Pathophysiology of respiratory failure

Pathophysiology of Respiratory Failure

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

ERS National Delegate of Egypt

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

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=∞

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.


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

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 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.


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


(PAO2 - PaO2)

Alveolar Hypoventilation

V/Q abnormality

NIF N P0.1

increased normal

N VCO2

PaCO2 >50 mmHg

Not compensation for metabolic alkalosis

Central

Hypoventilation

Neuromuscular

Problem

VCO2

V/Q

Abnormality

Hypermetabolism

Overfeeding

NNIF P0.1


Alveolar Hypoventilation

Brainstem respiratory depression

Drugs (opiates)

Obesity-hypoventilation syndrome

NIF

Central

Hypoventilation Neuromuscular

Disorder

N NIF

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.

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

Health & Medicine

Pathophysiology of respiratory failure