Exam 1 review
- DKA – Diabetic Ketoacidosis
o Patho: Happen mostly in Type 1 Diabetic patient. There is not enough insulin so
the body can’t allow the blood sugar into the cells for energy. So the blood sugar
become very high. So the body use protein and fat to break into energy.
 Remember: KETONES build up = ACIDOSIS.
o Risk factor:
 illness, infection, missed dosage insulin, untreated diabetes.
o S&S: (The onset is ABRUPT)
 Hyperglycemia (300-500 mg/dL)
 Polyuria and polydipsia -> cause increase thirst
 Ketosis and acidosis
 Dehydration, electrolytes loss, Increase urine output, Blurry vision,
hypotension from volume loss.
 Lack of insulin circulate in the body
 Metabolic acidosis cause GI symptoms - Acid breath “fruity breath”
 Kussmaul respiration: hyperventilated but not labored (trying to blow of
the Co2)
 Low pH, low bicarbonate and low PaCO2, increase creatine and
BUN.
o Treatment and intervention:
 First, Fluid replacement and electrolyte with NS
 Second, IV Regular Insulin
 Give IV potassium (K+) with fluid and insulin-> nurse monitor potassium
level.
 The insulin cause sugar and K+ to go in the cells, causing
hypokalemia unless we administer K+ with IV insulin.
 Third, start D5W when patient reach normal blood sugar (under 250-300)
 Give bicarbonate for metabolic acidosis.
 Monitor for hyperglycemia and hypoglycemia, neuro status, monitor HR
as hear issue can related to potassium level.
o Education:
 Teach pt to correctly take insulin even when they are sick and assess
blood sugar.
- HHNS – Hyperglycemic Hyperosmolar Nonketotic Syndrome
o Patho: happen mostly in Type 2 Diabetes patient. This is just high amount of
glucose in the blood. The problem with these patient is not insulin because they
can still produce insulin, its dehydration.
 Remember: No acidosis and no ketones
o Risk factor:
 Inadequate fluid intake, decrease kidney function, infection, stress, older
adults.
o S&S: ONSET IS GRADUAL
 Hyperglycemia (>600 mg/dL)
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 There is no metabolic acidosis. Btu can still have fruity smell.
 3 P’s -> polyuria, polydipsia, polyphagia)
 Dehydration (hypovolemia)
 Neurovascular changes (confusion, decrease LOC, headache)
o Treatment:
 Fluid and electrolytes monitor (K+)
 In patient with heart failure, we give ½ NS not NS because we
dont want fluid overload.
 We switch to D5W when blood sugar reach 250-300
 Give IV insulin and Potassium (K+)
 SubQ insulin.
SIADH – Syndrome of Inappropriate Antidiuretic Hormone Secretion
o Patho: this is when pituitary gland secretes to much ADH hormones. RETAIN
WATER. Causes are pulmonary disease (TB, pneumonia), brain/head injuries,
tumor.
 Patient retain fluid. Low serum osmolarity – low plasma– high urine
o S&S:
 Decrease urinary output of concentrated urine -> diluted blood
 Fluid volume overload, Weight gain without edema
 Hypertension, tachycardia
 Nausea and vomiting, Hyponatremia (-> confuse, seizures, headache,
coma, muscle weakness).
 High (>1.030) urinary specific gravity (normal specific gravity are .0051.030) -> more concentrated urine will increase this number increase.
 Low (<135) sodium in the blood – risk for heart failure.
o Intervention:
 Key: treating underlying cause and restrict fluid.
 Implement seizure precautions, neuro status.
 Elevate HOB 10 degree to promote venous return
 Restrict fluid intake – 800ml/day, monitor intake and output, daily
weight, edema, urine concentration.
 Meds: loop diuretic and vasopressin antagonists. Give 3% hypertonic
solution. Can also get Lasix – check BP, kidney function and sodium level.
 Diet: restrict fluid, increase salt and protein.
o Education:
DI – diabetes insipidus (DI- think Dry Inside)
o Patho: this is when pituitary gland secretes not enough ADH hormones. LOSS
WATER. Causes are head trauma (this is important because the pituitary gland is
in the brain), brain tumor, manipulation of the pituitary gland, infection to the
CNS (meningitis), renal failure.
 Patients get grid of excessive fluid. High serum osmolarity - High plasma
- low urine.
 Patient will be very thirsty and craving for cold water all the time.
o S&S:
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Excretes large amounts of diluted urine -> concentrated blood
polydipsia (increased thirst), polyuria (increased urine output)
dehydration, decreased skin turgor, dry mucous membranes.
Muscle pain and weakness, headache
Postural hypotension, tachycardia
Low (<1.005) urinary specific gravity (normal specific gravity are 1.0051.030) -> more diluted urine will increase this number decrease.
 High sodium (>145)
 Fluid deprivation test:
 Withhold fluids for 8-12 hours until 3-5% of body weight lost.
 Is there is increase specific gravity and osmolality of the urine. its
confirmed DI.
 Stop the test if there is excessive weight loss.
o Intervention:
 Key is to replace ADH hormone, ensure adequate fluid replacement,
treating underlying cause.
 Monitor intake and output (hourly urine output record) and daily weight,
vitals, monitor hypovolemic shock.
 Watch electrolytes imbalance. Monitor cardiac and hypotension.
 ADH replacement (replace the missing hormone)
 Vasopressin (we know the meds working when urine output
decrease)
 Desmopressin (can cause vaso-constriction)
 Adequate fluids
 IV hypotonic solution replacement – NS
 Restrict diuretic such as caffeine, alcohol)
o Education:
 It’s important to treat the underlying causes.
Chest trauma – trauma respiratory complication:
o Chest trauma can occur on its own or with trauma. Due to the disruption of the
airway, pt can have atelectasis.
 Blunt trauma: sternal/rib fracture, flail chest,
 Penetrating trauma: pneumothorax
o Intervention: Airways monitor and suctioning secretion, breathing, depth
 EKG, pulse ox, airway management.
 Patient might be combative. Fluid resuscitation. Stabilize the chest wall. –
in case of fracture ribs.
 Pain management, Monitor fluid imbalance. Coughing and deep
breathing
 Supportive care to managing the symptom more than surgery.
 DX: chest Xray, ABGs, pulmonary function test, breath sound.
 Pt might have constant cough, might need to be intubated.
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Atelectasis
o Closure or collapse of the lungs -> common in post-op pt.
 Obstructive -> by mucus
 Nonobstructive -> reduce ventilation.
o Chest X-ryas/ Ct, auscultation for decrease breath sounds and crackles.
o S&S: dyspnea, tachypnea, wheezing, tachycardia, cough, low o2 level.
o Education: early amputation turning and reposition in bed. Cough, incentive
spirometer.
o Meds: nebulizer with bronchodilators to assist with cough.
o Treat: chest tube, thoracentesis to drain fluid.
Pneumothorax – chest trauma
o Patho: lung collapse due to collection of air int eh pleural space.
 Causes -> trauma that blunt or penetrating, medical procedure like open
heart surgery or central line placement, gun shot or stab wound.
 Simple or spontaneous: from smoking, lung disease.
 Traumatic pneumothorax: blunt injuries rib fracture, penetrating the
chest – stab wound or gunshot) -> priority is to stop the flow of air
through the opening in the chest wall is lifesaving.
 Tension pneumothorax – complication of pneumothorax which pleural
space create a one-way valve that air collect in lungs and can’t escape->
result tension build up in the lung. This is medication emergency.
 S&S: jugular vein distension, compress on the heart (tachycardia,
hypotension, chest pain), compression on other lung (tachypnea,
hypoxia), trachea shifted.
 Management: chest tube, needle decompression to aspirate the
air.
 Beside tension, we have simple, spontaneous, and traumatic.
o S&S:
 Chest discomfort, dyspnea, tachypnea, anxious, use of accessory muscles,
hypoxemia, diminished or absent breath sounds,
o Management:
 Remove air or blood from the pleural sacs by inserting chest tube, sealed
with gauze impregnate with petrolatum for the open chest wound in
emergency. Or doing thoracentesis – needle for drainage.
o Intervention:
 Provide o2, positioning – fowler’s position
 Monitor chest tube drainage system.
Hemothorax – chest trauma
o Patho: lung collapse fu to a collection of blood in the pleural space.
 Causes: pneumothorax is often followed by hemothorax.
o Treatment: chest tube.
Sternal/ rib fractures
o Patho:
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o S&S:
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Rib fracture are the most common type of chest injuries resulting from
blunt trauma. Ribs 5-9 are the most common fracture because they are
least protected by the chest muscle.
If the fractured rub is splinted or displaced, it may damage the pleura,
lungs, and other internal organs.
Anterior chest pain, ecchymosis, crepitus, swelling, point tenderness,
pain.
 Pt more likely to breath shallow and avoid deep breath to prevent pain.
o Treatment
 Splint the chest, treat associated injuries, NSAIDs, opioids, nerve blocks.
 Chest binder might be use as supportive treatment to provide stability to
the chest wall and decrease pain.
Flail chest – chest trauma:
o Patho: Flail chest is frequently a complication of blunt chest trauma from
steering wheel injury – fracture of 3 or more adjacent ribs and sternum -> free
floating ribs and chest wall loosely stable.
 Paradoxical respirations (inwards movement of a segment of the thorax
during inspiration with outward movement during expiration)
o S&S:
 Paradoxical respirations, Severe pain in the chest
 Dyspnea, tachypnea, rapid and shallow respiration, tachycardia.
 The patient move air poorly, and movement of the thorax is asymmetric
and uncoordinated
o Management/ intervention:
 Controlling pain, ventilatory support (endotracheal intubation) – oxygen,
suctioning. -> to facilitate lung expansion.
 If affect small segment of the chest: ensure airway, positioning – Fowler’s
position, coughing, deep breathing, suctioning
 Physical assessment
Pulmonary contusion
o Patho:
 damage to lung from hemorrhage and localized edema. . blood
accumulate and interfere with gas exchange.
o S&S:
 hypoxemia, decrease breath sound, tachypnea, chest pain, blood-tinged
secretion, crackles, frank bleeding, respiratory acidosis. Might have signs
and symptoms of minor ARDS.
 Injuries will show on X-rays 1-2 days after injury happen.
o Intervention
 Airway, o2, pain, hydration via IV fluid and oral intake to mobilize
secretion.
Pulmonary hypertension:
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o Patho: pressure in the blood vessels from the heart to the lungs is high. The
heart has to pump harder to get blood though the narrowed vessels. The heart
muscle can weaken. Eventually result in right ventricle heart failure.
 Labs: chest X-rays, PAWP, pulmonary function test, echocardiogram.
Vasoreactivity test – high acuity for medication so we can start calcium
channel blocker.
o Risk factors: obesity, heart disease, vascular disease, lung disease, portal
hypertension, HIV infection.
o S&S:
 Symptoms start slowly and gets worse over time: dyspnea wit. Exertion
early on and with rest later. Substernal chest pain. Weakness, fatigue,
syncope and anorexia
 Signs of right-side ventricle heart failure: peripheral edema, ascites,
distended neck veins, crackles, heart murmur.
o Treatment
 Meds: vasodilators, calcium channel blockers, diuretic, anticoagulants,
digoxin -> improve ventricle ejection,
 There is no cure to this, just management S&S
o Intervention:
 Oxygen therapy, fluid restriction, encourage rest. Grouping care and
activity to prevent fatigue.
 O2 does not need at rest but need with exercise.
Chest tube:
o Chest tube is a tube that is inserted into the pleural space to remove excess air,
blood or fluid. This help re-expand the lungs.
 Use -> after thoracic surgery, cardiac surgery/CABG, spontaneous
pneumothorax, hemothorax, pleural effusion.
 Consist 3 chambers:
 drainage chamber: this is where the fluid is collected from the
patient
 water-seal chamber: allow air to be removed from the pleural
space without outside air entering the lungs.
o Tidaling (rise and fall with each breath) is good.
 If water stop fluctuating, it could mean the lung has
re-expand or the tubing is kinked.
o Excessive continue bubbling in the water seal chamber is
bad
 suction-control chamber:
o wet suction: use water to control suction (actually filling
the suction control chamber with water) -> will have
gentle bubbling
o dry suction: there is no water column. The suction is
controlled by a suction monitor below that balance wall
suction -> will have no bubbling.
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Complication:
 If the tube become dislodged -> cover the insertion site with
sterile dressing
 If the chamber become damaged -> place the tubing in sterile
water while waiting for a new system.
o Nursing: management of chest tube
 Maintain patency and function of the chest tube system. Assess for air
leaks, secure connection with tape
 Keep the canister below the chest – never strip or clamp the tubing.
 Check drainage suction, and water seal levels frequently
 Semi-fowler’s, turn Q2hours to enhance air and fluid remove
 Monitoring color and quantity of the drainage every hour, lung sound and
insertion site. REPORT BRIGHT RED BLOOD – but dark blood is expected.
 EDUCATION: Valsalva maneuver when remove chest tube – deep breath,
exhale, and bear down.
o Nursing monitor for post – op chest tube insertion:
 Improve gas exchange and breathing. Check ABGs 20 mins after chest
tube insertion.
 Turning: turn on “good side down” do not turn completely onto
operative side.
Thoracentesis:
o Remove air from pleural space with a needle.
o Complication such as pneumothorax can arise.
Oxygenation
o FiO2 – fraction of inspired o2 – the air you breath in.
 Room air has 21% o2
o PaO2 – the partial pressure of o2 in the arterial blood.
 80-100
o SaO2 – Hemoglobin saturation - % of hemoglobin that bound to o2
 95-100% (measure by pulse ox)
o Pt education:
 All o2 should be at least 15ft away from fire sources. Keep o2 tank away
from direct sunlight. When riving car, keep o2 on floor behind front seat.
Oxygen delivery system:
o Nasal cannula:
 flow rate 2-6.  use in non-acute or use humidifier air to decrease
dryness.
o Simple mask
 Flow rate 6-10  use in non-acute
o Non-rebreather mask
 Flow rate 10-15  use for acutely ill pt
o High flow oxygen therapy
 Flow rate up to 60  high flow nasal cannula.
o Venturi mask
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 Flow rate 2-15  for chronic lung disease – delivery o2 without intubate.
o Face tent.
 Flow rate at least 10 - for pt who don’t tolerate mask well.
Mechanical ventilation: chap 21
o A machine that helps a person breathe. The machine pump air into the lungs
unlike normal breathing.
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Negative-pressure ventilators
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Iron lung (drinker respirator tank)
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Body wrap (pneumo-wrap) and chest cuirass (tortoise shell)
Positive-pressure ventilators
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Pressure-cycled ventilators
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Time-cycled ventilators
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Volume-cycled ventilators
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Noninvasive positive-pressure ventilation
o Different type of ventilator: Noninvasive Positive-Pressure Ventilation
 Method of positive-pressure ventilation that can be given via facemasks that
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cover the nose and mouth, nasal masks, or other oral or nasal devices such
as the nasal pillow
Eliminates need for endotracheal intubation or tracheostomy
 Continuous positive airway pressure (CPAP)
o Provide a single set of pressure throughout your sleep and
pressure relief during exhale.
 Bilevel positive airway pressure (BiPAP)
o Provide constant set of pressure during inhale and exhale.
 Assisted control: the machine do it all for you
Assessment for all: respiratory, neuro status, comfort, communication.
 Patient first, then the ventilator
 If the patient develops respiratory distress, immediately remove the
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ventilator and provide ventilation with a bag-valve mask device
Assess vital signs, oxygen level (agitation, restlessness indicates
impaired oxygenation), capnography, breath sounds, ABG
Assess the area around the ET tube or tracheostomy site every 4
hours for color, tenderness, skin irritation and drainage
Provide psychological and emotional support
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 Nursing consideration:
 Monitoring LOC< vitals, lung sounds, ABGs, GI, nutrition.
 GI – give PPIs and H2 blockers to prevent stress ulcers and
decrease acid. (Omeprazole and Famotidine)
 Suctioning to remove secretion only when needed -> never
suction when inserting a catheter into the airway. Never suction
more than 10 secs. Give 100% before suction.
 Oral care – clean the mouth with chlorhexidine ever 2 hrs
 Turn/ reposition the pt every 2hrs. keep head of bed 30%
Endotracheal intubation – chapter 21-7:
o Endotracheal tube – oral intubation following Rapid sequence intubation (RSI) is the
technique of choice. Nasal route alternatively
o Preparing for intubation – basic life support, each intubation attempt no longer than
30 seconds
o Verifying tube placement – end-tidal carbon dioxide and chest X-ray are most
accurate ways. Stabilizing the tube – tube is marked at mouth or naris level
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o Note that the cuff pressure of endotracheal tubes should be checked every 6 to
8 hours and that a pressure between 20-25 mm Hg is suggested
 Higher pressure can cause tracheal bleeding, pressure necrosis. Low
pressure can increase risk for aspiration and hypoxia.
 Should not be sue more than 21 days to reduce risk of paralysis and nerve
damage in tracheal.
 The cuff is inflated to maintain the tube’s position and to minimize the
risk of aspiration.
o Nursing immediate after intubation:
 Check symmetry of chest expansion, breath sound, chest X-rays confirm
placement.
 Ensure high humidity, a visible mist should appear on T-piece.
 Monitor for signs of aspiration.
 Secure the tube to pt face with tape and mark the proximal end for
position maintained.
 Use sterile suction tech. reposition Q2hrs oral hygrines.
Tracheostomy:
o Surgical procedure in which an opening is made into the trachea. The indwelling
tube inserted into the trachea is called a tracheostomy tube
 Note that cuff pressure on tracheostomy tubes is maintained between
20-25 mm Hg every 8hrs. Tracheostomy cuff pressures exceeding 25 mm
Hg may cause injury to tissue and a cuff pressure of 15 mm Hg is
suggested to prevent aspiration. Not all persons with a tracheostomy
may require the cuff to be inflated.
o Nursing
 Maintain patency by proper sterile suctioning
 Administer analgesia and sedatives
 Provide an effective means of communication
Nursing care for both ET and Trach
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Weaning: page 535. 21-16
o Process of withdrawal of dependence upon the ventilator. Weaning is the
process of going from ventilator dependence to spontaneous breathing (patient
should be hemodynamically stable). Disconnect from the ventilator; weaning
with a T-piece for the patient with an ET tube or tracheostomy mask for the
patient with a tracheostomy tube. ABG 20 minutes after spontaneous breathing
o Three stages:
 Patient is gradually removed from the ventilator
 Then from either the endotracheal or tracheostomy tube
 And finally from oxygen
 Successful weaning is a collaborative process
Acute respiratory distress syndrome:
o Patho:
 This is a type of respiratory failure. The mortality rate is very high
because it happens suddenly.
 Severe inflammation in the lungs -> damage of alveoli capillary
membranes -> fluid leaks from blood vessels into the alveoli -> alveoli
sacs are filled with fluid -> gas exchange is inhibited -> blood is not
oxygenated -> hypoxemia -> eventually the organs will suffer from not
being oxygenated.
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Labs: chest X-rays, chest CT -> look for white out appearance,
echocardiogram -> to rule out cardiac issues.
o Risk factors:
 Sepsis shock, pneumonia, smoke inhalation, aspiration, drug overdose,
air embolism, major surgery.
o S&S:
 Keys:
 hypoxemia that result -> restlessness, confusion, agitation.
 Refractory hypoxemia (refractory – think resist to oxygen)-> low
o2 level despite receiving high amounts of O2. Labs will show
decrease PaO2, increase CO2
 Severe RAPID dyspnea (trouble breathing – must use accessory muscles)
and tachypnea, Labored breathing, crackles on auscultation, Intercostal
retractions
 Later stages: cyanosis, changes in mental status. Decrease all vitals
o Treatment:
 Meds:
 Vasopressors, analgesics
 sedatives -> to decrease o2 demand and decrease anxiety for
ventilated patients.
 Nebulizer with bronchodilators -> dilate bronchioles and assist
with coughing up secretion.
o Nursing intervention:
 Provide supplement o2 as an early intervention. Most pt with ARDS will
be on mechanical ventilation with PEEP, intubation.
 Prone position, reduce anxiety. Need to keep Pao2 above 60%
 For intubated patient:
 Turn and reposition, oral care, skin care, range of motion of
extremities.
 Monitor:
 ABGs, vitals, level of responsiveness, pulse ox.
 Risk for develop hypovolemia, decrease cardiac output.
 Management of pt on ventilator: Give medication, give paralytic,
take over breathing to lets body rest, or give sedatives.
 Doctor do intubation, we tell patient that what will happen and
what we do. We give sedative then paralytic before intubate
patient. We give sedative first so they are not awake and scare.
 Confirm placement with X-ray and put monitor for CO2 – 35 to 45,
color metric device, check bilaterally lung sound, ABGs within 20
mins after placement.
 Place NG tube to prevent air pressure in the stomach.
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Foley insert, turning every hours, give photonic, risk for skin
breakdown, daily ABG, Q4 blood sugar. Pressure on the ventilator
can be higher than 25%
o Different with acute respiratory failure is that ARDS is fluid in the lung. On the
other side, acute respiratory failure is just a vague symptoms where pt is restless
and fatigue and trouble breathing.
COVID-19
o Droplet transmission.
o S&S: mild pneumonia-like, respiratory distress, multi-organs failure.
o Precaution: contact, droplet, airborne.
o Test: nasopharyngeal swap, Nasopharyngeal wash/aspirate.
o Medication: Remdesivir, Corticosteroids, Bamlanivimab.