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PPNP 3 > Critical care - ARF & ARDS, NIV/HFNC > Flashcards

Critical care - ARF & ARDS, NIV/HFNC Flashcards

- Interpretation and management of acid-base imbalances- Acute respiratory failure- Adult respiratory distress syndrome - Nursing management for MV and HFNC- Management of Shock

1
Q

What are the components for intact ventilation?

A

Brain, respiratory centre, nerves between brainstem and respiratory muscles, intact and patent upper and lower airways, intact and non-collapsed alveoli

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2
Q

What is oxygenation? Physiology of oxygenation?

A

Simple diffusion process at pulmonary-capillary bed

Gaseous exchange across alveolar membrane to blood vessels

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3
Q

Diffusion requirements for oxygenation

A
  • Intact, non-thickened alveolar walls (no gaseous exchange occurs in alveolitis)
  • Minimal interstitial space and without additional fluid
  • Intact, non-thickened capillary walls
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4
Q

Physiology of perfusion

A

Process of circulating blood through the capillary bed

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5
Q

Perfusion requirements

A
  • adequate blood volume
  • adequate hemoglobin
  • intact, non-occluded pulmonary capillaries
  • functioning heart
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6
Q

relationship between heart and lungs (normal ventilation perfusion) (V/Q)

A

Pulmonary artery carries deoxygenated blood to the alveoli, oxygenated blood is carried to the heart via the pulmonary vein

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7
Q

What is a low V/Q ratio caused by?

A

e.g. Pneumonia/asthma/COPD

When ventilation is impaired (e.g. bronchospasm/ bronchitis), alveoli will not get adequate oxygen, unable to carry out gaseous exchange

–> Blood going back to heart is not 100% oxygenated

therefore, ventilation compromised, but perfusion (Q) is intact

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8
Q

What is the general treatment for LOW V/Q ratio?

A
  • give oxygen as the airways are only partially obstructed, so it is possible for oxygen to enter the alveoli by diffusion
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9
Q

What is very low V/Q ratio and what treatment

A

Usually caused by shunt (blood flows through the pulmonary circulation but does not come into contact with functional alveoli)

Multiple alveoli affected, blood reaching the heart poorly oxygenated

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10
Q

Why cannot use oxygen therapy for VERY LOW V/Q ratio?

A

True shunt is not responsive to oxygen therapy as the alveoli are collapsed and oxygen cannot gain entry into them

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11
Q

In what cases will perfusion (Q) be compromised? What is high V/Q ratio??

A

Perfusion compromised when pt is in shock, and no proper oxygenation, low PaO2, SaO2 as oxygen is not going into the body due to poor perfusion

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12
Q

Example of condition w high V/Q ratio

A

Pulmonary embolism

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13
Q

Will increasing oxygen to a pt in shock be the most effective way of increasing PaO2? If not, what should the treatment be?

A

NO!! Problem lies with perfusion! Give inotropes and colloids to build up perfusion!

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14
Q

What is non-invasive ventilation (NIV)?

A

A method of providing ventilatory support without the need for an invasive procedure, such as intubation. It delivers pressurized air/oxygen through a tightly fitting mask

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15
Q

Types of NIV

A

Modes of delivery:
CPAP (Continuous Positive Airway Pressure)

BiPAP (Bi-level Positive Airway Pressure)

Used for managing acute and chronic respiratory failure.

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16
Q

Nursing care of pts on NIV/HFNC (initiation)

A

Choose appropriate size of mask (NIV)
set up NIV/HFNC incl. audible alarms
Position patient: upright (high Fowler’s) if no contraindication
ABG post initiation

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17
Q

Nursing care of pts on NIV/HFNC (monitoring)

A

Continuous SpO2 monitoring
ABG for titration/weaning
Monitor for complications

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18
Q

What does NIV (BiPAP and CPAP) do?
Hint: delivers positive…

A

delivers positive pressure into lungs without need for endotracheal intubation (ETT)

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19
Q

Rationale for BiPAP/CPAP

A

Unload respiratory muscles during inspiration

Inspiratory Positive Airway Pressure (IPAP): Higher pressure during inhalation. Supports the work of breathing by assisting airflow into the lungs. This reduces the effort required by the respiratory muscles

CPAP: Airway stenting

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20
Q

What is BiPAP

A

(Bi-level Positive Airway Pressure)
Provides two levels of pressure:

Inspiratory Positive Airway Pressure (IPAP): Higher pressure during inhalation.

Expiratory Positive Airway Pressure (EPAP): Lower pressure during exhalation.

Offers inspiratory support to reduce respiratory muscle effort and exhalatory support to prevent airway collapse, improving ventilation and gas exchange

Helpful for patients with cardiopulmonary disorders such as CHF and lung disorders or certain neuromuscular disorders

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21
Q

Clinical indication for BiPAP

A

Ventilation (CO2) and/or oxygenation problems

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22
Q

What is CPAP

A

(Continuous Positive Airway Pressure)

CPAP provides a single CONTINUOUS pressure throughout both inhalation and exhalation.

Acts as a “stent” to keep the airway and alveoli open, reducing upper airway obstruction and improving oxygenation in conditions like obstructive sleep apnea or pulmonary edema.

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23
Q

Clinical indication for CPAP

A

Oxygenation problem

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24
Q

BiPAP vs CPAP

A

BiPAP has a greater ability to reduce PaCO₂ and influence systemic effects like vasoconstriction compared to CPAP

By increasing the depth of ventilation (tidal volume), BiPAP helps remove excess carbon dioxide (CO₂) from the blood more effectively.

Elevated PaCO₂ causes systemic vasodilation as the body attempts to remove CO₂.
BiPAP lowers PaCO₂ more effectively, thereby reversing CO₂-induced vasodilation and restoring vasoconstriction.

BiPAP: Preferred for conditions with hypercapnia (e.g., COPD exacerbations, neuromuscular disorders).

CPAP: More effective for conditions like obstructive sleep apnea (OSA) or acute pulmonary edema, where the primary issue is oxygenation and airway collapse, not CO₂ retention.

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25
Q

Complications of HFNC

A

Pneumothorax (mostly children & infants)
Device-related pressure injuries - apply Mepilex/pressure relieving
Dry oral mucosa - to ensure oral hygiene with oral swabs
Dry eyes - to ensure correct placement of straps
Haemodynamic instability, hypotension
Non-compliance, fear, claustrophobia

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26
Q

Definition of Acute Respiratory failure (ARF)

A

A state of disturbed gas exchange resulting in abnormal ABG values.

  • PaO2 < 60 mmHg (hypoxemia)
  • PaCO2 > 50 mmHg (hypercapnia)

with

  • pH < 7.35 on room air
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27
Q

Differences between Type 1 and 2 RF

A
  1. Type 1: Failure of OXYGENATION
    Type 2: Failure of VENTILATION
  2. Type 1: Normal or low PaCO2—Hypoxaemia WITHOUT hypercapnia

Type 2: High PaCO2 (>50 mmHg)—-Hypoxaemia WITH hypercapnia

28
Q

Causes of Type 1 RF

A

Causes (Respiratory dysfunctions):
* Bronchial Asthma
* Emphysema
* Chronic Bronchitis
* Pneumonia
* Acute Pulmonary Edema
* Heart Failure
* Pulmonary Embolism
* Cardiogenic Shock
* Adult Respiratory Distress
Syndrome (mixed of Type I & II)

29
Q

Causes of Type II RF (3 broad categories)

A

Pulmonary dysfunction
CNS dysfunction
Neuromuscular dysfunction

30
Q

Causes of Type II RF - Pulmonary Dysfunction

A
  • COPD
  • Emphysema
  • Chronic Bronchitis
31
Q

Causes of Type II RF - CNS dysfunction

A

Head injuries
Drug overdose

32
Q

Causes of Type II RF - Neuromuscular dysfunction

A
  • Obstructive Sleep apnea
  • Myasthenia Gravis
  • Guillain-Barre syndrome
  • Spinal cord trauma
33
Q

What is Type 3 respiratory failure?

A

results from lung ATELECTASIS in the perioperative period, resulting in PERIOPERATIVE respiratory failure

After GA, decreases in functional residual capacity lead to collapse of dependent lung units

34
Q

What is Type 4 respiratory failure?

A

caused by HYPOPERFUSION of respiratory muscles during circulatory shock (e.g., cardiogenic, septic, or hypovolemic shock)

35
Q

Management of Type 3 respiratory failure

A

frequent changes in position, chest physiotherapy, upright positioning, and control of incisional and/or abdominal pain.

Noninvasive positive-pressure ventilation may also be used toreverse regional atelectasis.

36
Q

Management of Type 4 respiratory failure + rationale

A

Intubation and mechanical ventilation

Allows redistribution of the cardiac output away from the respiratory muscles and back to vital organs while the shock is treated.

37
Q

Clinical manifestation (Early signs) of ARF

A
  • Restlessness
  • Fatigue
  • Headache
  • Dyspnea
  • Tachycardia
  • ↑B/P
  • Tachypnea
  • Use of accessory muscle
  • Nasal flaring
  • Paradoxical breathing (chest wall moves in when taking a breath and moves out when exhaling)
38
Q

Clinical manifestation (Late signs) of ARF

A
  • Confusion
  • Central cyanosis
  • Tachycardia
  • Tachypnea
  • Diaphoresis
  • Respiratory arrest
39
Q

Pathophysiology of hypoxaemia (Type 1)

A
  1. Alveolar hypoventilation
    e.g. opiate overdose
  2. Low inspired oxygen
    - Due to reduced oxygen availability in the inspired air
    e.g. Commercial flights, high altitude (decreased atmospheric pressure)
  3. Diffusion limitation
    - Due to impaired movement of oxygen from the alveoli into the blood across the alveolar-capillary membrane
    e.g. Idiopathic pulmonary fibrosis
  4. V/Q mismatch: Impaired ventilation (airflow), preserved perfusion
    e.g.Lobar pneumonia (One lobe receiving normal perfusion but decreased ventilation because air spaces are congested with inflammatory exudate)
  5. V/Q mismatch: Preserved ventilation, impaired perfusion
    e.g. pulmonary embolism
40
Q

Pathophysiology of hypercapnia (Type 2)

A

Hypercapnia results from alveolar hypoventilation, which can occur due to:

  1. Decreased neurorespiratory drive: respiratory centers in the brainstem regulate ventilation. A reduced drive leads to inadequate ventilation.
    e.g. encephalopathy, cerebral ischemia
  2. Capacity of the muscle pump (impaired by muscular dystrophy, electrolyte imbalances)
  3. Increase in load that cannot be overcome

Alveolar hypoventilation results in capacity < load:
- leading to respiratory failure where CO₂ builds up (hypercapnia), and oxygen levels drop

41
Q

Complications of long-standing chronic respiratory failure

A

Long-standing chronic respiratory failure –> Pulmonary vasoconstriction –> Pulmonary arterial hypertension –> Right ventricular function becomes impaired –> Right heart failure

42
Q

Investigations to be ordered for ARF

A
  • ABG
  • FBC
  • U/E/Cr
  • CXR
  • CT scan of lungs
  • Sputum, blood, urine c/s
43
Q

Treatment for Type 1 (hypoxaemic) and Type 2 (hypercapnic) RF

A

Type 1 (hypoxaemic) RF:
- long-term oxygen therapy for at least 15 hours a day for pts with stable condition of a resting PaO2 of 7.3kPa or lower

Type 2 (hypercapnic) RF:
- Domiciliary NIV for chronic hypercapnic RF

44
Q

Goals of management for ARF

A
  1. Maintain adequate airway patency
  2. Correct underlying cause
  3. Optimizing oxygen delivery
  4. Minimizing oxygen demand
  5. Preventing complications
45
Q

How to maintain adequate airway patency for ARF

A
  • chest physiotherapy to removed trapped secretions and allow expectoration of secretions or suctioning
  • administer bronchodilators to increase airway patency
    and mobilize trapped secretions
  • Administer non-invasive mechanical ventilation
  • Intubation and invasive mechanical ventilation (if unable to maintain airway)
46
Q

How to correct underlying causes of ARF

A

Investigations and
medical interventions to
identify and reverse the cause
of ARF

47
Q

How to optimise O2 delivery for ARF

A
  • Monitor for respiratory distress and auscultate for any adventitious lung sounds
  • Provide supplement O2
  • Positioning for comfort and to enhance V/Q matching
  • Blood transfusion to ensure optimal Hb to transport O2
48
Q

How to decrease O2 demand for ARF

A
  • Provide adequate bed rest
  • Timing of ADLs
  • Addressing sepsis, restlessness, patient-ventilator dysynchrony
49
Q

How to prevent complications for ARF

A

Monitor for potential complications from ARF:

– Immobility-related complication
– Fluid and electrolyte imbalances
– Nutritional imbalances
– Adverse effects from medications
– Ventilator-associated complications

50
Q

Definition of Acute Respiratory Distress Syndrome (ARDS)

A

a clinical syndrome of :

  1. severe dyspnea of rapid onset
  2. hypoxemia
  3. diffuse pulmonary infiltrates leading to respiratory failure

Is a subset of Acute Lung Injury (ALI)

51
Q

How to differentiate ARDS from Acute Lung Injury (ALI)

A

3 criteria to diagnose ARDS from ALI:

  1. PaO2/FiO2 ratio of <200 (ARDS) vs <300 (ALI)
  2. CXR indicating bilateral infiltrates (in ARDS)
  3. Pulmonary artery occlusion pressure (PAOP) < 18mmHg or no clinical evidence of left atrial hypertension (in ARDS)
52
Q

Pathophysiology of ARDS

A
  1. Injury to the alveolar capillary membrane –> damage Type 2 alveolar cells (responsible for producing surfactant) –> lack of surfactant will lead to decrease in alveolar compliance and recoil –> causes atelactasis –> reduce lung compliance –> cause ALI or ARDS

Atelactasis –> can also lead to hyaline membrane formation –> impairment of gas exchange –> further deteriorate ALI or ARDS

  1. Injury to the alveolar capillary membrane –> inflammatory mediators released –> cause bronchoconstriction –> impair gas exchange

inflammatory mediators also can cause –> vasoconstriction and obstruction –> pulmonary hypertension –> aggravate ALI or ARDS

Inflammatory mediators–> increase alveolar-capillary membrane permeability –> outward migration of blood cells and fluids from capillaries –> pulmonary edema –> reduce lung compliance and causes impairment in gas exchange

53
Q

Consequences of ARDS

A

1) Impaired gas exchange= V/Q mismatching

2) Decreased lung compliance

3) Pulmonary HTN

54
Q

Causes of ARDS

A
  • Bacteremia
  • Sepsis
  • Trauma, with or without pulmonary contusion
  • Fractures, particularly multiple fractures and long bone fractures
  • Burns
  • Massive transfusion
  • Pneumonia
  • Aspiration
  • Drug overdose
  • Near drowning
  • Post perfusion injury after cardiopulmonary bypass
  • Pancreatitis
  • Fat embolism
55
Q

How many stages are there in ARDS?

A

4

56
Q

First stage of ARDS

A

Phase: Injury (within 24 hrs)

  • Increased dyspnoea and RR
  • Worsen within 24 hour
  • Coarse bilateral crackles
  • CXR reveals shows patchy infiltrates
57
Q

Second stage of ARDS

A

Phase: Exudative (1-7 days)

  • Marked by mediator-induced interstitial & alveolar oedema and damage with hyaline membrane formation –> affect surfactant release
  • Increase permeability to proteins
  • Hypoxia resistant to supplement O2; require MV
58
Q

Third stage of ARDS

A

Phase: Proliferative
(1-2 weeks after initial
injury)

  • Hemodynamic instability
  • Evidence of SIRS (Temp>38 or <36, HR > 90; PaCO2 less than 32 mmHg, RR >20/min; Increased WBC )
  • Generalised oedema, lungs become more dense, fibrous, decreased lung compliance
  • Thickened alveolar membrane
59
Q

Fourth stage of ARDS

A

Phase: 4 Fibrotic (2-3 weeks after injury)

  • Lung is completely remodelled by sparsely collagenous and fibrous tissues
  • Increased dead space –> poor ventilation –> Increased airway pressure
60
Q

Diagnosis of ARDS

A

In initial stage, ARDS will resemble acute cardiogenic pulmonary edema clinically and radiographically.

Distinction usually made from clinical circumstances associated with onset but
occasionally additional diagnostic tests may help.

1) BNP: hormone released by heart; can find out if condition is because of HF or ARDS

2) Echo-cardiography: detect any ventricular dysfunction, valvular abnormalities, etc

3) PAC (Pul artery catherisation): To measure pressure within heart and lungs TRO cardiogenic involvement
If Wedge pressure >18 mmHg suggests cardio involvement (heart failure)

61
Q

Common management problems of ARDS

A
  • Decreased Compliance
  • Refractory Hypoxemia
  • High Mortality
62
Q

Strategies to manage the common management problems in ARDS

A
  • Low Tidal Volume Ventilation
  • Permissive Hypercapnea
  • Best PEEP Curve
  • Prone Positioning
  • Inhaled NO2
63
Q

Risk factors for mortality

A
  • Multi-organ Failure
  • Underlying Cause of ARDS
  • Degree of Hypoxemia is not a risk factor
64
Q

Goals of treatment of ARDS

A

Treatment is mainly supportive while waiting for lungs to “heal”

– Oxygenation
– Sedation/Comfort
– Prone positioning
– Fluid and electrolytes
– Nutrition
– Pharmacological treatment

Constant monitoring
Treating underlying causes of ARDS

65
Q

Explain the difference behind differing SpO2 and PaO2 levels.

e.g. SpO2: 90%
PaO2: 80

A

O2 saturation (SpO2) varies with the PaO2 in a nonlinear relationship

Possible V/Q shunt

66
Q

What is a shunt effect?

A

A shunt effect results from blood flowing from the right side to the left side of the heart without passing through ventilated areas of the lung.

Shunt is the extreme degree of V/Q mismatch where there is no ventilation. Poor response to oxygen therapy is the feature that differentiates shunt from other mechanisms of hypoxemia.

PPNP 3 (19 decks)

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