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exam 1 Flashcards

1
Q

PaO2-partial pressure of oxygen dissolved in the arterial blood
- measure by Arterial blood sample
SaO2-arterial oxygen saturation of hemoglobin
-Direct measurement of oxygen in blood
SpO2-indirect measurement of the oxygen content of blood
-Measured via pulse oximeter
Hypoxemia-abnormally low PaO2

A

vocab

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2
Q 
PaO2: 80-100 mmHg (70=hypoxemic)
SaO2: 92-99%
pH: 7.35-7.45
PaCO2 (lungs): 35-45 mmHg
HCO3 (bicarb/kidney): 22-26 mEq/L

pH: acid 7.35-7.45 alk
PCO2: alk 35-45 acid
PCO3: acid 22-26 alk

A

normal values for ABG

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3
Q

pH-measure of hydrogen ion concentration in the blood

  • When hydrogen ions accumulate, the pH drops-patient becomes acidotic
  • When hydrogen ions decrease-pH raises-patient becomes alkalotic

PaCO2-partial pressure of carbon dioxide in arterial blood
-Regulated by the lung function

Respiratory acidosis

  • Hypoventilation-carbon dioxide increases  respiratory acidosis
  • Occurs due to respiratory depression, decreased respiratory rate

Respiratory alkalosis
-Hyperventilation- carbon dioxide leaves body respiratory alkalosis

Bicarbonate- base

  • Helps regulate pH
  • Regulated by kidneys-metabolic process
  • When bicarbonate increases –> metabolic alkalosis
  • When bicarbonate decreases –> metabolic acidosis
A

functions/regulatory mechanisms

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4
Q 
Definition:
-PaCO2 >45mmHg (high)
-pH <7.35 (low)
-Build up of carbon dioxide in the lungs
Causes:
-*Over sedation or meds
-Pulmonary embolism
-*Hypoventilation
-Bronchial obstruction
-Heart failure
-Central nervous system depression
-Pulmonary edema
-Pneumothorax
-Cardiac arrest
-COPD (retains CO2)
-Pneumonia
Signs and symptoms
-Dyspnea
-*Lethargy
-Tachycardia
-Confusion
-Respiratory distress
-Drowsiness
-*Decreased responsiveness (can't breath r/t lethargy)
A

respiratory acidosis

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5
Q 
Definition
-PaCO2 <35mmHg (low)
-pH >7.45 (high)
Causes
-Anxiety (breath fast, altered LOC --> blowing off too much CO2 --> alkalosis)
-Pain
-*Hyperventilation
-Fever/sepsis
-*Excessive mechanical ventilation (r/t breathing too much)
Signs and symptoms
-Confusion
-Light headedness
-Sweating
-Dry mouth
-Decreased concentration
-Cardiac dysrhythmias
-Deep, rapid breathing
-Anxiety
A

respiratory alkalosis

See CO2 think lungs

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6
Q 
Definition
-HCO3 <22mEq/L (low)
-pH <7.35 (low)
Causes
1. Increased acids
-*Renal failure
-*Ketoacidosis (DKA/can be extremely low numbers)
-Starvation
-Alcoholism
2. Loss of base
-Diarrhea 
Signs and symptoms
-Headache
-Confusion
-Lethargy
-Stupor/coma
-*Kussmaul respirations (DKA)(rapid breathing r/t compensary mechanism for hyperventilation and to help kidneys)
A

metabolic acidosis
always low HCO3

metabolic = kidney and bicarb (bicarb is regulated by kidneys)

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7
Q 
Definition
-HCO3 >26 mEq/L
-pH >7.45
Causes
1. Gain of base
-Excess ingestion of antacids
2. Loss of acids
-*Vomiting
-*NG suctioning (can remove acid)
-Hypokalemia
-Hypochloremia
-Diuretics (effects kidneys)
Signs and symptoms
-Tetany
-Dizziness
-Lethargy
-Weakness
-Coma
-Nausea and vomiting
-*Depressed respirations (r/t compensation of lungs)
A

metabolic alkalosis

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8
Q

Body should try to compensate if the patient has alkalosis or acidosis
-Renal or respiratory will try to compensate
If the problem is respiratory the kidneys should try to compensate
If the problem is renal the lungs should try to compensate

Can be fully compensated, partially compensated or uncompensated
Fully: good r/t body trying to fix it
- know in Full if pH is normalized
Partial: trying, not working - all abnormal
Uncomp: pH abnormal, either CO2 or CO3 is normal

A

compensation

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9
Q

If there is a metabolic-based pH imbalance:

  • If it is metabolic acidosis- there will be an increase in respiratory rate and depth (high)
  • If it is metabolic alkalosis- there will be a decrease in respiratory rate and depth (low)
A

respiratory compensation

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10
Q

If there is a respiratory based pH imbalance:

  • Respiratory acidosis- there will be an increase in hydrogen secretion and HCO3 reabsorption (high)
  • Respiratory alkalosis- there will be a decrease in hydrogen secretion and HCO3 reabsorption (low)
A

metabolic compensation

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11
Q

pH-normal
CO2-abnormal
HCO3-abnormal
Because the pH is normal, it indicates that one system has compensated for the other

A

fully compensation

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12
Q

pH is abnormal
CO2 is abnormal
HCO3 abnormal

Because both CO2 and HCO3 are abnormal, this indicates that one system has tried to correct the other system but hasn’t been completely successful

*Nothing is normal on ABG’s

A

partially compensation

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13
Q

pH is abnormal
EITHER CO2 or HCO3 is abnormal (1 is normal 1 is abnormal)

There is no indication that one system tried to correct the other

A

uncompensation

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14
Q

Nursing care is directly related to the cause of the imbalance!
What can the nurse do?
-Respiratory acidosis
–cause: narcotic, hypoventilation
–give narcan, wake them up, cough/deep breath, ventilate
-Respiratory alkalosis
–cause: hyperventilation
–correct: antianxiety (Ativan), pain meds, treat fever, *change vent setting
-Metabolic acidosis
–cause: DKA, renal failure, not enough bicarb
–correct: give bicarb, DKA=fix electrolyte imbalance and S/S
-Metabolic alkalosis
–cause: NG suction, vomit
–correct: turn suction down, antiemetic’s

A

nursing care for each resp and metabolic acid and alkalosis

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15
Q

Sudden and life threatening
Poor gas exchange: retain CO2 (acidotic) , inadequate oxygen (hypoxemia)

In patients with normal baseline abgs:
-PaO2 55 or less
-Paco2 >50
-Ph <7.35 
In patients with chronic hypercapnia or hypoxemia:
-Indicated by acute deterioration
A

acute respiratory failure

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16
Q

Large airway obstructions (food, mucous, tonsils, OSA, trauma, tumor)
Bronchial diseases (chronic bronchitis or asthma)
Parenchymal disease (severe pneumonia, pulmonary fibrosis)
Cardiovascular disease (cardiac pulmonary edema, PE)
Diseases of the pleura and chest wall (pleural effusions, pneumothorax)
Disorders of the respiratory muscles and neuromuscular junction (myasthenia gravis, muscular dystrophy, meds that paralyze respiratory muscles)
Disorders of the peripheral nerves and spinal cord (MS, ALS, guillain barrb)
Disorders of the central nervous system (stroke, seizures, narcotics)

A

causes respiratory failure

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17
Q

Affects all organs/tissues
From causes of resp. failure
low O2 in the blood –> tissue death
low Pa02
S/S
-Dyspnea*
-Cyanosis
-Restlessness: r/t lack of O2 to brain and gas exchange issue
-Confusion: r/t lack of O2 to brain and gas exchange issue
-Anxiety: r/t lack of O2 to brain and gas exchange issue
-Tachypnea
-Tachycardia
-HTN
-dysrhythmias*: low O2 to heart and high ectopy (PAC, PVC, afib) so give O2

A

hypoxemia

acute respiratory failure

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18
Q 
Impairs cellular function
From alveolar hypoventilation and ventilation-perfusion mismatch 
Respiratory acidosis
hypoventilation causes high CO2
S/S
-Dyspnea
-Headache
-Htn
-Tachycardia
-Tachypnea
-Aloc-can become unconscious*
-Use of intercostal muscles
A

hypercapnia
acute respiratory failure

if less responsive automatically check CO2 levels

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19
Q

Abgs: see S/S from hypoxemia, hypercapnia
Cxr: check infection , pneumonia, cause (do this 1st)
Sputum culture: infection in sputum, pneumonia, organism
Pfts
Ct: shows PE*, tumor
Labs- cbc (WBC infection/pneumonia), electrolytes (ones that cause acid base imbalance)
bronchoscopy: to see in lungs to check for mucous plugs/infection/biopsy and can do a wash out

Medications to treat the underlying cause of the respiratory failure
If cause is due to narcotic overdose-give narcan or reversal agent*
If cause is due to bronchospasm (copd/asthma)-give bronchodilator and corticosteroids to lower inflammation*

A

diagnostic procedures and meds for acute respiratory failure

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20
Q
  • Increase oxygen-via nasal cannula, high flow mask, bipap (most invasive), ventilator
  • This will improve cardiac output and improve tissue oxygenation
  • Correct acid/base imbalance-ventilator will improve alveolar ventilation-may give sodium bicarb to improve resp and metabolic acidosis
  • Monitor fluid balance (pt on vent has fluid imbalance - monitor daily weight, I/O)
  • Treat underlying cause (if cardio/fluid OD give diuretics, if pneumonia give antibiotics)
  • Monitor respiratory status closely!! May need immediate intubation!
  • Will need to increase fio2 to increase pao2
  • -Titrate down when able to prevent co2 retention
  • Monitor oxygen saturations continuously* (put O2 on ear, foot, forehead and work with resp therapist)
  • Frequent respiratory/neurological assessments (work of breathing, neuro)*
A

oxygen and airway management

if brain has poor perfusion then breathing won’t work as well
high CO2 is biggest S/S for altered LOC

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21
Q

Fio2-fraction of inspired oxygen-can go up to 100%
-30-100
Tidal volume-volume of air between inspiration and expiration
-amount of air chest holds
Peep-positive end expiratory pressure
-end of breath spurt on vent to keep the alveoli open
Rate-respiratory rate
-physician changes rate based on condition and CO2 rate
-can’t go below, but can go above setting

VENT SETTINGS: ALWAYS KNOW MODE, F102, rate, tidal volume and PEEP

A

vent vocab

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22
Q

Controlled rate that we set / volume mode
Patient can trigger own breaths but cannot go under set amount
Own breaths will be given full tidal volume by ventilator
Fully supports patient
initial mode we use

A

assist control/CMV continuous mandatory ventilation ventilator modes

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23
Q

Set Rate and tidal volume / volume mode
Patient can trigger own breaths but spontaneous breaths will not be supported by set tidal volume
Can add pressure support to this setting-will reduce work of breathing for patient
can use for weaning

A

Synchronized intermittent mandatory ventilation mode (SIMV)

ventilator modes

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24
Q

Assists spontaneous breathing by giving a high flow of gas to selected pressure level
Patient’s effort determines rate and tidal volume
Can adjust the pressure to achieve best tidal volume and resp. rate for patient
Can be used as weaning tool-will increase endurance of lung muscles
We only set pressure. We do not set tidal or rate (the patient sets that themselves)

A

pressure support ventilation modes

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25
Q

Used with ards (lung compliance is decreased)
Used when the patient has oxygenation problems despite a high fio2 and high peep* (high peep causes barotrauma and decreased CO)
Awkward breathing pattern for patient-must sedate (patient will fight vent to breath)
high peep Creates high intra-thoracic pressures-may decrease cardiac output and oxygen delivery—-must monitor hemodynamics closely!
Results in decreased lung pressure and improved ventilation

A

pressure control ventilation mode

26
Q

Used in trauma and ards
to reduce airway pressure
Becoming more common
Allows spontaneous breathing throughout whole cycle-limit sedation
Time triggered, pressure limited, time-cycled
High pressure setting and low pressure setting
-High pressure has long set time interval
-Brief release to low pressure
-Breathing looks very awkward!

A

airway pressure release ventilation APRV vent modes

27
Q

Cpap-Peep (5-20 cm H20) supplied during spontaneous breaths)
Peep used to keep alveoli open
High levels of Peep decrease venous return to heart, decrease cardiac output.
-Watch for hypotension
High levels of peep leads to increase intrathoracic pressure and may cause pneumothorax-may need chest tube (no breath sounds on side)
Cpap is a weaning mode!
With peep watch for a low BP

A

Continuous positive airway pressure (CPAP) ventilator modes

28
Q

Nasal mask, prongs, full face mask
Used as a bridge to invasive mechanical ventilation
Used to help patients with hypoventilation, osa
May be needed post extubation
*Must be alert for aspiration - goes into lungs if pt does
Must have a gag reflex
can be used as bridge to ventilation or after ventilation
*switch meds to IV when on BIPAP cause PO will go into lungs
-wait 15 mins (TEG)
if they lose gag reflux must intubate r/t pt can’t maintain own airway
-cough/talk indicates gag reflux

A

BIPAP noninvasive mechanical ventilation

29
Q

Aspiration
Barotrauma and pneumothorax
Ventilator associated pneumonia (vap)
Decreased cardiac output
Immobility
Gastrointestinal problems
Intubation
Pneumonia
How do we prevent aspiration while intubated?
-Appropriate cuff inflation: et tube has cuff to keep in place and is maintained by pressure. If low pressure secretions can go down and cause aspiration
-Ng/og tube: for every vent pt to prevent aspiration
-**Oral care every 2 hours (chlorhexidine to bursh BID)
-Elevate hob 30-45 degrees

A

complications of vent - aspirations

30
Q

Positive pressure during inspiration-creates barotrauma
Peep-pressures increased & continue through expiration
High peep –> can rupture alveoli –> air escapes into pleural space –>collapses lung
Assessments for tension pneumothorax
-Breath sounds (can be diminished/absent on one side)
-Monitor for tracheal deviation (tension pneumo respiratory/circulatory collapse) (fix with needle decompression and chest tube)
-Crepitus (air escapes into subq)
-Assess for bradycardia/hypotension

A

vent complications - barotrauma/pneumothorax

31
Q

Mechanical ventilation for at least 48 hrs (if before 48 hours pt came in with it)
Chest x-ray-new or progressive infiltrates
Temp higher than 100.4 (38 degrees C)
Leukocytosis
Purulent sputum/cough
Worsening gas exchange
How do we prevent vap?
-Oral care q 2 hours
-Elevate head of bed 30-45 degrees
-Vent bundle (og, oral care, DVT/stress ulcer orders)
-Og vs ng tube (*pause 1st before laying down to prevent aspiration)

A

complications ventilator associated pneumonia VAP

32
Q

Intubation

  • Medications (give sedation meds 1st paralytic 2nd)
  • -they lower BP (emergency r/t decreased CO and perfusion issues)
  • -BP meds include fluid and vasopressors
  • Increased thoracic pressure –> decreased venous return

What are other signs of decreased cardiac output (besides hypotension)? bradycardia, low UO, slow cap refill, altered LOC, weak pulse

A

vent complications decreased cardiac output

33
Q 
Muscle wasting
Weakness
Contractures - foot drag
skin integrity
Pneumonia (caused from immobility)
Dvt
Pe
*Constipation (chart BM)
*Ileus

How do we prevent this problem??
- reposition q 2 hours side to side, prevent pressure ulcer, make them move (ROM, up to chair)

A

vent complications immobility

34
Q

Distention (r/t swallowing air)
Decreased motility/ileus
Vomiting

Must keep bowels moving normally!
Enteral nutrition - tube feeding makes pt have diarrhea. If pt doesn’t have BM know theres an obstruction, ileus, etc.
- dietitian tells us what to give
- good nutrition promotes healing

A

vent complications gastrointestinal

35
Q

Starts day 1
Assess daily
Weakened diaphragm –> weak respiratory muscles
Often wean during day and rest at night
Stop trial if the patient cannot tolerate
Limit sedatives: sedation vacation
*can’t wean if one 100% F102 (30% f1o2 they’re ready to wean)
must place them on ‘weaning trial’ - 2 hours
Sedation vacation
-Which modes? wake up, see if it’s a true wean. if patient can’t tolerate (s/s tachypnea) put back on CMV. if on CMV and breath fast/fight vent then sedate
Patient must be able to maintain own airway
-Alert, gag reflex, lift head off pillow, follow commands (shows muscle and alert)
Breathing tests by respiratory therapists
Abg’s
Nurse and rt in room
Must have oxygen readily available - ambu bag
Must have resuscitation equipment
Suction prior to clear airway
Have patient cough while taking tube out
Stay and assess/monitor
-What are priority assessments?
– oxygenating ok, work of breathing is good
OG comes out with et but NG can stay in unless it gets dislodged

A

weaning from the vent

36
Q

Acute onset
Sepsis is most common cause of ards
- sepsis is inflammatory process and capillaries weap and intravascular fluid moves to alveoli –> impaired gas exchange and ventilation issue
Changes in lung vascular tissue, increased lung edema, impaired gas exchange
Alveolar-capillary membrane damage –> increased membrane permeability –> fluids move to alveolar space –> air spaces fill with fluid –> decreased oxygenation
Increase in airway resistance –> impaired ventilation
Alveoli become full of fluid –> impaired ventilation

A

acute respiratory distress syndrome ARDS

37
Q 
Cxr= patchy/ground glass, ‘white out’ 
*Sirs --> systemic inflammatory response syndrome-occurs due to systemic insult
Patients with ards will have s/s of sirs
Sirs criteria: must have 2 or more of the following (page 591)
-Temp >100.4 or <96.8
-HR >90bpm
-Rr >20 
-Wbc >12,000 or <4000

Sirs –> sepsis –> ards

A

Acute respiratory distress syndrome & systemic inflammatory response syndrome (sirs)

38
Q

Stage one:
-Increased dyspnea, tachypnea
-Bilateral crackles
-Dry cough
– hard to catch r/t looks like other resp/gas exchange issues
Stage 2:
-*Refractory hypoxemia: hypoxemia that is resistant to supplemental oxygen administration (hypoxemia is PaO2 <80)
–Will need to be mechanically ventilated (can give peep on vent to keep alveoli open)
–pao2 will be getting worse no matter how much oxygen they are given
Stage 3:
-Hemodynamic instability (low BP, high heart rate), increased hypoxemia, decreased lung volumes (FI02 give 100%, peep (makes BP go down with high peep) so must maintain BP with vasopressors)
-white out on chest xray
Stage 4:
-fibrotic stage (after 10 days), more organ involvement
-not easy to vent fibrotic lungs
-multiorgan failure: lungs, brain, kidneys, LFT are high r/t no liver function, and low gut motility

A

stages of ARDS

39
Q

Treat underlying cause
Oxygen
-Refractory hypoxemia: must give correct amount of oxygen
-Mechanical ventilation
-Peep: to prevent collapse of alveoli
-Fio2: try to oxygenate as much as possible
–need to keep drawing ABGs
Cardiac output: Enhance preload (volume/stretch in ventricle) & contractility (squeeze/contract is poor so decreased CO) and normalize afterload (resistance heart overcomes to open valve - ARDs have increased afterload so we want to normalize)
-ARDS pt is dry so has decreased preload
Respiratory Assessments
Positioning: Prone for late stages - 1-1 nursing
-improves oxygenation/gas exchange
-lots of complications: aspiration, extubate, restricted mobility, swelling/edema* so high chance of cardiac arrest and hard to CPR prone
Meds: Antibiotics, bronchodilators, mucolytics, steroids
Sedate/psychosocial: helps improve gas exchange and oxygenation*
Assess pain: assess sedation by neuro RASS scale
Nutrition-Assess gut perfusion by checking residual so no tube feeding while moving prone
Circulation/perfusion assessments: monitor C.O., VS q 15 mins, EKG (hypoxemia=dysrhythmias)
Fluids & electrolytes: maintain fluid balance
-monitor ABG, lactate, BUN/CR, LFT to check perfusion
Mobility/safety if tolerated, check skin integrity
Teaching : with fam on stages and expectations

A

NM for ARDS and acute respiratory failure

40
Q

Caused by combination of forces:
-acceleration: velocity of moving object
-deceleration: decrease in velocity
-shearing: 2 objects rub against each other
-crushing: pressure between 2 objects
-compressive resistance: ability of an object to resist
Direct impact causes the greatest injury
Three collisions involved in one crash: First – car with another object. Second- occupants body with interior of the car. Third- internal tissues with the rigid body surface structure.

A

blunt force trauma

41
Q

Produced by foreign objects penetrating the tissue
The external appearance of the wound DOES NOT reflect the extent of the internal injury.
Damage is going to depend on 3 factors:
-Density and compressibility of tissue injured: what did it hit
-Missile’s velocity: how fast did it hit (gun/stab/etc.)
-Fragmentation of primary missile: like bullets
Think of what’s going on inside (internal bleeding?) - it can be much worse inside than what it looks on the outside

A

penetrating injury

42
Q

EMS typically first to arrive- Obtain history of events
-How many involved, wearing seatbelt, scene, alcohol/drugs used? - can make blood thin, entrance/exit wound
-Very important step - can predict what injury occurred
Perform all the pre hospital management of the patient which will include:
-Pre hospital priority of maintaining ABC’s while making sure to maintain C-spine precautions (if no c-spine, can lead to lifelong damage).
– EMS gets pt. to hospital as quick as possible
– 1st*: must ensure airway is secured and pt. not bleeding out
– must think if pt. has adequate gas exchange/perfusion
-They will do a very fast primary assessment and secondary assessment of patient
-Consider what type of facility the patient needs to go to – Level 1 Trauma center is top choice

A

initial assessment and management of trauma

43
Q

Primary survey
Follow ABCDE’s
-1st: Airway-jaw thrust, chin lift, maintain c-spine precautions
-Breathing-respirations, color, breath sounds
– breath sounds (are they clear?), symmetrical sounds/rise, work of breathing, color (are they cyanotic)
-Circulation-pulse, blood pressure, cap refill, uncontrolled bleeding
– if poor, check for bleeding, pulses (bleeding causes increased HR and decreased BP)
-Disability- LOC, pupil size
– pupils equal/reactive, is pt. unresponsive/confused?
-Exposure- remove clothing, inspection
– to check skin color (pale/diaphoretic = poor perfusion), entrance/exit wound, temp tells if pt. has good perfusion (if in shock, temp decreases r/t vasoconstriction

Keep room warm to prevent vasoconstriction

A

patient arrival to hospital after trauma

Primary Survey

44
Q

Head to toe assessment
Turn patient and remove backboard
- push spin all the way down to perform a good spinal exam
- digital/rectal exam to check for bleeding
CTs/Ultrasounds performed
- CAT/other diagnostics you can’t do at bedside
Reassess* constantly in every stage, esp with head injuries

once pt. is stable, then do this thorough assessment

A

Secondary survey in trauma

45
Q

Admissions to ICU (reassess pt.)
Head to toe assessment to ensure all injuries are identified, labs, and to ensure nothing was missed
Response to resuscitation
Checking for injury identifications

A

Tertiary survey in trauma

46
Q

Trauma patients usually have fluid volume deficit r/t blood loss
- hypovolemic shock r/t fluid depletion
- hemorrhagic shock r/t bleeding out/blood loss
Maintain perfusion
Factors that affect choice of fluid are : how the volume loss occurred and which solutes need to be replaced.
- must figure out what fluid loss pt is in and why it occurred
- replaced fluids must be put in warmer r/t giving fluid fast. Do this to prevent hypothermia
Complications of aggressive fluid resuscitation: hypothermia* (want to stay away from this r/t vasoconstriction) and coagulopathy (r/t possible hemodilution)

A

fluid resuscitation

47
Q

Crystalloids (1st thing we go to)
-Typically used for trauma patient.
-Types of Crystalloids include: Isotonic (NS, lactated ringers - good volume expanders), Hypotonic, and Hypertonic
-Amount used is typically a 2L bolus.
Colloids
-Colloids contain albumin, dextran, and hetastarch.
-They have a longer duration of action and more efficient in expanding plasma volume.
-No clear evidence that they are superior to crystalloids
-Complications include anaphylaxis and coagulopathy (has more complications than others)
-Cost more
Blood products
-Excellent resuscitation fluid
– Volume expander to help perfusion/coagulation - blood carries O2 so helps gas exchange/perfusion r/t O2 carrying ability)
-Hemodynamically unstable or showing signs of tissue hypoxia despite crystalloid infusion
-Crossmatched preferred- O neg for women of childbearing age, O positive for male and post menopausal women.
– Sometimes can’t cross match in trauma

A

types of fluids for trauma

48
Q
  • *priority will always be airway management.
  • Tracheobronchial Trauma: caused by blunt or penetrating trauma. If severe it is associated with high mortality rate (r/t airway issue)
  • -*Dyspnea is early and usually only sign
  • -*Cyanosis will be late sign.
  • Nursing care for these injuries will be: assessment of oxygenation and gas exchange (up to nurse to put on vent, oxygenate, etc.)
  • Bony Thorax Fractures: Rib fractures, sternal fractures, and flail chest-common in trauma patients.
  • Common concerns for nurses caring for these patients are ineffective ventilation and secretion control
  • -Airway management
  • -Pain management
  • -Oxygen therapy
  • Pleural Space Injuries- caused by disruption of an intrathoracic structure that allows air or blood to build up in the pleural layers leading to a negative intrathoracic pressure.
  • *Types include: Pneumothorax, Hemothorax, and Hemopneumothorax
  • *Mechanism of injury may lead nurse to suspect these injuries and nurse needs to continuously reassess
  • Chest x-ray usually shows injuries
  • *Chest tubes and needle decompression are usual treatments
  • Blunt Cardiac Injuries: S/S chest pain (most common), watch for dysrhythmias/heart working right
  • Penetrating Cardiac Injuries: very low survival r/t bleeding to death
    • if make it to hospital, surgery right away
  • Cardiac Tamponade: pericardiac sac fills with blood - heart can’t squaaze well (emergency, so go to OR)
  • Aortic Injuries: 80% die r/t aorta is vital in supplying blood and it can’t - straight to OR
A

Assessment and management of specific trauma injuries
Thoracic trauma

pt was in MVA, hit steering wheel hard. Think to check thoracic and recheck r/t expecting complications

49
Q 
Esophagus and Diaphragm (airway concern)
Stomach and Small Bowel
Duodenum and Pancreas
Colon
Liver
Spleen
Kidneys
Bladder
A

abdominal injuries in trauma

50
Q

Esophagus and Diaphragm-rare and difficult to diagnose
-*Nursing considerations –pay close attention to airway, ventilation, oxygenation, and hemodynamic support
Patient NPO
-NG tube
-Antibiotics (can lead to infection)
Diaphragm rupture- more common in blunt injury and occurs more frequently on left side due to not being protected by liver
-Patient may have respiratory distress, dyspnea, decreased breath sounds on affected side, positive bowel sounds in thorax, palpation of abdominal contents when inserting chest tube, and paradoxical movement of abdomen when breathing

A

esophagus and diaphragm injuries in trauma

diaphragm ruptures must be surgically repaired

51
Q

Gastric injuries-rare, small bowel are more common
-Small bowel or gastric injuries present with blood in ng or vomiting of blood (blood in stool or NG)
-Surgery is usually necessary
Duodenum and Pancreas are closely related
-CT will usually show injury
-NSG considerations for duodenum and pancreas-post surgical care and maintaining patency of drains
-Skin assessment-make sure pancreatic fluid isn’t causing cutaneous fistula due to high enzymes, also fluid assessment and electrolyte balance
Colon injuries-usually caused by penetrating trauma.
-Repair may be considered if patient is stable and if injury is small and doesn’t have fecal contamination.
-Colostomy may be needed depending on injury/where it’s at, or injection r/t closeness to bowel
-NSG considerations are going to focus on post surgical care and preventing infection

A

stomach, small bowel, duodenum, pancreas injuries in trauma

52
Q

Liver most commonly injured
-S/S-right upper quadrant pain, rebound tenderness, hypoactive or absent bowel sounds or signs of hypovolemic shock.
-If hemodynamically stable-managed without surgery. Liver will heal itself.
- probably will need to replace blood
-NSG care-include replacement of blood products and monitor HCT and coag. studies.
-Assess drainage, observe for complications.
Spleen-also most injured along with liver
-Tendency to lose blood rapidly
-S/S-left upper quadrant pain radiating to left shoulder(Kehrs sign) hypovolemic shock, & increased WBC count
-Course of action dependent on severity and if patient is stable
-NSG care-close monitoring for hypotension & signs of bleeding, bedrest, NPO, monitor H/H

A

liver and spleen injuries in trauma

lose blood easily with liver and spleen issues

53
Q

Kidney injuries- lead to hemorrhage, hematoma, intravascular thrombus
Most injuries can be managed with observation
Fluid balance must be maintained
Low dose dopamine may be ordered to promote renal perfusion
Bladder can be lacerated, ruptured, or contused usually because bladder is full at time of injury
Blood at urethral meatus, scrotal hematoma, or displaced prostrate gland need to be further examined before putting in a foley
*Nursing care-monitoring for infection and I/O, fluid blanace

A

kidney and bladder injury with trauma

anytime kidney injury, concern with adequate fluid balance and kidney function

54
Q

Fractures: continually assess to prevent
-esp pelvic fracture r/t extensive blood loss
-Treat: control bleeding, prevent infection (open fracture more prone to bleeding so do wash out)
Compartment Syndrome
- 1st S/S: numbness/tingling - check pulses to see how good perfusion is
Deep Venous Thrombosis: huge risk DVT –> PE (potential comp of trauma)
- monitor for PE S/S and swelling, warmth, low BP, high HR
Pulmonary Embolus ^
Fat embolism syndrome: fat embolism sits in lungs/peripheral tissues
-S/S*: hypoxemia, neuro decline, rash (petiche on head/neck/thorax)
Maxillofacial Trauma: common r/t no protection to face
-concern: airway/breathing

A

musculoskeletal injuries

55
Q

Early (responsible for death)
-Head injuries
-Hemorrhage
Late
-Hypovolemic Shock (may be r/t missed injury)
-Infection and Septic Shock (possible with penetrating wound)
-ARDS r/t main cause of sepsis
-SIRS: body’s response to trauma
-MODS
Psychosocial Considerations r/t trauma is always unpredicted so give good therapeutic communication

A

complications of multiple trauma

56
Q

Effective triage is one of the first procedures that critical care nurse uses in responding to disaster. Need to be sure that salvageable patient are appropriately categorized.
Need to make sure patients are in appropriate place
Determine the priority of the patient’s treatment based on patient severity

Minor- Victims who can get up and walk–GREEN
-Walking wounded, minor injury
Delayed- Victims who are breathing but may have an irregular pulse and can respond to commands—YELLOW
- urgent needs but not life threatening injuries - are breathing and can respond to commands
Immediate- Victims whose breathing indicates impending shock or possible suffocation—RED
- airway issues
Dead- Victims whose breathing, perfusion, and mental status are absent and or unresponsive—BLACK
- 90% burned, no breathing/perfusion/mental status

A

Triage

57
Q

Process of discharging patients when the hospital or unit is full or when there is a disaster

A

reverse triage

58
Q

Explosions and Blast Attacks- can have primary, secondary, and tertiary effects
Nuclear or Radiological Attacks- can be accident too, but medical consequences depend on nuclear or radiation source
Primary: hearing, pulmonary contusion, GI contusion
Secondary: struck by flying objects/debris
Tertiary: when body flies through air and strikes another object
Chemical Attacks- designed to irritate, incapacitate, injure, or kill. Readily accessible and easy to find and transport without being considered unusual
-Contamination incidents require different approach- caregivers need to be careful not to spread contamination. Need to perform a decontamination on patient (and on nurse)
-Staff needs to wear PPE and respirators may be needed if patient is highly contaminated
-Example: Cyanide

A

unnatural disasters

59
Q 
Intentional release of a biologic agent
-Anthrax
-Botulism
-Hemorrhagic fever
-Plague
-Small pox
-Tularemia
Why are these agents a threat? spread fast (can be aero sterilized), we have very little immunity which makes us susceptible
A

bioterrorism

60
Q

Deliberate release of microorganisms into a community to produce death, disease, or poisoning.
-Anthrax- 3 types-inhalation, cutaneous, GI
– inhalation = more sick pt r/t gas exchange issue
Treatment: Antibiotic therapy, support gas exchange/acid-base balance, IVF, decontamination

A

biological attacks

61
Q

High fever, headache, flushing maculopapular rash, conjunctival infection, progresses to diffuse hemorrhagic disease and to MODs.
Treatment: supportive care, Ribavirin maybe helpful in some cases. May need to be in isolation for weeks.

A

viral hemorrhagic fevers (ebola, yellow fever)

multisystems (7 decks)

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