Test 2 Flashcards

1
Q

Pulmonary Embolism - PE

A

A collection of particulate matter that enters the venous system and lodges in the pulmonary vessels

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2
Q

Clinical Signs and Symptoms of a PE –

dependent upon number and size of emboli

A

Symptoms:
▪ impending doom – restlessness - apprehension
▪ dyspnea with …
▪ abrupt onset ▪ pleuritic chest pain ▪ tachycardia
▪ cough
▪ hemoptysis

Signs:
▪ tachypnea	▪ pleural friction rub	▪ S3 or S4
▪ fever		▪ petechiae			▪ ↓SaO2
▪ diaphoresis  
▪ ST and T wave changes if severe
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3
Q

Priority Problems of a PE

A

▪ Hypoxemia r/t mismatch of perfusion and alveolar respiration
▪ Hypotension due to reduced forward flow of blood
▪ anxiety
▪ potential for bleeding due to anticoagulants

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4
Q

What is PaO2 and Fio2?

A

partial pressure arterial O2 (get this from your ABGs)

Fio2 = fraction of inspired o2 (A patient on room air = fio2 = .21)

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5
Q

Diagnosis of a PE:

A
▪ Abnormal ABG’s 
   	▪ early respiratory alkalosis
   	▪ later respiratory acidosis 
		see Fraction of Inspired oxygen (PaO2-FiO2)
   	▪ eventually metabolic acidosis

▪ Chest X-ray
Non specific x 24 hrs unless very large PE
▪CT Scan, MDCTA (very specific)

▪ TEE, Doppler ultrasound
▪Lung scan (ventilation/perfusion scan), pulm angiogram

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6
Q

Nursing Care for PE:

A

improve ventilation and perfusion, minimize risk of additional clot formation, prevent complications

▪ respiratory assessment
        ▪ administer O2	▪ crackles
▪ cardiac assessment
        ▪ S3 S4
▪ anticoagulation medications
        ▪ IV heparin
        ▪ warfarin
        ▪ thrombolytic
▪ surgical management
       ▪ vena cava filter
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7
Q

Acute Respiratory Failure definition:

A

pulmonary system fails in one or both functions; oxygenation and CO2 elimination

Acute Resp. Failure
Ventilatory Failure
Oxygenation Failure
Combined Failure

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8
Q

Acute Respiratory Failure

A

▪ Clinically Defined
PaO2 < 60mmHg OR PaCO2 > 50mmHg
SaO2 < 90% with ABG pH < 7.30

▪ Manifestations often subtle at onset and
progress rapidly

Patient is always hypoxemic

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9
Q

what is V/Q?

A

“V” - ventilation-air that reaches the lungs

“Q” - perfusion-blood that reaches the lung

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10
Q

What is normal V and normal Q?

A
Normal V (ventilation) is 4 L of air per minute
Normal Q (perfusion) is 5L of blood per minute.  
Normal V/Q ratio is 4/5 or 0.8.  

When the V/Q is higher than 0.8, it means ventilation exceeds perfusion.
When the V/Q is < 0.8, there is a VQ mismatch caused by poor ventilation.

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11
Q

Ventilatory Failure:

A

normal perfusion & abnormal ventilation

▪ PaCO2 > 45mmHg in patients with otherwise healthy lungs

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12
Q

Oxygenation Failure:

A

normal ventilation with abnormal perfusion

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13
Q

What are possible causes of oxygenation failure?

A
Impaired diffusion at alveolar level
Right to left shunt in pulmonary vessels
Low O2 concentration atmospheric air
Failure of Hgb to bind to Oxygen
V/Q mismatch  
	Acute Respiratory Distress Syndrome (ARDS) classic case
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14
Q

Combined Ventilatory & Oxygenation Failure:

A

Diseased bronchioles & alveoli (oxygenation failure)
-ex. Ephysema, asthma

Increased work of breathing leads to ineffective respiratory muscle function (ventilatory failure)

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15
Q

What are the CNS signs and symptoms of V/Q mismatch?

A

▪ Irritability
▪ Confusion
▪ Impending doom
▪ Somnolence

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16
Q

What are the respiratory signs and symptoms of V/Q mismatch?

A

▪ Dyspnea
▪ Increased Depth - hypoxemia
▪ Decreased Depth - hypercapnia

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17
Q

What are the cardiovascular signs and symptoms of V/Q mismatch?

A
▪ Tachycardia - early
▪ HTN - early
▪ Bradycardia - late
▪ Hypotension - late
▪ Arrhythmias
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18
Q

Acute Respiratory Distress Syndrome (ARDS):

A

syndrome of lung inflammation and injury, potentially fatal non-cardiac pulmonary edema. Often associated with acute lung injury (ALI)

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19
Q

Characteristics of ARDS?

A
▪ acute and refractory hypoxemia
		despite 100% FIO2 
▪ dyspnea
▪ decreased lung compliance
▪ alveolar collapse
▪ bilateral infiltrates “white out” →
▪noncardiac-associated bilateral 
		pulmonary edema
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20
Q

Pathophysiology of ARDS:

A

activation of the systemic inflammatory response in response to direct or indirect lung injury

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21
Q

Phases of ARDS:

A
Phases:
Early changes of SOB and increased HR 
Infiltrates, pulm. Edema
Increasing hypoxemia (days 2-10)
Pulmonary fibrosis
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22
Q

What are Direct Mechanisms of ARDS:

A
lead to alveolar inflammation and injury:
▪ aspiration
▪ inhalation injury
▪ contusion
▪ embolism
▪ radiation
▪ reperfusion injury
▪ oxygen toxicity
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23
Q

What are indirect Mechanisms of ARDS:

A
activation of SIR from outside the lung, tissue destructive cytokines travel to the lungs
▪ shock
▪ sepsis
▪ trauma
▪ pancreatitis
▪ drug overdose
▪ massive blood transfusion
▪ disseminated intravascular coagulopathy
24
Q

Diagnosis of ARDS:

A

▪ Abnormal Chest X-ray

▪ Abnormal ABG’s

▪ Refractory hypoxemia
▪ despite supplemental O2

▪ Abnormal Pulmonary Function Tests
▪ ↓ compliance
▪ ↓ FRC

25
Q

Nursing Priority of ARDS:

A

Early Recognition!

Collaborative management
Support and improve oxygenation:
	▪ mechanical ventilation
	▪ positioning
Medications &amp; fluids
Nutritional support 
Prevention of complications
	 ▪ multi-organ system dysfunction/failure
	 ▪ ventilator acquired pneumonia
26
Q

How is lung cancer diagnosed and treated?

A

Diagnosis
∙ chest x-ray ∙ biopsy ∙ CT
∙ bronchoscopy ∙ thoracoscopy ∙ PET
∙ MRI

Treatment
∙ non-surgical - chemotherapy, radiation therapy, targeted therapy, photodynamic therapy
∙ surgical – removal of tumor, lobectomy, pneumonectomy

27
Q

Cerebral Angiography

A
  • Images of cerebral circulation
  • Use: checks patency/adequacy of circ.

-Prep: good hydration
check circulation distal extremity
NPO
allergies

28
Q

Post cerebral angiography

A
  • keep leg straight
  • observe site for hematoma
  • check distal circulation
  • neuro assessment
  • pressure dressing
29
Q

CSF normal findings

A
  • Clear, colorless
  • Normal pressure
  • Few WBC
  • No RBC
  • Composition similar to plasma
30
Q

Cerebral blood supply

A

brain receives 750 ml/min of blood = 20% of CO

31
Q

Monro-Kellie Hypothesis

A
  • The skull does not expand
  • Within this closed system are 3 fluctuating components: blood (move into sinuses), brain (swell), CSF (shunted or absorbed quicker)
  • If one component increases, one or both of the others decrease
32
Q

Cerebrospinal Fluid

A
  • Volume 120ml to 150ml
  • Body produces about 500ml daily
  • Cushions brain and spinal cord
  • Absorbed through arachnoid villa
  • Returned to systemic circulation by internal jugular
33
Q

Cerebral Perfusion Pressure

A
  • Changes in MAP or ICP affect CPP
  • Normal MAP = 70 to 105 mmHg
  • Normal ICP = 5 to 15 mmHg
  • Normal CPP = 60 to 100 mmHg

*any increase/decrease in CPP means brain isn’t being adequately perfused

34
Q

Autoregulation

A
  • Ability of the brain to maintain cerebral blood flow despite changes in CPP
  • Achieves this by altering diameter of arterioles (response to changes in cerebral environment)
  • Autoregulation does not work if CPP < 50mmHg or > 150mmHg
35
Q

Intracranial Pressure (ICP)

A
  • Pressure exerted by brain tissue, CSF, blood against the inside of the skull
  • Normal 5-15mmHg
  • Prolonged elevation causes ischemia due to decreased cerebral blood flow
36
Q

Cushing’s Triad

A
  • Elevated SBP
  • Widening pulse pressure- (normal =30-40mmHg)
  • Bradycardia
  • LATE sign of increased ICP
37
Q

Herniation Syndromes

A
  • Cingulate- lateral shift of 1 hemisphere
  • Uncal- uncus of temporal lobe pushed over edge of tentorium
  • Central- downward displacement of basal ganglia
  • Cerebellar-cerebellar tonsils pushed toward through -foramen magnum
38
Q

Guillian-Barre’ Syndrome

A
  • Acute autoimmune disorder
  • Destruction of myelin –impairs impulse conduction (communicate)
  • Descending
  • Affects respiratory function
  • Ascending GBS
  • Most common
  • GBS “ground to brain symptoms”
39
Q

Stages of Guillian-Barre’ Syndrome

A
  • Initial Period (1-4 weeks), Definitive symptoms begin
  • Plateau Period (days to 2 weeks)
  • Recovery Period (6 months to 2 yrs): Remyelinization , Axonal regneration
40
Q

GB Plan of Care

A
  • Diagnostic testing
  • Priority nursing care: Respiratory care - priority, Pain management, Communication and emotional, Nutritional
  • Involvement of family, other team members
  • Education
  • Medical treatments—plasmapheresis (take out antibodies and replace them with new ones, complications - bleeding, ecchymosis)
41
Q

Treatment for GBS

A

-Plasmapheresis:
Removes circulating antibodies assumed to cause disease
Plasma selectively separated from whole blood; blood cells returned to patient without plasma
Plasma usually replaces itself, or patient is transfused with albumin

42
Q

Early Signs of Intracranial Pressure

A
  1. change in mentation, may be subtle
  2. change in LOC
    restlessness, fidgety, barely off normal
3. addition of other signs and symptoms
pupil changes
visual changes
motor weakness of 1 or > limbs
headache
43
Q

Later signs of worsening intracranial pressure increase

All of the above plus:

A
  1. nausea, vomiting
  2. deteriorating LOC
  3. confusion
  4. papilledema
  5. hemiplegia
  6. decerebrate posturing
  7. decorticate posturing
44
Q

Late Symptoms of increased Intracranial pressure

A
  1. Cushing’s reflex:
    - Increased systolic blood pressure
    - Increased pulse pressure
    - bradycardia
45
Q

Pathophysiology of SCI

A
  • Injury interrupts blood supply - damage to blood vessels
  • Clots accumulate in damaged vessels
  • Chemical mediators produce ischemia
  • Necrosis and neuron death occurs
  • CPP may be decreased by neurogenic shock
46
Q

Key Assessment Findings in SCI

A
  • Neurological system- level of sensation, motor ability, breathing
  • Cardiovascular system- neurogenic shock (lose sympathetic tone- vessels dilate=bp falls)
  • Respiratory system- vent, deep breathing, RT, quad cough, incentive spirometry
  • GI/GU systems- spinal shock= bowel sounds will be absent, distended abdomen, loss of emptying of bladder, urinary retention, UTI
47
Q

Spinal Shock (Syndrome)

A

mainly a loss of reflexes, minutes within injury can last up to weeks, flaccid paralysis, loss of sensation, loss of motor response
temporary

48
Q

drug Management of SCI

A
  • steroids: decreases inflammation but decrease immune, prone for stress ulcers, elevated glucose
  • dextran:expand plasma, increase cap blood flow to spinal cord
  • atropine sulfate: bradycardia
  • dopamine: elevate bp
  • muscle relaxant: after shock has resolved
49
Q

Priority Problems for Long-Term Management of SCI

A
  • Difficulty breathing
  • Impaired physical mobility (safety)
  • Spastic or flaccid bladder and bowel
  • Impaired adjustment
50
Q

Autonomic Dysreflexia

A
  • develops massive sympathetic discharge from kinked catheter, constipation
  • severe HTN, hr drop, headache, nasal stuffiness, flushing
  • first thing to do!!!!- raise the head of bed (to decrease hemorrhagic bleed in head)
  • loosen tight clothing, assessing for cause, check for fecal impaction, urinary retention
51
Q

antidote for heparin

A

protamine sulfate

52
Q

antidote for warfarin

A

vitamin k

53
Q

antidote for tpa

A

FFP

54
Q

Medications for CO

A

Digoxin, inotropic (dobutamine, dopamine)

55
Q

Right brain injury= left side of body is effected

A
Hemiplegia
Impairment in creativity
Confused on date time place
Cannot recognize faces
Loss of depth perception
Trouble staying on topic 
Can’t see thing on left side- left side neglect
Trouble with grooming
Emotional unstable
Impulsive
Denial
Not able to interpret nonverbal language
56
Q

left sided brain injury

A
Right hemiplegia
Aphasia- trouble formulating words and comprehending them
Aware of limits
Severe depression
Trouble understanding written text
Issues with writing - agraphia
Impaired math
Memory intact
Trouble seeing on right side of body
57
Q

Drug Therapy for strokes

A
Thrombolytics
Anticoagulants
Lorazepam, other antiepileptics
Calcium channel blockers
Stool softeners
Analgesics (for pain)
Antianxiety drugs