilator setting TOO HIGH or TOO FAST K+ goes down with alkalosis. K+ moves into the cells (ICF) and increased renal

excretion of K+ occurs as the renal system tries to conserve the H+. If alkalosis is

corrected, K+ will shift out of the cells and back into the circulating volume

Metabolic Acidosis (Loss of base HCO3- or excessive acid production) Possible Causes:

o Ketoacidosis

o Shocko Severe Diarrhea

o Impaired Kidney Function

K+ will go up Kidneys will compensate acidosis by increasing the HCO3-

Diabetes, poor perfusion, poor ventilation, and real failure canall causeACIDOSIS.

Metabolic Alkalosis (loss of acid) Possible Causes:

o Nasogastric (gastric) suctioningo Prolonged vomiting

o Thiazide diuretic use

o Overdose of Bicarbonates with CPR

o Excessive antacids

Hypocapnia decreased levels of CO2. Most commonly seen when

hyperventilation secondary to hypoxia as a result of acute pulmonary conditions.

MECHANICAL VENTILATION

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ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) & ACUTE LUNG

INJURY (SIRS)

ARF: caused by failure to adequately ventilate and/or oxygenate Ventilatory failure is due to a mechanical abnormality of the lungs or chest wall,

impaired muscle function (the diaphragm), or a malfunction in the respiratory

control center of the brain

Oxygenation failure can result from a lack of perfusion to the pulmonary capillary

bed (a pulmonary embolism) or a condition that alters the gas exchange medium

(pulmonary edema, pneumonia)

Both inadequate ventilation and oxygenation can occur in individuals with diseased

lungs (asthma, emphysema). Diseased lung tissue can cause oxygenation failure and

increased work of breathing, eventually resulting in respiratory muscle fatigue and

ventilatory failure Criteria is based on ABG values

o ABGS indicating ARF:

Room air, PaO2 less than 60 mm Hg, and SaO2 less than 90%, or

PaCO2 greater than 50 mm Hg in conjunction with a pH less than

7.30

ARDS: state of acute respiratory failure with a mortality rate of 25-40%

Indicators:

o Dyspnea

o Bilateral noncardiogenic pulmonary edema

o Reduced lung compliance

o Diffuse patchy bilateral pulmonary infiltrateso Severe hypoxemia despite administration of 100% oxygen

Risk Factors

Patients who have experienced:

Pneumonia or pulmonary emboli

Trauma

Sepsis

Aspiration of stomach contents

Near drowning

Drug overdoses Multiple blood transfusions

Pancreatitis

Assessment:

RR (labored or rapid breathing)

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Increased work of breathing (nasal flaring, intercostal retractions, use of accessory

muscles)

Hypotension and tachy

Scattered crackles at the lung bases

Labs

ARF, ARDS, SARS ABG sample

Room air, PaO2 less than 60 mm Hg, SaO2 less than 90%

PaCO2 greater than 50 mm Hg and pH less than 7.30 (hypoxemia, hypercarbia)

Sputum culture (used to rule out infection)

CBC (elevated WBC count may indicate infection or inflammation)

Diagnostic Procedures

Chest XRAY

o Results may include: pulmonary edema (ARF, ARDS), cardiomegaly (ARF),

diffuse infiltates and white out or ground glass appearance (ARDs),infiltrates (SARS)

o Nursing actions:

Assist in positioning client; interpret and communicate results

ECG

o Rules out cardiac involvement

Hemodynmamic monitoring

o Swan Ganz catheter

Placed to measure pulmonary artery pressures and cardiac output

Pulmonary capillary wedge pressure with ARDS is usually low or

within the expected reference range (4-12 mmHg) Continuous hemodynamic monitoring is important for fluid

management

o Nursing actions

Monitor ECG during catheter insertion

Have resuscitation meds ready

Monitor

Confirm cath placement

Nursing Care

Maintain patent airway and monitor RR Q hour

Suction PRN

Assess and document sputum color, amount, and consistency

Oxygenate before suctioning to prevent further hypoxmia

Mechanical ventilation often required.

o Positive end expiratory pressure (PEEP) is often used to prevent alveolar

collapse during expiration

o Follow facility protocol for monitoring and documenting ventilator

settings

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Monitor for pnemothorax (as PEEP may cause lungs to collapse)

Obtain ABGs as prescribed and following each ventilator setting adjustment

Maintain continuous ECG monitoring for changes that may indicate increased

hypoxemis, especially when repositioning and suctioning

Monitor vitals and SaO2 continously

Position client to facilitate ventilation and perfusion Prevent infection

o Hand hygiene

o Suctioning techniques

o Oral care Q2 hrs

o PPE

Promote nutrition

o Bowel sounds

o Monitor elimination patterns

o Daily weights

o Record urine outputo Administer enteral and/or parenteral feedings

o Prevent aspiration with enteral feedings (elevate HOB 30-45)

Confirm NG tube placement prior to feeding

Emotional support

Therapeutic Procedures

Intubation and mechanical ventilation

o Artificial airway insertion with mechanical ventilation

o Nursing actions

Monitor ECG, SaO2, breath sounds, and color

Sedate as needed

Reassure patient

Suction ready

Preintubation

Oxygenate with 100% oxygen

Assist ventilation with manual resuscitation bag and face

mask

Have emergency equip ready

Postintubation

Assess bilateral breath sounds, symmetrical chest

movement, and check xray to confirm placement of

endotracheal tube

Secure endotracheal tube per guidelines

Assess balloon cuff for air leaks periodically

PEEP

Positive pressure is applied at the end of expiration to

keep the alveoli expanded

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Decreased cardiac output can activate the renin-angiotension-

aldosterone system, leading to fluid retention and or decreased

urine output

Nursing actions: I&Os, wt, hydration status

Education: advise pt to avoid using Valsalva maneuver (straining

with bowel mvement) because it can further increaseintrathroacic pressure

o Barotrauma

Ventilation with positive pressure causes damage to the lungs

(pneumothorax, subcutaneous emphysema)

Nursing actions:

Oxygenation status and chest xray

Assess for subcutaneous emphysema (crackles and/or air

movement felt under skin)

Document all ventilator changes made (high pressure

ventilation alarm may indicate pneumothorax)o Immobilization

Can result in muscle atrophy, pnemonia, and pressure sores

Actions

Reposition and suction Q2

Routine skin care

Implement ROM

2 phase condition:

1. Acute exudative phase

a. Activation of neutrophils (PMNs-polymorphonuclear neutrophils)

b. The bodies nonspecific first responders to infection, injury, or

inflammation

c. Neutrophil activity

i. Release pro-inflammatory cytokines (TNF & interleukins) & other

substances

ii. Activate macrophages

iii. Neutrophils migrate into pulmonary circulationthrough

endothelial walls of pulmonary capillariesinto lung

d. Resultsi. Alveolar-capillary membrane damage (fluid starts leaking into

alveoli)

ii. Edema and flooded alveoli

iii. Inactivated surfactant (type II cells)

iv. Inflammation in lungs

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v. Create classic features of ARDS: hypoxemia, decreased lung

compliance, increased respiratory rate

2. Fibroproliferative phase Towards the end of acute exudative phase, collagen and fibrin deposits begin to

collect in lungs

In FP phase, fibrin matrix develops (hyaline membrane) in alveoli

Results:

o 1. Lungs become even stiffer (harder to ventilate)

o 2. Increased hypoxia and increased CO2

Xray findings:

o As alveoli fill with fluid, see white patches on xray

o white outsometimes used to described what is seen on xray

o physical findings at this time: significantly decreased breath sounds

Medical Care

maintain respiratory function

o intubation and ventilation using positive pressure

o identify and treat causative factors

Nursing Care

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Three mainstays:

o Prevent complications (infections, aspiration, skin breakdown,

contractures, nutrition)

o Provide adequate support (family care)

o Allow the disease time to resolve (tincture of time)

ACUTE COMPLICATIONS OF DIABETES MELLITUS

Review insulin/Glucose Utilization

o Insulin moves glucose into cell

o If insulin not present cells deprived of glucose which is needed for

energy

o Without insulin, glucose levels in the blood begins to rise

o As cells are deprived of glucose, the liver produces glucagon

o Glucagon increases BG by breaking down stored glucose in the liver

(glycogenolysis)

o Eventually, non carbs (fats & proteins) are converted to glucose

(gluconeogenesis)

The Polys

Polyuria: excessive urination (with glycosuria)

Polydipsia: excessive thirst (from dehydration and hyperglycemia)

Polyphagia: excessive hunger (from using non-CHO sources for energy)

Ketoacidosis

Without insulin, fat is used for energy (gluconeogenesis)

Ketones result from breakdown of fatty acids

3 specific ketone bodies are produced

o Acetone (fruity breath)

o B hydroxybutyrate

o Acetoacetate

Ketones & Acid Base Balance As ketones breakdownproduce H+ ionsdrop in pH

Serum bicarbonate decreases in attempt to maintain pH

Result is severe metabolic acidosis

Ketoacidosis

As bicarbs decrease, breathing becomes deep and rapid (Kussmaul respirations) to

release acid in form of CO2

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Acetone: doesnt cause acidosis (eliminated in lungs fruity breath)

Ketones eliminated in urine:ketonuria

Ketones in blood: ketoneumia

Two major complications

DKA: Diabetic Ketoacidosis (Type 1 DM) HHNS: Hyperglycemic hyperosmolar state (Type 2 DM)

o Also called HHNKS: Hyperglycemic, hyperosmolar non-ketotic syndrome

Similarities:

o Both most often caused by infection/stress

o Both have elevated blood glucose

o Both present with dehydration, polyuria, polydipsia, and electrolyte loss

o Both have altered mental status

Differences

DKA HHNS

BG >300 (300-800) BG >600 (600-2000)Serum & urine ketones No ketones

Fruity acetone breath No fruity breath

Acidosis (pH

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As H+ moves into cell K+ moves out (to maintain ion

balance)serum K+ increases

Also, insulin is needed to move K+ into the cell

Without insulin, K+ remains outside of cell

Net result: RELATIVE hyperkalemia

What does this mean? Ex. Patient with type I DM presents with BG 350 mg/dl, pH

7/20, HCO3 15 and K+ 3.9 mEq

Some protocols: Need K+ > 3.5 before giving initial insulin

bolus

Why? Usually pH corrects itself with adequate hydration

and insulin replacement

o Hyponatremia

Na loses from:

Osmotic diuresis

Vomitting/diarrhea Correct with infusion of 0.9 NaCl

- need to do all three of these simultanenously

Nursing Care

Monitor!

o Response to therapy

Fluid volume status: hourly urine output

Insulin levels: monitor BG hourly

Electrolytes (Na & K)monitor hourly

Mental status & LOCsudden complaints of HA may signalcerebral edema. Hyponatremia may cause mental status changes

Cardiac statuscontinous EKG monitoring because of K probs

Patient and Family Education

o Listen: to gain insight into possible cause of hyperglycemic episode

o Possible issues: cost/availability of meds, not able to recognize stress/

infection, drug holiday, knowledge deficit, apathy or memory probs

(older adults)

Diabetes oral meds all rely on the insulin the body makes (so they will not be useful in

patients with type 1 diabetes. Most of these meds can be used in combo with each

other and with insulin

Oral medications

Medications

Action

Advantages

Possible side effects

Meglitinides

Repaglinide

Stimulate the release

of insulin

Work quickly

Severely low blood sugar

(hypoglycemia); weight gain;

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(Prandin)

Nateglinide (Starlix)

nausea; back pain; headache

Sulfonylureas

Glipizide (Glucotrol)

Glimepiride

(Amaryl)

Glyburide (DiaBeta,

Glynase)

Stimulate the release

of insulin

Work quickly

Hypoglycemia; weight gain;

nausea; skin rash

Dipeptidy peptidase-4

(DPP-4) inhibitors

Saxagliptin

(Onglyza)

Sitagliptin (Januvia)

Linagliptin

(Tradjenta)

Stimulate the release

of insulin; inhibit the

release of glucose

from the liver

Don't cause weight gain

Upper respiratory tract

infection; sore throat;

headache; inflammation of

the pancreas (sitagliptin)

Biguanides

Metformin

(Fortamet,

Glucophage, others)

Inhibit the release of

glucose from the liver;

improve sensitivity to

insulin

May promote modest

weight loss and modest

decline in low-density

lipoprotein (LDL), or "bad,"

cholesterol

Nausea; diarrhea; rarely, the

harmful buildup of lactic acid

(lactic acidosis)

Thiazolidinediones

Rosiglitazone

(Avandia)

Pioglitazone (Actos)

Improve sensitivity to

insulin; inhibit the

release of glucose

from the liver

May slightly increase high-

density lipoprotein (HDL),

or "good," cholesterol

Heart failure; heart attack;

stroke; liver disease

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Alpha-glucosidase

inhibitors

Acarbose (Precose)

Miglitol (Glyset)

Slow the breakdown

of starches and some

sugars

Don't cause weight gain

Stomach pain; gas; diarrhea

Injectable medications

Medications

Action

Advantages

Possible side effects

Amylin mimetics

Pramlintide (Symlin)

Stimulate the release

of insulin; used with

insulin injections

May suppress hunger; may

promote modest weight

loss

Hypoglycemia; nausea or

vomiting; headache; redness

and irritation at injection site

Incretin mimetics

Exenatide (Byetta)

Liraglutide (Victoza)

Stimulate the release

of insulin; used with

metformin and

sulfonylurea

May suppress hunger; may

promote modest weight

loss

Nausea or vomiting;

headache; dizziness; kidney

damage or failure

monitor lipid levels for avandiamust be cautious if pt has past history of

heart failure

alpha inhibitors- believed to help with weight loss, when person ingests a lot

of starches really helps in the breakdown

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Drugs for Diabetes Mellitus

What is diabetes? Basically, a lack of insulin or ineffective use of insulin causingsugar to build up in the blood.

Functions of Insulin:

Allows glucose into cells

Allows glucose to enter liver

Prevents fat breakdown Stores excess calories as fat

Who gets diabetes?

Type I Diabetes

No insulin, must be given by injection, prefer use of SQ insulin pump

Ketone prone

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Autoimmune disease

Type II Diabetes

Insulin resistance

Deficient insulin secretion

Obesity contributes significantly, losing weight decreases insulinresistance

Blood sugar control = 70-140 mg/dl. The ADA recommends keeping blood sugaras close to 110 as possible.Hemoglobin A1C expressed as a %, reflects the average blood glucose over thepast 3 months.

ADA now recommends that A1C be used to diagnose type 2 and screen forprediabetes. Normal Hemoglobin A1C =5%.5.7-6.4 pre-diabetic. < 7.0 is thetarget for a diabetic..

A1c (%) Blood glucose(mg/dL)

6 126

7 154

8 183

9 212

10 240

Complications of diabetes mellitus (DM):

Stroke

ESRD (end stage renal failure) Heart disease

Diabetic Retinopathy, neuropathy

Foot/leg amputation

Oral Agents for Diabetes

Sulfonylureas-increase insulin secretionmechanism of action-improves insulin production from functioning beta cellsnot a good agent to be used alone; hypoglycemia reaction

*Glyburide(micronase) should be taken with meals

*Glipizide (glucotrol) should be taken before meals end up gaining weight

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Biguanides-decrease hepatic glucose production, will not cause hypoglycemiamechanism of action-while in a fasting state, will diminish overproduction ofglucose from the liver.-only comes in certain dose ratios

*Metformin(glucophage, glucophage XR)-lactic acidosis serious side effectContraindicated with contrast dye - Must HOLD if IV contrast dye given. In orderto use dye must be greater than 1.5

Thiazolidinediones TZDs glitazones-mechanism of action-decreases insulin resistance at the cell level. May causefluid retention, use caution with history of CHF.*rosiglitazone(avandia)-liver function tests required!pioglitazone(Actos)

BLACK BOX WARNINGfor Avandiaincreased risk of heart disease andstroke. May cause fluid retention/edema, therefore contraindicated in pts. withCHF.September, 2010FDA advised people to stop taking unless they were not ableto lower blood sugar with any other treatment.In Europe, the FDA equivalent has stopped the use of this drug. (EuropeanMedicines Agency)

Evidence- based Recommendation: TZDs ( avandia and actos) are NOT first-line options. Metformin is first line recommendation.

Combination Drugs*Glucovance-Glyburide/metformin -sulfonylurea + biguanide

*Avandamet-rosiglitazone/metformin TZD + biguanide

Types of Insulin

Short or Rapid ActingLispro (Humalog)- onset 15, peaks 30-1.5hrs.

Aspart (Novolog)-onset 10, peaks 1-3 hrs.Regular (Humulin R, Novolin R, Regular Iletin II)-onset 30-1 hr, peaks 2-4hrs.

Intermediate- NPH, Lente

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Long Acting-Glargine (Lantus)- peakless, duration 24 hrs.

Combo Mixtures-

Insulin Pumps -3X as many diabetics are now using insulin pumps. Type 1

&2.Pumps use rapid acting insulinLispro (Humalog), Aspart (Novolog). 50%delivered at a continuous basal rate, the remaining ia given as a BOLUS atmeals or snacks. Pumps are not for everyone. They are ore expensive andrequire more training.Medicare and most insurers do cover pumps.

Euglycemic protocol- sliding scale insulin used for non-diabetic and diabeticpatients.

Protocol extended beyond the diabetic population If patients show very high blood sugars after surgery; due to stress

of surgery; used to help them recover quickly

Hypoglycemiarecognize signs/symptoms. Including: headache, confusion,blurred vision, fatigue, hunger, irritability, shakinessCauses- too much insulin, skipping meals, not eating food,Treat if blood glucose is < 60 mg/dl. 15 grams of a simple CHO (6 ounces of

juice or fruit juice; regular soda). If not able t o swallow safely1 mg. glucagonIM or 25 gms. 50% dextrose IV.-recheck in 15 minutes-If patient is not responding well and cannot swallowgive IM glucagon; thepatients families are given

Hyperglycemia-

As blood glucose increases, the blood (intravascular space)becomes more hyperosmolar

Cellular dehydration occurs as the hyperosmolar intravascularspace draws fluid from the more dilute intracellular and interstitialspaces

Recognize signs and symptoms:o Polyuria, polydyspia, unexplained weight loss, sore that is

slow to heal (or doesnt heal)

If doesnt get treated, very high blood sugars can cause disruption

in fluid and electrolyte; causing them to become comatpossiblyhave a seizure

Insulin Aspart

Adult, adolescents, child

Intermittent SQ or continuous SQ

Rapid Acting

Onset 10-20 mins

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Duration 3-5 hours

2-4 inj daily just prior to meal

Intermittent SQ 50-70% of total daily insulin may be given Aspart; remainder should

be intermediate of long acting insulin

Continuous: external insulin pump via continuous SQ infusion insulin dose should be

based on previous regimen

Insulin Lispro

Adult, adolescence, child

SQ 15 min before meals

Continuous SQ infusion (external insulin pump)

With infusion total daily dose should be based on previous regimen

50% given at meal related boluses remainder in basal infusion

Rapid acting

Onset 15-30 mins

Peak 30 mins to 1.5 hours Duration 3-5 hours

Insulin Glargine

Adult and child

SQ 10 international units/day

Range 2-10 international units/day

Long acting

Onset 1.5 hours

No peak

Duration >24 hours

Regular Insulin

Adult

IV 5-10 units/hr until desired response then switch to SQ

SQ 30 mins before meal

Short acting

Onset 30 mins

Peak 2.5-5 hours

Duration 7 hours

Whenregular insulin is administered IV monitor glucose, K+, often to prevent fatalhypoglycemia, and hypokalemia

Side Effects: blurred vision, dry mouth, flushing, rash, swelling, redness, peripheral

edema, hypoglycemia, anaphylaxis

Interactions:

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alcohol, beta blockers, anabolic steroids, MAOIs increase hypoglycemia

Thiazides, thyroid hormones, oral contraceptives, epinephrine DECREASE

hypoglycemia

Decrease K+ and Ca+ lab values

Nursing Considerations Assess urine ketones during illness; insulin requirement may increase during stress,

illness, and surgery

Assess hypoglycemic reaction that can occur during peak time (sweating, weakness,

dizziness, chills, confusion, headache, nausea, rapid weak pulse, fatigue, tachy

Assess hyperglycemia, acetone breath, polyuria, fatigue, polydipsia, flushed, dry

skin, lethargy

ORGAN TRANSPLANT

Facts:

Anyone can be a potential donor regardless of race, age, or med history

All major religions in US support

Organ, eye, & tissue donation can only be considered if you are deceased

When on waiting list, what matters is: severity of illness, time spent waiting, blood type, andother important med info (not financial or celeb status)

Open casket funeral IS possible

No cost to donor or family for organ or tissue donation

A donor card and drivers license with an organ donor designation may notsatisfy yourstates requirementsIn Wisconsin:

Registering indicates legal consent for donation

A WI citizen who is at least 15 yrs of age and has a drivers license and state ID canregister

If a minor, parents can override decision

Over 40 state donor registries

Registry is maintained by the WI Dept of Health Services in cooperation with WI Dept ofTransportation

Immunology The immune system distinguishes self from non-self and protects host from

foreign threats Antibody: A protein molecule produced by the immune system in response

to a foreign body, such as a virus or a transplanted organ Antigen: An antigen is any substance that causes your immune system to

produce antibodies against it. T-cell: Cells in thymus that attack antigens on cell membranes B-cell: Cells in bone marrow that differentiate into plasma cells which

produce antibodies

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Human Leukocyte Antigens (HLA) Human Major Histocompatibility complexis a cluster of genes on

chromosome 6 that encodes HLAs Molecules found on cells in the bodies that are inherited genetically.

Determines compatibility between a donor and recipients. Main antigens looked at in transplantation:

o 1. HLA-Ao 2. HLA-Bo 3. HLA-DR

A person receives a total of 3 antigens from each parent, so each person has6 antigens

Panel Reactive Antibody Definition: Measure of a patients level of sensitization to donor antigens. The % of cells from a panel of blood donors against which a potential

recipient serum reacts

PRAreflects the % of the general population that a potential recipient makesantibodies against.o Can range from 0-100%o Usually >80% is considered highly sensitized

The higherthe PRA, the more sensitizeda patient is to the general donorpool (thus, the more difficult it is to find a suitable donor)

A patient may become sensitized as a result of pregnancy, a bloodtransfusion, or a previous transplant.

Crossmatch Definition: a blood test to determine compatibility between donor and

recipient

Occurs directly prior to transplantation (+) crossmatch incompatibility

o hyperacute antibody mediated rejection may occur if transplantproceeds

(-) crossmatch transplant can occur

End Stage Organ Failure Kidney

o Hemodialysis, Peritoneal Dialysis, or Renal Transplantation (livingor deceased donor)

o GFR less than 15% or Dialysiso Diabetes, Hypertension, Polycystic Kidney Diseaseo RISK- age younger than two, older than 7, advanced untreatable

cardiac disease, active cancer, chemical dependency, chronicinfections or systemic disease, coagulopathies and certain immunedisorders

Pancreaso Insulin therapy, Pancreas Transplantation, or Islet cell

Transplantationo Uncontrolled Type I Diabetes Mellitus

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Blood Flow ComplicationsThrombosis Definition: blood clot in an artery or vein Signs:

o Kidney Sudden decrease in UO Increased creatinine Hematuria

o Pancreas Sudden elevation in BG Acute abdominal pain Increased serum amylase

o Liver Increased ALT/AST

Diagnosis: U/S, Scan Treatment:OR, AnticoagulationHematoma Definition: collection of blood in the abdomen Signs: hypotension/tachycardia, increased pain, decreased Hct Diagnosis: CT Treatment: OR, RBC infusions

Surgical ComplicationsAnastomotic Leak Definition: tear at connection of donor and recipient anatomy Signs:

o Kidney Increased creatinine Decreased UO Yellow fluid draining from incision (with higher creatinine

than serum) Increased pain

o Pancreas Fever Elevated WBC Elevated serum amylase Abdominal pain

o Liver

Abdominal pain Increased LFTs Increased bilious drainage from JP (with higher bilirubin

than serum) Diagnosis: U/S, Scan, CT Treatment:

o Kidney: Foley/nephrostomy tubeo Pancreas:drain placement

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o Liver:ERCOo OR, IV Abx

Obstruction Definition: blockage of flow Signs:

o Kidney Increased creatinine Decreased UO hydronephrosis

o Liver Increased Alk phos & bilirubin

Diagnosis: U/S, Scan, ERCP Treatment: based on time of event in postop period, ERCP/PTC (liver)

Goal of Ideal Immunosuppression

Immunosuppression Induction

o Basiliximab (Simulect) Monoclonal Binds T cell receptor for interleukin-2 IV infusion intraop and on POD #4 Few GI side effects

o Antithymocyte Globulin (Thymoglobulin) Polyclonal T cell depletion IV infusion intraop and up to 10 days postop Premeds

Chills, fever, pulmonary edema, thrombocytopenia,leukopenia

Maintenanceo Prednisone

First major immunosuppressant Now try to supplement with others and decrease dose Steroid-free protocols PO and IV Inhibits T cells production Many side effects:

Hyperglycemia, hypertension, weight gain & swelling,mood changes, osteoporosis, dyslipidemia, gastric

ulcerso Mycophenolate Mofetil (Cellcept, Myfortic)

Inhibits proliferation of B & T cells PO & IV GI side effects less with Myfortic S/E: leukopenia, thrombocytopenia, anemia

o Calcium Inhibitors

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Tacrolimus (Prograf, FK-506) or Cyclosporine (Gengraf,Neoral)

Inhibit production and release of IL-2 & T-cellactivation and proliferation

Take with or without food consistently Tacrolimus is more potent than cyclosporine Many drug interactions Side effects:

o Nephrotoxicityo Hyperkalemia, hypomagnesaemiao Hypertension, hyperlipidemiao Hyperglycemia

12 hour trough levels drawn to maintain appropriateimmunosuppression

Rejection Treatmento Hyperacute Rejection

Preformed antibodies to ABO blood group antigens or HLA

antigens are present Very rare due to crossmatching Occurs within hours of revascularization Must remove kidney Occurs within 48 hours after surgery Findings: fever, hypertension, and pain at the transplant site Tx is immediate and removal

o Acute Cellular Rejection T cell mediated injury Most common type of rejection Most common in first 3 months after transplant (occurs 1

week to 2 years after surgery)

Findings- olguria, anuria, low-grade fever, hypertension,tenderness over transplanted kidney, lethargy, azotemia,and fluid retention.

Increases risk for chronic rejection Diagnosed by biopsy Can be mild to severe but is almost always reversible Treatment:

Corticosteroids, Increased CNI, Thymoglobulin Decreased doses of immunosuppressive meds

o Antibody Mediated (Humoral) Rejection Antibodies injure organ Diagnosed by positive C4D stain on biopsy

Monitor levels of donor specific antibodies Treatment:

Plasmapheresis Immunoglobulin

o Chronic Rejection Slow decline in organ function Gradually occurs over months to years

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Findings- gradual return of azotemia, fluid retention,electrolyte imbalances, and fatigue

May be related to multiple acute rejection episodes and CNInephrotoxicity

No tx except retransplantation (tx conservative until dialysisrequired)

Symptoms of rejection: Kidney

o Increased creatinineo Decreased UOo Increased wt and swellingo Fevero Pain over organ

Pancreaso Increased serum amylaseo Increased blood glucoseo Fevero

Pain over organ Liver

o Increased LFTso Fevero Pain over organ

Hearto Fatigueo Hypotensiono Jugular venous distentiono S3 heart soundso Arrhythmias

Lung

o Fevero Decreased oxygenationo Infiltrates on CXRo Pulmonary edema

Infection Solid organ transplant patients are at high risk for infections Prophylaxis

o Pretransplant: immunizationso Peritransplant: antibioticso Posttransplant:

TMP/sulfa (val)ganciclovir

(val)acyclovir clotrimazole

Bacterial Infection Mostly want to prevent against Pneumocystis Carinil Pneumonia (PCP) Symptoms of PCP:

o Fever, dyspnea, cougho Elevated EBCSo Patchy interstitial infiltrates on chest X-ray

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Prophylaxis and Treatmento TMP/Sulfa (Bactrim)

Usually once daily for 1 yearo Pentamidine inhalation

Once monthly for 6 months

Viral Infections-CMV Cytalomegalovirus (CMV) is the most common opportunistic infection in

transplant patients CMV infection vs CMV disease

o CMV Infection: detection of virus via molecular techniques orchanges in serology

o CMV Disease: requires clinical signs and symptoms Fever, leukopenia/neutropenia, organ involvement

Diagnosis: CMV PCR, Biopsy Risk Factors:

o CMV negative recipients from a positive donor

o Patients who received Thymo Prophylaxis (strongerimmunosuppresants) o Dosed based on risk factorso 3 monthso Valgancicloviro Acyclovir

Treatmento IV Ganciclovir

5 mg/kg IV Q12Ho Valganciclovir

900 mg PO BIDBK Virus

Definition: Polyomavirus causing a latent kidney infection that reactivateswhen patient is immunosuppressed

Usually occurs 6 month post transplant Symptoms: increased creatinine Diagnosis: Biopsy Treatment:

o Decreased immunosuppressiono Leflunomide and cidofovir

Fungal Infections Fungal infection of the mouth and tongue Prophylaxis/Treatment

o Nystatino Clotrimazoleo BID for 3 months

Post-transplant Lymphoproliferative Disorder Definition: Malignancy after transplant possibly related to EBV infection

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Symptoms: fever, malaise, leukopenia, adenopathy, sore throat, graftdysfunction

Diagnosis: Biopsy Treatment: Decrease immunosuppression, Chemo

Other Complications Delayed Graft Function

o Definition: insufficient kidney function post transplant due towarm ischemic time

o Treatment:based on duration, diuretics, HD HTN Hyperlipidemia Diabetes

Retransplantation Failure

o Immediate post op complication

o Rejectiono Recurrent diseaseo Primary non-function

Immunologic Factorso Increased PRA/Highly sensitizedo Exhausted possible living donor options

Patient Education Begins immediately upon admission Primary nursing and responsibilities

o Med review with SA sheets with each med passo Review of daily labs and VS, record in book

o Discharge planning Daily classes

o Pharmacy-medicationo Nursing- homecare, lab values and fluid balance, and

complications Evidence based practice and patient education

Recent Advances in Transplantation Most advances related to increasing donor pool Living liver Donation after cardiac death Extended criteria donors CDC high risk donors ABO/HLA incompatible Paired kidney exchange

ATI post procedure-renal Assess/monitor VS every 15 mins initially and advance to every hour;

maintain BP within parameters

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Intake and output hourly (UO should be greater than 30 mL/hrnotifyprovider of oliguria as evidenced by UO of 100-400 mL in 24 hr)

Urine appearance and odor hourly (initially pink and bloody, graduallyreturning to normal in a few days to several weeks)

ACUTE/CHRONIC RENAL FAILURE

Review of kidney function:

Regulation of fluid volume- Na+ & H20

Elimination of waste products-nitrogen wastes

Regulation of BP- renin & aldosterone response

Erythropesis-erythropoetin production

Metabolism of vit D- kidneys necessary to metabolize vit D to its active form which is neededfor calcium absorption

ACUTE KIDNEY INJURY

Involves rapid loss of kidney function

Normal GFR- Glomerular filtration rate 125 mL/min, which is reflected by urinary creatinineclearance

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o 6X increase risk of deatho 40-60% mortality if dialysis is require

ARF SyndromesPrerenal ARF

Volume Depletion

Decreased Effective Blood Volume Altered Intrarenal Hemodynamics

Intrinsic ARF

Acute tubular necrosis

Ischemia, nephrotoxicity, interstitial nephritis, glomerulonephritis

Postrenal ARF

Obstructiono Upper tract obstructiono Lower tract obstruction

Least common cause of AKI

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o Patients usually oliguric/anuric

Post-opo 1-5% CABG patients require dialysis-mortality rate is almost 65%o Risk factors: prior renal disease, 70% left main disease, hx of PVD, cardiogenic

shock

Rhabdomyolysis

o Occurs from crushing injurieso Traumatic cell injuryo ARF with CPKs >100,000o Nontraumatic causes: pressure from immobilizationo Need aggressive volume replacement

NSAIDS & COX II

o Inhibit production of prostaglandins which normally vasodilateo Result is afferent arteriole vasconstrictiono NSAIDS can result in: acute renal failure, nephrotoxic syndrome with nephritis

Contrast Dye

o Same risk factorso Volume of contrasto Esp cautious if creatinine >2.0

Amphotericin B

o Incidence about 30%o 50% less tocivity when liposomal preparation used (amphotericin B liposome)o risk factors dose and duration related

Amnioglycosideso 10-15% of patients, treated for 7-10 dayso Less toxicity with once daily dosingo Other risk factors: diabetes, CHF, volume depletion, NSAIDS, ACE inhibitors

(bilateral renal stenosis)

Management of ARF

Closely monitored fluid infusion

Minimal use of vasopressors

Avoid hypotension

Low dose dopamine (either it will work or it wont)

Diuretics-loop and osmotic

Peritoneal dialysis

Hemodialysis

Watch weight- 1 kg (2.2 lb) daily weight increase is approx 1 L of fluid retained

Provide diet high in carbs and moderate in fat

Fluid restriction

MedsCardiac Glycoside (Digoxin)

Increases contractility of myocardium and promotes UO

Take apical pulse 1 min prior to med; notify if HR less than 60

Notify if vision changes or sensitivity to light or behavior changes

Sodium Polystyrene (Kayexalate)

Increase elimination of potassium

Cautious with pts w HF, HTN, edema, & taking Digoxin

Erythropoietin alfa (Epogen, Procrit)

Stimulates production of RBCs, given for anemia

Contraindicated in pts with uncontrolled HTN and used cautiously in pts w bone marrowcancer

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Have blood drawn 2x weekly to monitor hemo and hct

Iron supplement (Ferrous Sulfate)

Increases level of iron in blood

Adm after dialysis if possible

Stool softener used with cause causes constipation

Aluminum hydroxide gel (Amphojel)

Phosphate binder used to increase elimination of phophate

Use stool softener

Contraindicated in pts with GI disorders

Diuretics (except in ESRD) (Lasix)

Excrete excess fluidsLab Tests

Urinalysiso Hematuria, proteinuria, and alterations in specific gravity

Serum creatinineo Gradual increase of 1-2mg/dL per every 24-48 hr for ARF

BUNo 80-100 mg/dL within 1 week with ARF

Serum electrolyteso Decreased sodium (dilutional) and calcium, increased potassium, phosphorus,

magnesium

Complete Blood Count (CBC)o Decreased hemoglobin and hematocrit from anemia

DIALYSIS

Dialysis

Movement of fluid/molecules across a semipermeable membrane from one

compartment to another Used to correct fluid/electrolyte imbalances and to remove waste products in renal

failure

Treat drug overdoses (Lithium, ethylene glycol, aspirin)

Two methods available: Hemodialysis, Peritoneal Dialysis

Begins when pts uremia can no longer be adequately managed conservatively

Initiated with GFR (or creatinine clearance)

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Osmosis: Movement of fluid from an area of lesser concentration to an area ofgreater concentration of solutes

Ultrafiltration: Water and fluid removal; Results when there is an osmotic gradientacross the membrane

PERITONEAL DIALYSIS

Peritoneal access is obtained by inserting a catheter through the anterior wall Technique for catheter placement varies

Usually done via surgery

Continuous exchanges usually needed

Portable system but is time consuming

Solution

Available in 1 or 2 L plastic bags with glucose concentration of 1.5%, 2.5%, &4-25%

Electrolyte composition similar to plasma

Solution warmed to body temp

CyclesThree phases of PD cycle1. Inflow (fill)

Prescribed amount of solution infused through established catheter over about 10minutes

After solution infused, inflow clamp closed to prevent air from entering tubing2. Dwell (equilibration)

Diffusion and osmosis occur between patients blood and peritoneal cavity

Duration of time varies depending on method3. Drain

15-30 minutes

may be facilitated by gently

massaging abdomen or changingposition

Peritoneal Dialysis Systems

Automated peritoneal dialysis(APD)

o Cycler delivers thedialysate

o Times and controls fill, dwell, & drain

Continuous ambulatory peritoneal dialysis (CAPD)o Manual exchange

Nursing Actions

Assess dry weight, serum electrolytes, creatinine, BUN, and blood glucose

Instruct- may feel fullness when dialysate is dwelling. May be discomfort initially withdialysate infusion.

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AV Fistula vs. graft

DOUBLE LUMEN VENOUS

CATHETER

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Hemodialysis Dialyzers

Long plastic cartridge that contains thousands of parallel hollow tubes or fibers

Fibers are semipermeable membrane

Resuable- approx 20 treatments

Costly

Labor intensive-processing, cleaningHD Procedure

Two needles placed in fistula or graft

Needle closer to fistula or red catheter lumen pulls blood from patient and sends todialyzer

Blood returned from dialyzer to patient through second needle or blue catheter

Before treatment, nurse should:o Complete assessment of fluid status, condition of access, temperature,

skin condition. Check patency of access device. Administration of drugs-hold

During treatment:o Be alert to changes in conditiono Perform vital signs every 30-60 mins

HD Complications

Hypotensiono Actions- replace fluid volume with transfusion of IV fluids or colloid as

prescribed, slow rate. Lower HOB. Discontinue if severe.

Muscle cramps Loss of blood

o (Anemia); administer erythropoietin to stimulate production of RBCS.Monitor for hypotension and tachy.

o Diet foods high in folate (beans, green veggies)

Hepatitis

Sepsis

HEMODIALYSIS

SYSTEM

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Disequilibrium syndrome: caused by too rapid a decrease of BUN and circulatingfluid volume. May result in cerebral edema and increased ICP

HD Advantages HD Disadvantages

Quick & efficient

Weekly exchanges as an output 3-4x/week

Prolongs life

No limit as to how long one can remainon dialysis

Allows wait for kidney transplant

Exchange rate 3-4 hours

AV fistula takes 6 weeks to cure

AV graft ready in 2 weeks

Stresses a compromised cardiosystem

Does not remove phosphorous

Access may clot

Heparin required

May need dietary restrictions

Dialyzable drugs

Hemodialysis

Requires an invasive access

AV fistula

AV graft Dual-lumen venous catheter

Heparin is required

Weekly exchanges as an outpatient 3-4xo Usually 3 times per week, for 3-5 hours. Two needles inserted one into

artery and one in vein.

Instruct pt to notify of muscle cramps, headaches, nausea, dizziness

If bleeding apply light pressure, notify provider if bleeding continues after 30 minutes

Nursing Implications

Check for patency of access devices

Monitoring v/s weight

Expected following dialysis- decreased in BP, wt, and lab values Typical meds:

o Phosphate binder*o Vitamin D (calcitrol)o Epoetin alfa (Epogen)o Iron supplemento Folic acido Protamine sulfate ready if needed to reverse heparino Renal diet? What is it? increase in dietary protein

Tips for Dialysis Patient Care (Access Device)

DO NOT draw blood for a dialysis access

DO NOT obtain BP readings from an arm with a access device (ex. Fistula or graft)

Medications

BP meds should be help prior to dialysis

Administer antibiotics AFTER dialysis treatment

Pain medications are often dialyzed off during dialysis

DO NOT use morphine with dialysis patients, drug metabolites are not dialyzed off

Phosphate binders MUST be taken with food (ex. Tums, calcium acetate, Fosrenal,Renvia)

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EKG

ECG: Monitors cardiac activity

Can be monitored by a standard 12 lead ECG (resting ECG),

ambulatory ECG (Holter monitoring), continuous cardiac

monitoring, or telemetry

Electrocardiography uses electrocardiograph to record

electrical activity of heart over time. Connect by wires (leads)

to skin electrodes placed on the chest and limbs of a pt

Telemetry tracing:allows pt to ambulate while maintaining proximity

to monitoring system

ECG

Three basic parts:

Speed/rate

Regularity

Rhythm

Areas of note:

Sinus atrial node

AV node ventricle

Indications: bradycardia, heart block, A fib, Supra tachy, ventricular

tachy, ven fib

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Patient presentation: cardiovascular disease, MI, hypoxia, acid-base

imbalances, electrolyte disturbances, chronic renal failure, liver, or

lung disease, pericarditis, drug or alch abuse, hypovolemia, shock

The life threatening effects of dysrhythmias are generally related todecreased cardiac output and ineffective tissue perfusion

Cardiac dysrhythmias are a primary cause of death in pts suffering

acute MI and other sudden death disorders

12 lead ECG Prep:

Position in supine position with chest exposed

Wash skin to remove oils

Attach one electrode to each extremity by applying electrodes to flatsurfaces above wrists and ankles and other six electrodes to chest,

avoiding chest hair (may need to be shaved on males)

Intraprocedure:

o Instruct pt to remain still and breathe normally

o Monitor for s/s of dysrhythmia (chest pain, decreased LOC,

and SOB) & hypoxia

Postprocedure

o Remove leads, print report, notify MD

o Apply holter monitor if on telemetry unit or needs

continuous

o Continue to monitor for s/s dys or hypoxia

Basics of ECG

P wave

o Atrial contraction (depolarization)

o Systole

QRS

o Ventricular contraction (depolarization)

o Systole

QT

o Repolarization

o Diastole

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Reading a ECG

Each small box: 0.04

Each large box: 0.20

Normal PR: .12 to .20

Normal QRS: 0.04-.12

Sinus Rhythms

Normal Sinus Rhythms

Regular

Rate 60-120

Every P matches up with a

QRS

ST

elevation

STEMI

heart

attack

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PR-normal

QRS-normal

other sinus rhythms

Sinus Tachycardia Same as normal sinus rhythm but rate

>120

Treatments:

o Remove trigger: stress, caffeine, hypovolemia, hypotension,

hyperthyroidism, fever

o Meds:Beta blockers (Class II antiarrhthymic)

Supra-Ventricular Tachycardia

A tachy similar to sinus tachy but doesnt originate from the SAnode (usually involves the AV node)

Treatments:

o Valsalva maneuver-trigger the vagus nerve

o Metoprolol

o Adenosine

o ATI- amiodarone, adenosine, and verapamil (w/pulse)

Electrical management- synchronized cardioversion

Significance of Sinus Tachycardia

Can be an early sign of more significant issues (shock, internal

bleeding, etc)

May become uncompensated

May lead to an MI

Sinus Bradycardia

Same qualifications as

sinus rhythm but

rate is

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o Meds:Atropine & isoproterenol

o Treat if client is symptomatic

Significance:

o May be normal- particularly in athletes

o Can complicate orthostatic hypotensiono Symptoms may be severeincluding syncope, impaired

renal perfusion, etc

o May require a pacemaker-SSS

o Electrical management-pacemaker

Atrial Arrhythmias

Atrial Flutter-the artria contract very quickly causing a saw tooth

patterno No P wave present

o QRS are regular and normal

o Rate is variable

o If rate is > approx 180 or patient is having severe symptoms

it is considered uncompensated A. flutter.

Atrial fibrillation:atria fibrillate (quiver)- a jagged irregular line

in p wave area

o No p wave present

o QRS are regular and normal

o Rate is variable

o If rate is >approx 180 or patient is having severe symptoms

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it is considered A. fib

Significance of Atrial Arrthythmias

Reduces cardiac output by eliminating atrial kick

Can decrease BP, may lead to CHF or MI

Coagulation risks with lack of turbulent flow of blood in atria

Causes: age, enlarged heart, cardiac injury

Treatments

Cardioversion

o Synchronized, direct electrical shock

Meds

o Amiodarone (IV or PO)/Dronaderone (PO) (Class III)

o Tikosyn/Doefetilide (PO)

o Betablockers- metoprolol (IV/PO)

o Calcium channel blockers- Diltiazem (IV/PO) (Class IV)

o ATI- amiodarone, adenosine, and verapamil (w/pulse) Ablation

o Radio frequency or cyro (cold) to kill cells of aberrant

pathway

Ventricular Arrhythmias

Ventricular tachycardia

o Fast rate HR>100

o QRS still present-often wide (>.12) and irregular

o No synchronization with P waves and QRSo P waves may not be recognizable

o ATI- amiodarone, adenosine, and verapamil (w/pulse)

o W/o pulse- amiodarone, lidocaine, epinephrine--defib

o

o

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Preprocedure

If have a fib of unknown duration must

anticoagulate prior to therapy to prevent

dislodgement of thrombi into bloodstream

Monitor for pulmonary or systemic emboli following Embolism

o Cardioversion can dislodge blood clots

potentially causing:

Pulmonary embolism (dyspnea,

chest pain, air hunger & decreasing

sa02)

CVA ( decreased LOC, slurred

speech, and muscle

weakness/paralysis) MI (chest pain and ST segment

depression or elevation)

o Decreased CO & heart failure

s/s of decreased CO- hypotension,

syncope, increased HR

s/s HF- dyspea, productive cough,

edema, and venous distention

meds to increase output (inotropic

agents) and decrease cardiac

workload

o Defibrillation

The delivery of an unsynchronized, direct

countershock to the heart. Stops all electrical activity

of the heart allowing SA node to take over and re-

establish a perfusing rhythm.

Indications- ventricular fib or pulseless ventricular

tachy

o Postprocedure for C&D

Document: postprocedure rhythm, number of

attempts, energy settings, time, & response

Pts condition and state of consciousness following

Skin condition under electrodes

Implantable Cardioverter Defibrillator (ICD)

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o Education is extremely important

o Variety of emotions:

Fear of body image change

Fear of recurrent dysrhythmias

Expectation of pain w/ ICD discharge Anxiety about going home

o Participation in support groups is encouraged

Ablation/Cardiac catheterization

Meds

o Beta blockers

o Emergency drugs (epinephrine,

lidocaine,etc)

Pacemakers

Used to pace the heart when the normal conduction

pathway is damaged or diseased; battery operated

device that electrically stimulates the heart when

the natural pacemaker of the heart fails to

maintain acceptable rhythm

o Composed of two parts:

Pulse generator houses the E source (battery) and

control center

The electrodes are wires that attach to the myocardial

muscle on one side and connect to the pulse generator

on the other

o Pacing circuit consists of a power source, one or more

conducting (pacing) leads, and the myocardium

o Electrical signal (stimulus) travels from the pacemaker,

through the leads, to the wall of the myocardium

o Myocardium is captured and stimulated to contract

Initially indicated for symptomatic bradydysrhythmias

Other indications: complete heart bloc, sick sinus syndrome, sinus

arrest, asystole, atrial tachy, ventricular tachydys

client presentation:

o symptoms- dizzinesss, palpitations, chest pain or pressure,

anxiousness, fatigue nausea, difficulty breathing

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o signs- brady, tachy, abnormal ECG, dyspnea/tachypnea,

restlessness, distended jugular vein, vomiting, hypotension,

diaphoresis, decreased CO

Antiachycardia and overdrive pacing

o Antiachycardia pacing: delivery of a stimulus to theventricle to terminate tachydysrhythmias

o Overdrive pacing: pacing the atrium at rates of 200-500

impulses per minute to terminate atrial

tachys

Temporary pacemaker: Power source outside the

body

o Power source provided by external battery

back

o Instruct- keep dry, do not touch dials. Notable to shower.

o Only used in controlled environments with

continous monitoring

o Transvenous (endocardial)

Pacing wires are threaded through a large central

vein (subclavian, jugular, or femoral) and lodged into

the wall of the R ventricle (ventricular pacing), right

atrium (atrial pacing), or both chambers (dual)

o Epicardial

Pacemaker leads are attached directly to heart during

open heart surgery. Wires run externally through

chest incision and may be attached to an external

impulse generator if needed

Commonly used during and immediately following

open heart surgery

o Transcutaneous (External)

Pacing energy is delivered through the thoracic

musculature to the heart via two electrode patches

placed on skin

Requires large amount of E, which can be painful

Used only in emergency resuscitation of pt who dos

not have pacing wires inserted

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Assess pt for hiccups, which may mean generator is pacing the

diaphragm

Complications: (insertion)

Infection or hematoma

Pneumothorax or hemothorax arrhythmias

Patient teaching for Pacemaker & ICD Care

Avoid lifting arm above shoulder post-op (do not raise arm on

surgical side above shoulder for 1-2 weeks)

Avoid large strong electronic magnetic fields (Not able to have MRI

scan)

Microwave ovens are safe to use

May set off metal detector at airport Wear Medic Alert ID or bracelet at all times

Permanent

o 10 years on average

o take pulse daily at same time

o teach to set rate of pacemaker. Notify MD if HR less than 5

beats below pacer rate

o anyone touching client when device delivers shock, will

feel slight electric shock

o no contact sports or heavy lifting for 2 months

Extras

There can be blocks

o If the AV node fails to/incompletely conducts the signal

o These are named for their severity

There can be normal extra/early beats

o PVC- extra/early beat in the ventricle

o PAV-extra/early beat in the atria

Pacemakers

o Noted by a white vertical line before the P or QRS waves

o Conduction of electrical impulses through the SD node may