Oxygenation - ABGs, ARDS, mechanical ventilation

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Test 2 - sem 3

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47 Terms

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What is ARDs

Acute respiratory distress syndrome

Sever inflammation process causing alveolar damage

Sudden pulmonary edema (fluid in the lungs)

Hypoxia, where oxygen supplements do NOT help!

Mortality rate = 36-44%

Mild → death

Muti-system damage/failure

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Alveolar collapse

Atelectasis

No breath sounds

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Is ARDS a controlled inflammatory response?

No

It is either direct or indirect

The result is respiratory failure and refractory hypoxia

Requires immediate medical interventions

There are three specific stages: exudative, proliferative, and fibrotic phase

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Direct causes of ARDs

Aspiration

Chest trauma

PNA

Inhalation injury

Pulmonary embolus (PE)

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Indirect causes of ARDs

SEPSIS

Shock

Pancreatitis

Burns

Mass blood transfusions

Cardiopulmonary bypass

Drug/alcohol overdose

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Phase 1 of ARDs

Exudative in 72 hours of exposure/onset of the causative agent

Clinically you will see someone who can’t breath and additional O2 support does not improve their saturations

Respiratory distress

Air hungry

Protein is lost that helps keep fluid in cells → 3rd spacing

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Phase 2 of ARDs

Proliferate in the repair process

1-3 weeks

Individualized and weaning off vent or transitioning to oxygen therapy

Frequent monitoring

Decreased blood pressure and cardiac output

Severe V/Q mismatch result in severe tissue hypoxia and lactic acidosis

After 2-3 weeks the damage is permeant

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Phase 3 of ARDs

Fibrotic scarring causes impaired gas exchange

Pulmonary hypertension worsens

Positioning patient is a type of therapy (turning/positioning Q2H, repositioning of ET tube to prevent mouth ulcers)

Prone positions helps lung expansion, require planned teamwork

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Even getting O2 on a patient with ARDs…

this doesn’t help patient and they will continue to get worse

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Clinical manifestations

Patient experience one of the causative factors →

SEVERE DYSPNEA WITH RAPID ONSET (less than 7 days) →

SUPPLEMENTAL O2 INCREASES FO NOT IMRPOVE BREATHING

Hypoxia, tachypnea, tachycardia (compensation) →

Bilateral infiltration of CXR

<p>Patient experience one of the causative factors →</p><p>SEVERE DYSPNEA WITH <strong>RAPID ONSET </strong>(less than 7 days) →</p><p><strong>SUPPLEMENTAL O2 INCREASES FO NOT IMRPOVE BREATHING </strong>→</p><p>Hypoxia, tachypnea, tachycardia (compensation) →</p><p>Bilateral infiltration of CXR</p>
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Diagnostic testing for ARDs

Intercostal retractions, crackles

BNP levels

Echo

ABG’s, CBC

Chest x-ray

Pulmonary artery catheterization

Transthoracic echocardiography (TTE)

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Goal of ARD therapy

Identification and treatment of underlying condition

Aggressive, supportive care

  • Endotracheal intubation

  • Mechanical ventilation: peep support

  • Circulatory support

  • Appropriate fluid volume

  • Nutritional support

  • PaO2 >60mmhg, or O2 stat >90%

  • Get consult, HOB up, suction, steroids, antibiotics

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ARDs nursing care/treatment

Close ICU monitoring: frequent oxygen saturation assessments, no improvement with supplemental O2 application

Frequent assessment: worsening lung sounds; rales/rhonchi present-intubation

Management of underlying cause

Anticipate and prepare for intubation

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Nursing diagnosis

Impaired gas exchange

Anxiety

Imbalance nutrition, less than body requirements

Potential skin breakdown

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What is PEEP

Positive End Expiratory Pressure

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How to provide PEEP

PEEP at the end of each breathe to ensure alveoli does not collapse

Routes:

  • CPAP

  • BiPAP

  • Mechanical Ventilation

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Vent modes

Synchronized Intermittent Mandatory Ventilation (SIMV)

Assist Control (AC) mode

*The use of PEEP helps increase functional residual capacity and reverse alveolar collapse by keeping the alveoli open, resulting in improved arterial oxygenation and reduction in the severity of the ventilation-perfusion imbalance

*After 2 weeks - the talk of tube coming out and trac going in

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RN role during intubation

Know your patient directives

Anticipate the need for intubation

Know where the emergency equipment is located and the process for emergency situations

Ensure patient receives all the care you have available to provide (current orders and scope of practice)

Talk to your patient, tell them what is going on, why it’s happening, what we are doing to “fix” it, and that you’ve got their back

Ensure that they providers and the respiratory therapist know the changing patients status and have the supples they need

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Nursing care on intubation

Close ICU monitoring

Oxygen administration

Nebulizer therapy

Proper positioning

Frequent turing

Oxygen monitoring

Pain management

Hemodynamic monitoring

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Medications

Paralytic (so they don’t move)

General anesthetic

Antipyretics

Antibiotics

Diuretic

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Ventilatory management

Control patient anxiety - “fighting” the vent

Potential sedation:

  • lorazepam (Ativan)

  • midazolam (Versed)

  • propofol (Diprivan)

  • Short-acting barbiturates

  • Potential paralytics (neuromuscular blocking)

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Prone positioning

“Good” lung down

Laying on stomach

Un-prone when they stop responding well

Can still do everything like normal

Face to the side

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Nutrition

35-45 kcal/kg/day to meet caloric requirements

TPN and lipids/external feeding

Tube feeding is preferred due to gut being the best absorption, but if it isn’t working then we go through the central/PICC line

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ARDs phonetic

Atelectasis  

Refractory hypoxemia

Decrease lung compliance

Surfactant decreased

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Normal pH level

7.35-7.45

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Acidosis

>7.35

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Alkalosis

<7.45

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PaCO2

35-45

Lungs

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HCO3

22-26

Kidneys

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Respiratory buffers

Takes minutes-hours to kick in

Control H+ levels with CO2

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Renal buffers

Takes slower to kick in, but lasts longer

Control H+ levels with HCO3

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Hyperventalation

Blowing off CO2

Decreases H+ ions

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Hypoventilation

Holding on to CO2

Increase H+ ions

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How do kidneys increase H+ ions

Reabsorb HCO3, so hydrogen is excreted

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How do kidneys decrease H+ ions

Excreted HCO3, so hydrogen is absorbed

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PaCO2 and HCO3 both abnormal…

Respiratory

Opposite

Metabolic

Equivalent/Equal

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Fully compensated

The pH has returned to the normal range, but both CO2 and HCO3 are abnormal

The body has successfully corrected the imbalance, though the “fingerprints” of compensation remain

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Partially compensated

The pH is still abnormal, but both CO2 and HCO3 are abnormal, showing that the body is trying to fox the problem

The compensatory system (lungs or kidneys) is working, but it hasn’t fully corrected the imbalance yet

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Uncompensated

The pH is abnormal and either CO2 or HCO3 is abnormal but the other value is still normal

The body has not yet started to correct the imbalance

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What is cystic fibrosis

Autosomal recessive genetic mutation

Get it from parents (1/4 children have it with parents that have it or carry it)

Disruption in the transport of chloride, sodium and water → build up of mucous

Effect the pancreas and lungs

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How many people does CF effect

30,000 people in the US

1 in every 3,500 babies (prenatal screening)

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What happens in CF

Mucosal surface alteration

Exocrine gland dysfunction

  • Sweat glands = more chloride → salty sweat and electrolyte imbalance

  • GI tract

  • Pancreas = absorption is blocked → malnutrition

  • Respiratory tract

  • Males = infertile

  • Females = hard for sperm to enter due to thick cervical mucous

Water transplant abnormalities

THICK, TENACIOUS SECRETIONS

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Nursing assessment for CF

Health history

  • Salty taste to skin

  • Abdominal pain

  • Difficulty passing stool

  • Poor weight gain despite diet

  • Chronic cough

  • Respiratory infection

  • Fever

  • Pulmonary meds

  • Bone pain

Physical examination:

  • Inspection (barrel chest, clubbing nails)

  • Auscultation (diminished lung sounds, tachycardia, bowel sounds)

  • Percussion

  • Palpation (asymmetrical chest with atelectasis, tender liver)

Labs/diagnostic tests

  • Increase chloride

  • Decreased O2 stat

  • Chest x-ray → hyperinflatration

  • Pulmonary function test

  • Bronchial walls thicken

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Nursing management for CF

Minimize pulmonary complications

  • Promote growth and development

  • Mobilize secretions multiple times a day

Maintain patent airway

  • brochodilators, antibiotics, CPT, bilateral lung transplant

Prevent infection

  • Pulmonary hygiene

NO CURE

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Respiratory medication management

Bronchodilators

  • Albuterol, Levalbuterol

Mucolytics

  • Dornase Alpha, Hypertonic Saline

Antibiotics 

Aerosolized Antibiotics

  • Tobramycin

Dilate → mucolytics → mucous clearance → inhale antibiotics

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Maintaining growth

Pancreatic Enzyme Supplements: Pancrealipase

  • Every time you eat

High fat, high protein diet; ADEK Vitamins

Tube feeds/TPN

Increase calories

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Promoting family coping

Daily interventions

Frequent hospitalizations

Surgical management

Relationship strain

Anticipatory grieving