pathophysiology of respiratory failure

Pathophysiology of Respiratory Failure

Gamal Rabie Agmy ,MD ,FCCP Professor of Chest Diseases, Assiut University

Non Respiratory Functions

Biologically Active Molecules: *Vasoactive peptides

*Vasoactive amines

*Neuropeptides

*Hormones

*Lipoprotein complexes

*Eicosanoids

Non Respiratory Functions

Haemostatic Functions

Lung defense :

*Complement activation

*Leucocyte recruitment

*Cytokines and growth factors

Protection

Vocal communication

Blood volume/ pressure and pH regulation

Respiratory Functions

*Oxygenation

*CO2 Elimination

Definition

*Failure in one or both gas exchange functions:

oxygenation and carbon dioxide elimination

*In practice:

PaO2<60mmHg or PaCO2>50mmHg

*Derangements in ABGs and acid-base status

Definition

Respiratory failure is a syndrome of

inadequate gas exchange due to

dysfunction of one or more essential

components of the respiratory system

Types of Respiratory Failure

Type 1 (Hypoxemic ): * PO2 < 60 mmHg on room air.

Type 2 (Hypercapnic / Ventilatory): *PCO2 > 50

mmHg

Type 3 (Peri-operative): *This is generally a subset of

type 1 failure but is sometimes considered

separately because it is so common.

Type 4 (Shock): * secondary to cardiovascular

instability.

The respiratory System

Lungs Respiratory pump

Pulmonary Failure

• PaO2

• PaCO2 N/

Ventilatory Failure

• PaO2

• PaCO2

Hypoxic Respiratory

Failure

Hypercapnic Respiratory

Failure

Cardiogenic pulmonary edema

Pneumonia

pulmonary ARDS

extra pulmonary ARDS

Atelectasis

Post surgery changes

Aspiration

Trauma

Infiltrates in immunsuppression

Hypoxic

Respiratory

Failure Pulmonary fibrosis

Brainstem

Spinal cord

Nerve root Airway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Type 3 (Peri-operative)

Respiratory Failure

Residual anesthesia effects, post-

operative pain, and abnormal

abdominal mechanics contribute to

decreasing FRC and progressive

collapse of dependant lung units.

Type 3 (Peri-operative)

Respiratory Failure

Causes of post-operative atelectasis include; *Decreased FRC

*Supine/ obese/ ascites

*Anesthesia

*Upper abdominal incision

*Airway secretions

Type 4 (Shock)

Type IV describes patients who are intubated and

ventilated in the process of resuscitation for

shock

• Goal of ventilation is to stabilize gas

exchange and to unload the respiratory

muscles, lowering their oxygen consumption

*cardiogenic

*hypovolemic

*septic

Hypoxemic Respiratory Failure (Type 1)

Causes of Hypoxemia

1. Low FiO2 (high altitude)

2. Hypoventilation

3. V/Q mismatch (low V/Q)

4. Shunt (Qs/Qt)

5. Diffusion abnormality

6. low mixed venous oxygen due to cardiac desaturation with one of above mentioned factors.

Physiologic Causes of Hypoxemia

Low FiO2 is the primary cause of ARF at high altitude and toxic gas inhalation


Physiologic Causes of Hypoxemia

However, the two most common causes of hypoxemic respiratory failure in the ICU are V/Q mismatch and shunt. These can be distinguished from each other by their response to oxygen. V/Q mismatch responds very readily to oxygen whereas

shunt is very oxygen insensitive.


V/Q: possibilities

0

1

∞

V/Q =1 is “normal” or “ideal”

V/Q =0 defines “shunt”

V/Q =∞ defines “dead space” or “wasted ventilation”


V/Q Mismatch

V/Q>1 V/Q<1

V/Q=o V/Q=∞

Optimal V/Q matching

Dead Space

Why does “V/Q mismatch” cause

hypoxemia?

• Low V/Q units contribute to

hypoxemia

• High V/Q units cannot compensate

for the low V/Q units

• Reason being the shape of the

oxygen dissociation curve which is

not linear

Hypoxic respiratory failure

• Gas exchange failure

• Respiratory drive responds

• Increased drive to breathe – Increased respiratory rate

– Altered Vd /Vt (increased dead space etc)

– Often stiff lungs (oedema, pneumonia etc)

Increased load on the respiratory pump which can push it into fatigue and precipitate secondary pump failure and hypercapnia


Types of Shunt

1. Anatomical shunt

2. Pulmonary vascular shunt

3. Pulmonary parenchymal shunt


Common Causes for Shunt

1. Cardiogenic pulmonary edema

2. Non-cardiogenic pulmonary edema (ARDS)

3. Pneumonia

4. Lung hemorrhage

5. Alveolar proteinosis

6. Alveolar cell carcinoma

7. Atelectasis

Causes of increased dead space

ventilation

*Pulmonary embolism

*Hypovolemia

*Poor cardiac output, and

*Alveolar over distension.

Ventilatory Capacity versus Demand

Ventilatory capacity is the maximal

spontaneous ventilation that can be

maintained without development of

respiratory muscle fatigue.

Ventilatory demand is the spontaneous minute

ventilation that results in a stable PaCO2.

Normally, ventilatory capacity greatly

exceeds ventilatory demand.

Ventilatory Capacity versus Demand

Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both).

Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing.

Components of Respiratory System

*CNS or Brain Stem *Nerves

*Chest wall (including pleura, diaphragm)

* Airways * Alveolar–capillary units

*Pulmonary circulation

Type 2 ( Ventilatory /Hypercapnic

Respiratory Failure)

Causes of Hypercapnia

1. Increased CO2 production (fever, sepsis, burns, overfeeding)

2. Decreased alveolar ventilation

• decreased RR

• decreased tidal volume (Vt)

• increased dead space (Vd)

Hypercapnic Respiratory

Failure

• Depressed drive: Drugs, Myxoedema,Brain stem lesions and sleep disordered breathing

• Impaired neuromuscular transmision: phrenic nerve injury, cord lesions, neuromuscular blokers, aminoglycosides, Gallian Barre syndrome, myasthenia gravis, amyotrophic lateral sclerosis, botulism

• Muscle weakness: fatigue, electrolyte Derangement ,malnutrition , hypoperfusion, myopathy, hypoxaemia

• Resistive loads; bronchospasm, airway edema ,secretions scarring ,upper airway obstruction, obstructive sleep apnea

• Lung elastic loads:PEEPi, alveolar edema, infection, atelectasis

• Chest wall elastic loads:pleural effusion, pneumothorax, flail chest, obesity,ascites,abdominal distension

Hypercapnic Respiratory Failure

(PAO2 - PaO2)

Alveolar Hypoventilation

V/Q abnormality

PI max

increased normal

Nl VCO2

PaCO2 >50mmHg

Not compensation for metabolic alkalosis

Central

Hypoventilation

Neuromuscular

Disorder

VCO2

V/Q

Abnormality

Hypermetabolism

Overfeeding

NPI max


V/Q abnormality

Increased Aa gradient

Nl VCO2

VCO2

V/Q

Abnormality

Hypermetabolism

Overfeeding


V/Q abnormality


Nl VCO2

VCO2

V/Q

Abnormality

Hypermetabolism

Overfeeding

• Increased dead space ventilation

• advanced emphysema

• PaCO2 when Vd/Vt >0.5

• Late feature of shunt-type

• edema, infiltrates


V/Q abnormality


Nl VCO2

VCO2

V/Q

Abnormality

Hypermetabolism

Overfeeding

• VCO2 only an issue in pts with ltd ability to eliminate CO2

• Overfeeding with carbohydrates generates more CO2

Hypoxemic Respiratory Failure

Is PaCO2 increased?

Hypoventilation (PAO2 - PaO2)?

Hypoventilation alone

Respiratory drive

Neuromuscular dz

Hypovent plus another

mechanism

Shunt

Inspired PO2

High altitude

FIO2

(PAO2 - PaO2) No

No Yes

Is low PO2 correctable

with O2?

V/Q mismatch

No Yes

Yes


(PAO2 - PaO2)


V/Q abnormality

NPI max

increased normal

N VCO2

PaCO2 >50 mmHg

Not compensation for metabolic alkalosis

Central

Hypoventilation

Neuromuscular

Problem

VCO2

V/Q

Abnormality

Hypermetabolism

Overfeeding

PI max



Brainstem respiratory depression

Drugs (opiates)

Obesity-hypoventilation syndrome

PI max

Central

Hypoventilation

Neuromuscular

Disorder

N PI max

Critical illness polyneuropathy

Critical illness myopathy

Hypophosphatemia

Magnesium depletion

Myasthenia gravis

Guillain-Barre syndrome

NIF (negative inspiratory force). This is a measure

of the patient's respiratory system muscle

strength.

It is obtained by having the patient fully exhale.

Occluding the patient's airway or endotracheal

tube for 20 seconds, then measuring the maximal

pressure the patient can generate upon

inspiration.

NIF's less than -20 to -25 cm H2O suggest that the

patient does not have adequate respiratory muscle

strength to support ventilation on his own.

Evaluation of Hypercapnia

P0.1 max. is an estimate of the patient's respiratory drive.

This measurement of the degree of pressure drop during the first 100 milliseconds of a patient initiated breath. A low P0.1 max suggests that the patient has a low drive and a central hypoventilation syndrome.

Central hypoventilation vs. Neuro-muscular weakness

central = low P0.1 with normal NIF

Neuromuscular weakness = normal P0.1 with low NIF

Evaluation of Hypercapnia

n The P (A—a)O2 ranges from 10 mm Hg in young patients to approximately 25mm Hg in the elderly while breathing room air.

n P (A-a)O2 if greater than >300 on 100% = Shunt < 300 = V/Q mismatch

• RULE OF THUMB

The mean alveolar-to-arterial difference [P(A—a)o2] increases slightly with age and can be estimated ~ by the following equation:

Mean age-specific P(A—a)O2 age/4 + 4

A-a Gradient

Increased Work of Breathing

Work of breathing is due to physiological work and imposed work. Physiological work involves overcoming the elastic forces during inspiration and

overcoming the resistance of the airways and lung tissue Imposed Work of Breathing

In intubated patients, sources of imposed work of breathing include:

n the endotracheal tube,

n ventilator Circuit n auto-PEEP due to dynamic hyperinflation with airflow obstruction, as is

commonly seen in the patient with COPD. Increased Work of Breathing n Tachypnea is the cardinal sign of increased work of breathing

n Overall workload is reflected in the minute volume needed to maintain

normocapnia.

Pediatric considerations

The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons.


Neonates are obligate nose breathers. This nose breathing occurs until the age of 2-6 months because of the close proximity of the epiglottis to the nasopharynx. Nasal congestion can lead to significant distress in this age group.


The airway size is smaller. Size is one of the primary differences in infants and children younger than 8 years when compared with older patients.

The epiglottis is larger and more horizontal to the pharyngeal wall. The cephalad larynx and large epiglottis makes laryngoscopy more challenging.

Pediatric Consideration

Infants and young children have a narrow subglottic area. In children, the subglottic area is cone shaped, with the narrowest area at the cricoid ring. A small amount of subglottic edema can lead to significant narrowing, increased airway resistance, and increased work of breathing. Older patients and adults have a cylindrical airway that is narrowest at the glottic opening.

Pediatric Consideration


In slightly older children, adenoidal and tonsillar lymphoid tissue is prominent and can contribute to airway obstruction.

The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, lung lymphatics, and the pulmonary circulation.


Infants and young children have fewer alveoli. The number dramatically increases during childhood, from approximately 20 million after birth to 300 million by 8 years of age. Therefore, infants and young children have less area for gas exchange.

The alveolus is smaller. Alveolar size increases from 150-180 mcm to 250-300 mcm during childhood.


Collateral ventilation is less developed, making atelectasis more common. During childhood, anatomic channels form to provide collateral ventilation to alveoli. These pathways exist between adjacent alveoli (pores of Kohn), bronchiole and alveoli (Lambert channel), and adjacent bronchioles. This important feature allows alveoli to participate in gas exchange in the presence of an obstructed distal airway.

Smaller intrathoracic airways are more easily obstructed. With age, the airways enlarge in diameter and length.


Infants and young children have less cartilaginous support of the airways. As cartilaginous support increases, dynamic compression during high expiratory flow rates is prevented.

The respiratory pump includes the nervous system with central control (ie, cerebrum, brain stem, spinal cord, peripheral nerves), respiratory muscles, and chest wall.

The respiratory center is immature in infants and young children, which leads to irregular respirations and the risk of apnea.


The ribs are horizontally oriented. During inspiration, less volume is displaced, and the capacity to increase tidal volume is limited when compared with that in older patients.

The surface area for the interaction between the diaphragm and thorax is small, which limits displacing volume in the vertical direction.


The musculature is less developed. The slow-twitch fatigue-resistant muscle fibers in the infant are underdeveloped.

The soft compliant chest wall provides little opposition to the deflating tendency of the lungs. This leads to a lower functional residual capacity than in adults

• Cardiogenic pulmonary edema

• Non cardiogenic pulmonary edema

• Pneumonia

• Acute pulmonary thromboembolic disease

• Acute allergic alveolitis

• Severe bronchial asthma without diaphragmatic fatigue

• Acute milliary TB and lymphagitis tuberculosa reticularis

Acute Type 1 RF

• Fibrosing alveolitis

• Other causes of IPF

• Chronic allergic alveolitis

• Thromboembolic pulmonary hypertension

• Chronic pulmonary edema

• Lymphangitis carcinomatosis

ChronicType 1 RF

• Upper airway obstruction

• Acute severe asthma with diaphragmatic fatigue

• Acute CNS disorder

• Myathenia gravis

• polyneuritis

• AE of COPD

• Pneumothorax

Acute Type 2 RF

• Chronic bronchitis

• Emphysema

• Pickwikian syndrome

• kyphoscoliosis

• Chronic neuromuscular diseases

• Progressive respiratory diseases preterminally

Chronic Type 2 RF

• Clinical picture of causative disease

• Manifestations of hypoxaemia.

1-Central cyanosis if reduced hemoglobin is

>5gram%.

2- Restlessness, irritability,, impaired

intellectual functions. Acute severe

hypoxaemia may cause convulsions,

coma and death.

3- Hyperventilation and tachypnae through

stimulation of chemoreceptors

Clinically

• 4-Tachycardia,arrythmias,increased COP and dilatation of peripheral vessels

• 5-Pulmonary vasoconstriction with pulmonary hypertension

• 6-Secondary polycythaemia with predisposition to DVT and pulmonary embolism

Clinically

Manifestations of hypercapnia:

• 1-Drowsines,flapping tremors, coma(CO2 narcosis) and papillodema due to increased CSF formation secondary to cerebral vasodilatation and increased cerebral blood flow.

• 2-Paradoxical action on peripheral blood vessels: Vasodilatation through direct action and vasoconstriction through sympathetic stimulation and the predominant action is the local one.

• 3-Tachycardia,sweating and generalized vasodilatation with hypotension due to sympathetic stimulation.

• 4-Gastric dilatation and may be paralytic ileus.

Clinically

• for the cause

• arterial blood gas analysis.

• non-invasive methods

Investigations

Investigations

http://www.emedicine.com/cgi-bin/foxweb.exe/makezoom@/em/makezoom?picture=/websites/emedicine/med/images/Large/11251_1125med2011-01.jpg&template=izoom2

http://www.emedicine.com/cgi-bin/foxweb.exe/makezoom@/em/makezoom?picture=/websites/emedicine/med/images/Large/14082_1408med2011-02.jpg&template=izoom2

• Treatment of the underlying

cause

• Correction of hypoxaemia

• Treatment of complications

Complications of RF: • 1-Cardiac arrythmias due to severe

hypoxaemia and acidaemia secondary to CO2 retention.

• 2-Pulmonary hypertension and cor pulmonale due to pulmonary vasoconstriction as aresult of hypoxaemia and acidaemia.

• 3-DVT and pulmonary embolism due to polycythaemia secondary to chronic hypoxaemia.

• 4-Complications of oxygen therapy and mechanical ventilation.

• Controlled O2 therapy

• Uncontrolled O2 therapy

Oxygen Therapy

Oxygen Therapy

Different equipments of oxygen supply::

A) Central oxygen in hospitals.

B) Home oxygen, includes :

1. Compressed gas cylinders.

2. Liquid oxygen cylinders.

3. Oxygen concentrators.

4. Small devices.

Compressed gas cylinders

Liquid oxygen cylinders

easier to refill, but of

higher cost

An oxygen concentrator works by taking in room air

which has an oxygen concentration of around 21% and

passing it through a series of molecular, bacterial and

dust filters to remove any dust particles and unwanted

gases. Purified oxygen with a concentration of up to

95% is then delivered to the patient via a flowmeter,

with mask or nasal cannulae.

Aquagen Opure O2 Oxyshot

These three forms of oxygen in small devices

applied by ingestion in Aquagen, inhalation in

Opure O2, and spray in Oxyshot.

Indications for acute oxygen

therapy

• Respiratory failure(PaO2<60 mmHg;

SaO2<90%).

• Cardio-respiratory arrest.

• Hypotension and low cardiac output.

• Metabolic acidosis(HCO3<18 mmol/L).

• Respiratory distress.

• Myocardial infarction.

• Sickle cell crises.

Nasal cannula:

The most commonly used.

Simple inexpensive, easy.

The FiO2 from 24%-44%

increasing the flow more

than 6L/min doesn't raise

FiO2 than 44 %, and may

result in drying of mucous

secretions.

Simple face mask

Face mask with reservoir bag

and one way valve.

Venturi mask Ideal for type II respiratory failure (hypercapnia)

as in COPD

Different colors of venturi control parts adjusted

to certain O2 flow to deliver different

concentrations of O2.

Treanstracheal oxygen catheter: •Bypass the anatomical dead space of upper airway,using it as an

oxygen reservoir during respiration.

•Lack of nasal or facial irritation due to oxygen flow.

•Infrequency of catheter displacement during sleep.

Invasive ventilator

Endotracheal tube

Invasive ventilator with endotreacheal tube:

•Give up to 100% oxygen under positive pressure.

•Used in sever cases when there is deterioration of spontaneous breathing with decreased pH, raised CO2, and persistent hypoxaemia.

Non invasive ventilator with face

mask

Hyperparic Oxygen A medical treatment in which the patient is entirely

enclosed in a pressure chamber breathing 100% O2

at > 1.4 times atmospheric pressure.

Hyperbaric oxygen (HBO) therapy uses a

monoplace (single-person) chamber pressurized

with pure O2 or a larger multiplace chamber

pressurized with compressed air in which the

patient receives pure O2 by mask, head tent, or

endotracheal tube.

Indications • CARBON MONOXIDE POISONING .

•ARTERIAL GAS EMBOLISM AND

DECOMPRESSION SICKNESS.

•Gas gangrene.

•Crush injury.

•Compromized skin grafts and flaps.

•Mixed aerobic anerobic soft tissue infections.

•Nonhealing ischaemic wounds.

•Burns.

•Smoke ionhalation.

Rationale for ventilatory assistance

Respiratory load

Respiratory muscles

capacity

Alveolar hypoventilation

PaO2 and PaCO2

Abnormal

ventilatory drive

Mechanical ventilation unloads the

respiratory muscles

Respiratory load Respiratory muscles

Mechanical

ventilation

pathophysiology of respiratory failure

Health & Medicine