Critical care - ARF & ARDS, NIV/HFNC

Question 1

What are the components for intact ventilation?

Answer 1

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

Question 2

What is oxygenation? Physiology of oxygenation?

Answer 2

Simple diffusion process at pulmonary-capillary bed

Gaseous exchange across alveolar membrane to blood vessels

Question 3

Diffusion requirements for oxygenation

Answer 3

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

Question 4

Physiology of perfusion

Answer 4

Process of circulating blood through the capillary bed

Question 5

Perfusion requirements

Answer 5

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

Question 6

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

Answer 6

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

Question 7

What is a low V/Q ratio caused by?

Answer 7

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

Question 8

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

Answer 8

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

Question 9

What is very low V/Q ratio and what treatment

Answer 9

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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

Example of condition w high V/Q ratio

Answer 12

Pulmonary embolism

Question 13

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

Answer 13

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

Question 14

What is non-invasive ventilation (NIV)?

Answer 14

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

Question 15

Types of NIV

Answer 15

Modes of delivery:
CPAP (Continuous Positive Airway Pressure)

BiPAP (Bi-level Positive Airway Pressure)

Used for managing acute and chronic respiratory failure.

Question 16

Nursing care of pts on NIV/HFNC (initiation)

Answer 16

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

Question 17

Nursing care of pts on NIV/HFNC (monitoring)

Answer 17

Continuous SpO2 monitoring
ABG for titration/weaning
Monitor for complications

Question 18

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

Answer 18

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

Question 19

Rationale for BiPAP/CPAP

Answer 19

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

Question 20

What is BiPAP

Answer 20

(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

Question 21

Clinical indication for BiPAP

Answer 21

Ventilation (CO2) and/or oxygenation problems

Question 22

What is CPAP

Answer 22

(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.

Question 23

Clinical indication for CPAP

Answer 23

Oxygenation problem

Question 24

BiPAP vs CPAP

Answer 24

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.

Question 25

Complications of HFNC

Answer 25

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

Question 26

Definition of Acute Respiratory failure (ARF)

Answer 26

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

Question 27

Differences between Type 1 and 2 RF

Answer 27

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

Question 28

Causes of Type 1 RF

Answer 28

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)

Question 29

Causes of Type II RF (3 broad categories)

Answer 29

Pulmonary dysfunction CNS dysfunction Neuromuscular dysfunction

Question 30

Causes of Type II RF - Pulmonary Dysfunction

Answer 30

* COPD * Emphysema * Chronic Bronchitis

Question 31

Causes of Type II RF - CNS dysfunction

Answer 31

Head injuries Drug overdose

Question 32

Causes of Type II RF - Neuromuscular dysfunction

Answer 32

* Obstructive Sleep apnea * Myasthenia Gravis * Guillain-Barre syndrome * Spinal cord trauma

Question 33

What is Type 3 respiratory failure?

Answer 33

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

Question 34

What is Type 4 respiratory failure?

Answer 34

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

Question 35

Management of Type 3 respiratory failure

Answer 35

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.

Question 36

Management of Type 4 respiratory failure + rationale

Answer 36

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.

Question 37

Clinical manifestation (Early signs) of ARF

Answer 37

* 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)

Question 38

Clinical manifestation (Late signs) of ARF

Answer 38

* Confusion * Central cyanosis * Tachycardia * Tachypnea * Diaphoresis * Respiratory arrest

Question 39

Pathophysiology of hypoxaemia (Type 1)

Answer 39

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

Question 40

Pathophysiology of hypercapnia (Type 2)

Answer 40

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

Question 41

Complications of long-standing chronic respiratory failure

Answer 41

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

Question 42

Investigations to be ordered for ARF

Answer 42

* ABG * FBC * U/E/Cr * CXR * CT scan of lungs * Sputum, blood, urine c/s

Question 43

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

Answer 43

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

Question 44

Goals of management for ARF

Answer 44

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

Question 45

How to maintain adequate airway patency for ARF

Answer 45

- 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)

Question 46

How to correct underlying causes of ARF

Answer 46

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

Question 47

How to optimise O2 delivery for ARF

Answer 47

- 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

Question 48

How to decrease O2 demand for ARF

Answer 48

- Provide adequate bed rest - Timing of ADLs - Addressing sepsis, restlessness, patient-ventilator dysynchrony

Question 49

How to prevent complications for ARF

Answer 49

Monitor for potential complications from ARF: – Immobility-related complication – Fluid and electrolyte imbalances – Nutritional imbalances – Adverse effects from medications – Ventilator-associated complications

Question 50

Definition of Acute Respiratory Distress Syndrome (ARDS)

Answer 50

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)

Question 51

How to differentiate ARDS from Acute Lung Injury (ALI)

Answer 51

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)

Question 52

Pathophysiology of ARDS

Answer 52

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 2. 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

Question 53

Consequences of ARDS

Answer 53

1) Impaired gas exchange= V/Q mismatching 2) Decreased lung compliance 3) Pulmonary HTN

Question 54

Causes of ARDS

Answer 54

- 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

Question 55

How many stages are there in ARDS?

Answer 55

4

Question 56

First stage of ARDS

Answer 56

Phase: Injury (within 24 hrs) - Increased dyspnoea and RR - Worsen within 24 hour - Coarse bilateral crackles - CXR reveals shows patchy infiltrates

Question 57

Second stage of ARDS

Answer 57

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

Question 58

Third stage of ARDS

Answer 58

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

Question 59

Fourth stage of ARDS

Answer 59

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

Question 60

Diagnosis of ARDS

Answer 60

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)

Question 61

Common management problems of ARDS

Answer 61

- Decreased Compliance - Refractory Hypoxemia - High Mortality

Question 62

Strategies to manage the common management problems in ARDS

Answer 62

- Low Tidal Volume Ventilation - Permissive Hypercapnea - Best PEEP Curve - Prone Positioning - Inhaled NO2

Question 63

Risk factors for mortality

Answer 63

- Multi-organ Failure - Underlying Cause of ARDS - Degree of Hypoxemia is not a risk factor

Question 64

Goals of treatment of ARDS

Answer 64

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

Question 65

Explain the difference behind differing SpO2 and PaO2 levels. e.g. SpO2: 90% PaO2: 80

Answer 65

O2 saturation (SpO2) varies with the PaO2 in a nonlinear relationship Possible V/Q shunt

Question 66

What is a shunt effect?

Answer 66

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.