N440 Exam #1

Shock
Arterial blood gases
Mechanical ventilation
Adult respiratory distress syndrome
Acute complications of Diabetes Mellitus-Euglycemic protocols

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 breakdown produce 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
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 <7.30)
No acidosis
Kussmaul respirations
No Kussmaul respirations
Bicarbonate <15
Bicarb >20
Treatment
1. Rapid rehydration
o fluid deficit
as much as 6 L in DKA or 7-10 L (HHNS)
1 L NS fluid bolus
Further replacement depends on DKA or HHNS
With HHNS may give 10 L in 10 hrs
As BG approaches 200-250 mg/dl
Change IV fluid to D5.45 NaCl at approx 250-500 ml/hr
2. Gentle insulin administration IV
o Initial insulin bolus (regular insulin)
o Continuous IV infusion approx. 7-10 U/hr
o Goal is to decrease BF 50-70 mg/dl each hour. Once BG approx. 200
mg/dl change rate 3-6 U/hr
o Too fast BG correction cerebral edema
3. Monitor/restore electrolyte loss
o Restore electrolyte balance
K+ shifts with acidosis
As H+ (from ketones) more H= moves into cell from
vascular space
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 signal
cerebral 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

Stimulate the release

Work quickly

Severely low blood sugar

Repaglinide
(Prandin)

of insulin

(hypoglycemia); weight gain;

nausea; back pain; headache

Nateglinide (Starlix)
Sulfonylureas

Glipizide (Glucotrol)

Glimepiride

Stimulate the release

Work quickly

of insulin

Hypoglycemia; weight gain;

nausea; skin rash

(Amaryl)

Glyburide (DiaBeta,
Glynase)

Dipeptidy peptidase-4

Stimulate the release

(DPP-4) inhibitors

of insulin; inhibit the

infection; sore throat;

Saxagliptin

release of glucose

headache; inflammation of

(Onglyza)

from the liver

the pancreas (sitagliptin)

Sitagliptin (Januvia)

Linagliptin

Don't cause weight gain

Upper respiratory tract

(Tradjenta)
Biguanides

Inhibit the release of

May promote modest

Nausea; diarrhea; rarely, the

Metformin

glucose from the

weight loss and modest

harmful buildup of lactic

(Fortamet,

liver; improve

decline in low-density

acid (lactic acidosis)

Glucophage, others)

sensitivity to insulin

lipoprotein (LDL), or
"bad," cholesterol

Thiazolidinediones

Improve sensitivity to

May slightly increase

Heart failure; heart attack;

Rosiglitazone

insulin; inhibit the

high-density lipoprotein

stroke; liver disease

(Avandia)

release of glucose

(HDL), or "good,"

Pioglitazone (Actos)

from the liver

cholesterol

Alpha-glucosidase

Slow the breakdown

Don't cause weight gain

inhibitors

of starches and some

Acarbose (Precose)

Miglitol (Glyset)

sugars

Stomach pain; gas; diarrhea

Injectable medications

Medications

Action

Advantages

Possible side effects

Amylin mimetics

Stimulate the release

May suppress hunger;

Hypoglycemia; nausea or

Pramlintide

of insulin; used with

may promote modest

vomiting; headache; redness

(Symlin)

insulin injections

weight loss

and irritation at injection

site

Incretin mimetics

Stimulate the release

May suppress hunger;

Nausea or vomiting;

Exenatide (Byetta)

of insulin; used with

may promote modest

headache; dizziness; kidney

Liraglutide (Victoza)

metformin and

weight loss

damage or failure

sulfonylurea

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

Drugs for Diabetes Mellitus

What is diabetes? Basically, a lack of insulin or ineffective use of insulin causing
sugar 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

Autoimmune disease

Type II Diabetes
Insulin resistance
Deficient insulin secretion
Obesity contributes significantly,
resistance

losing

weight

decreases

insulin

Blood sugar control = 70-140 mg/dl. The ADA recommends keeping blood sugar
as close to 110 as possible.
Hemoglobin A1C expressed as a %, reflects the average blood glucose over the
past 3 months.
ADA now recommends that A1C be used to diagnose type 2 and screen for
prediabetes. Normal Hemoglobin A1C =5%.5.7-6.4 pre-diabetic. < 7.0 is the
target for a diabetic..
A1c (%)
6
7
8
9
10

Blood glucose
(mg/dL)
126
154
183
212
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 secretion
mechanism of action-improves insulin production from functioning beta cells
not 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

Biguanides-decrease hepatic glucose production, will not cause hypoglycemia

mechanism of action-while in a fasting state, will diminish overproduction of
glucose from the liver.
-only comes in certain dose ratios
*Metformin(glucophage, glucophage XR)-lactic acidosis serious side effect
Contraindicated with contrast dye - Must HOLD if IV contrast dye given. In order
to use dye must be greater than 1.5

Thiazolidinediones TZDs glitazonesmechanism of action-decreases insulin resistance at the cell level. May cause
fluid retention, use caution with history of CHF.
*rosiglitazone(avandia)-liver function tests required!
pioglitazone(Actos)
BLACK BOX WARNING for Avandia increased risk of heart disease and
stroke. May cause fluid retention/edema, therefore contraindicated in pts. with
CHF.
September, 2010 FDA advised people to stop taking unless they were not able
to lower blood sugar with any other treatment.
In Europe, the FDA equivalent has stopped the use of this drug. (European
Medicines Agency)
Evidence- based Recommendation: TZDs ( avandia and actos) are NOT firstline options. Metformin is first line recommendation.

Combination Drugs
*Glucovance-Glyburide/metformin-sulfonylurea + biguanide
*Avandamet-rosiglitazone/metformin TZD + biguanide

Types of Insulin

Short or Rapid Acting

Lispro (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 2-4
hrs.
Intermediate- NPH, Lente

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

Combo MixturesInsulin 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 at
meals or snacks. Pumps are not for everyone. They are ore expensive and
require more training.
Medicare and most insurers do cover pumps.
Euglycemic protocol- sliding scale insulin used for non-diabetic and diabetic
patients.
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
Hypoglycemia recognize signs/symptoms. Including: headache, confusion,
blurred vision, fatigue, hunger, irritability, shakiness
Causes- 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. glucagon
IM or 25 gms. 50% dextrose IV.
-recheck in 15 minutes
-If patient is not responding well and cannot swallowgive IM glucagon; the
patients families are given
Hyperglycemia As blood glucose increases, the blood (intravascular space)
becomes more hyperosmolar
Cellular dehydration occurs as the hyperosmolar intravascular
space draws fluid from the more dilute intracellular and interstitial
spaces
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 comatpossibly
have a seizure
Insulin Aspart
Adult, adolescents, child
Intermittent SQ or continuous SQ
Rapid Acting
Onset 10-20 mins

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 fatal
hypoglycemia, and hypokalemia
Side Effects: blurred vision, dry mouth, flushing, rash, swelling, redness, peripheral
edema, hypoglycemia, anaphylaxis
Interactions:

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

Arterial Blood Gases

pH 7.35-7.45
PaCO2 35-45 mmHg
HCO3 22-26 mEq/L
PaO2 80-100 mm/Hg
O2 sat >95-100%
If pH normal - fully compensated
If pH abnormal, but both systems moving in diff directions partial compensated
CO2 respiratory
HCO3 metabolic
ROMES (Respiratory opposite, metabolic equal)

Acute 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 infiltrates
o 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)
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
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 output
o 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
PEEP is added to the ventilator setting to increase
oxygenation and improve lung expansion
Wont be able to speak while endo tube in
Kinetic therapy
A special kinetic bed that rotates laterally alters clients
position to reduce atelectasis and improve ventilation
Nursing actions
o Begin slowly and gradually increase the degree of
rotation as tolerated
o Monitor ECG, SaO2, breath sounds, and BP
o Stop is pt becomes distressed
o Routine skin care to prevent skin breakdown
o Sedate as needed
Outcomes
o Pt will be able to breath independently with no
resp assistance

o Pt able to maintain an SaO2, greater than 90% on

room air
o Free of infection
o Maintain optimal physical and mental functioning
Complications
Endotracheal tube
o Trauma during inhalation or long term intubation
Can cause damage to trachea and vocal cords
Nursing actions: consider tracheostomy for LT ventilation
o Aspiration pneumonia
Actions: check cuff for leaks, assess suction contents for gastric
secretions, verify NG placement
o Infection
o Blocked endotracheal tube
The high pressure alarm on the ventilator may indicate a blocked
endotracheal tube
Nursing actions: suction secretions to relieve a mucous plug or
insert an oral airway to prevent biting on the tube
Altered position of endotracheal tube
Nursing action: position Q 1-2 hours, assess breath sounds, SaO2
and chest movement, secure endo tube per guidelines
Mechanical Ventilation
o Increased intrathoracic pressure
Positive pressure (PEEP) increases intrathoracic pressure, which
can cause a decreased blood return to the heart, decreased
cardiac output and/or hypotension
Decreased cardiac output can activate the renin-angiotensionaldosterone 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 increase
intrathroacic 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 circulation through
endothelial walls of pulmonary capillaries into lung
d. Results
i. Alveolar-capillary membrane damage (fluid starts leaking into
alveoli)
ii. Edema and flooded alveoli
iii. Inactivated surfactant (type II cells)
iv. Inflammation in lungs
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 out sometimes 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
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)

Shock Syndrome
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 damage organ failure
o Death
Diagnosis
MAP <60
Clinical s/s of hypoperfusion of vital organs
SBP + (2DBP)/3=MAP
Compensatory Mechanisms: Synpathetic Nervous System (SNS)-Adrenal Response Fight
or Flight Response
SNS-hormonal: Renin-angiotension system
o Decreased renal perfusion
o Releases renin angiotension I angiotension II potent vasconstriction
and releases aldosterone adrenal cortex sodium and water retention
o ADH acts on renal tubules to retain H20 ^ BP
SNS-hormonal: Adrenal Cortex
o Anterior pituitary releases adrenocorticotropic hormone: ACTH
o Stimulates adrenal Cx to release glucocorticoids
o Blood sugar increases to meet increased metabolic needs
Stages of Shock
Initial stage
o Tissues are underperfused, decreased CO2, increased anaerobic
metabolism, lactic acid is building
Compensatory stage
o Reversible
o SNS activated by low CO, attempting to compensate for the decrease
tissue perfusion
Progressive stage
o Failing compensatory mechanisms: profound vasoconstriction from the
SNS ISCHEMIA
o Lactic acid production is high metabolic acidosis
Irreversible or refractory stage
o Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur
o Death is IMMINENT

Ventilation

Lab Values
CVP (central venous pressure) 2-8mm
Amount of blood flow to right side of heart
Normal pulmonary wedge 6-12
Wedges into pulmonary artery, reflects pressure in the L side of the heart
D-dimer <250ng/mL
Sedimentation rate <20 mm/hr
BUN 5-25 mg/dl
Creatinine0.5-1.5
WBCs 4500-10,000
RBCs
Platelets 150,000-400,000
Hemoglobin (Hb) 13.5-17.5 M 12.0-16.0 F
Hematocrit (Hct) 41-53 M 36-46% F
Potassium 3.5-5.0
Sodium 135-145
Phosphorus 2.5-4.5 mg/dl
Alanine amniotransferase (ALT) serum 4-35 units/liter
Aspartate aminotransferase (AST) serum 8-33 units/liter