Respiratory system

Respiratory Failure

• Dr.Dhaher JS Al-habbo
• FRCP London UK
• Assistant Professor in Medicine
• DEPARTMENT OF MEDICINE

Respiratory Failure

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination.
In practice, it may be classified as either hypoxemic or hypercapnic.
Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (Pa O2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (Pa CO2).
Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema pneumonia, and pulmonary hemorrhage.

Respiratory Failure

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air.
The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia.
Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders eg, asthma and COPD.

Respiratory Failure

Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3.
Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased.
The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases.
The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long-standing disorder.


Respiratory Failure
Pathophysiology:
Respiratory failure can arise from an abnormality in any of the components of the respiratory system;
Airways,
Alveoli,
Central nervous system (CNS),
Peripheral nervous system,
Respiratory muscles,
Chest wall

Respiratory Failure

Pathophysiology:
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

Respiratory FailureRespiratory physiology

Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue.
Normally, ventilatory capacity greatly exceeds ventilatory demand.
The act of respiration engages 3 processes:
Transfer of oxygen across the alveolus
Transport of oxygen to the tissues
Removal of carbon dioxide from blood into the alveolus and then into the environment


Respiratory FailureRespiratory physiology
Gas exchange;
Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place.
After diffusing into the blood, the oxygen molecules reversibly bind to the hemoglobin.
Each molecule of hemoglobin contains 4 sites for combination with molecular oxygen; 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen.

Respiratory FailureRespiratory physiology

Alveolar ventilation;
At steady state, the rate of carbon dioxide production by the tissues is constant and equals the rate of carbon dioxide elimination by the lung.
Hypoxemic respiratory failure;
The V/Q mismatch and shunt.
These lead to widening of the alveolar-arterial PO2 gradient, which normally is less than 15 mm Hg.
They can be differentiated by assessing the response to oxygen supplementation or calculating the shunt fraction after inhalation of 100% oxygen.

Respiratory FailureRespiratory physiology

Severe airway obstruction is a common cause of acute and chronic hypercapnia.
Acute epiglottitis and tumors involving the trachea;
lower-airway disorders include COPD, asthma, and cystic fibrosis.
Disorders of the peripheral nervous system;
Guillain-Barré syndrome, Muscular dystrophy,Myasthenia gravis , severe kyphoscoliosis, and morbid obesity.



Respiratory Failure Physical Examination
Cyanosis, a bluish color of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated hemoglobin in the capillaries or tissues is at least 5 g/dL.
Dyspnea, an uncomfortable sensation of breathing, often accompanies respiratory failure. (hypoxemia and/or hypercapnia) contribute to the sensation of dyspnea. Asterixis may be observed with severe hypercapnia. Tachycardia and a variety of arrhythmias may result from hypoxemia and acidosis.

Respiratory Failure Physical Examination

Confusion and somnolence may occur in respiratory failure. Myoclonus and seizures may occur with severe hypoxemia.
The increased pulmonary vascular resistance increases afterload of the right ventricle, which may induce right ventricular failure.
This, in turn, causes enlargement of the liver and peripheral edema.
The entire sequence is known as cor pulmonale.

HYPOXEMIC RESPIRATORY FAILURE(TYPE 1)

PaO2 <60mmHg with normal or low PaCO2  normal or high pH
Most common form of respiratory failure
Lung disease is severe to interfere with pulmonary O2 exchange, but over all ventilation is maintained
Physiologic causes: V/Q mismatch and shunt

HYPOXEMIC RESPIRATORY FAILURE CAUSES OF ARTERIAL HYPOXEMIA

1. FiO2
2. Hypoventilation; ( PaCO2) Hypercapnic
3. V/Q mismatch; Respiratory failure (eg.COPD)
4. Diffusion limitation ?
5. Intrapulmonary shunt - pneumonia - Atelectasis - CHF (high pressure pulmonary edema) - ARDS (low pressure pulmonary edema)


Classification of Respiratory Failure
Type I or Hypoxemic (PaO2 <60 at sea level): Failure of
oxygen exchange
Increased shunt fraction (Q S /QT )
Due to alveolar flooding
Hypoxemia refractory to supplemental oxygen
Type II or Hypercapnic (PaCO2 >45): Failure to
exchange or remove carbon dioxide
Decreased alveolar minute ventilation (V A )
Often accompanied by hypoxemia that corrects with
supplemental oxygen

Classification of Respiratory Failure

Type III Respiratory Failure: Perioperative respiratory failure
Increased atelectasis due to low functional residual capacity (FRC) in the setting of abnormal abdominal wall mechanics.Often results in type I or type II respiratory failure
Can be ameliorated by anesthetic or operative technique, posture, incentive spirometry, post-o perative analgesia, attempts to lowerintra- abdominal pressure

Classification of Respiratory Failure

Type IV Respiratory Failure: 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.


Respiratory Failure Laboratory Studies
Arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms.
A complete blood count (CBC) may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure.
Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure.
Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function.
.

Respiratory Failure Laboratory Studies

Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure.
An elevated creatine kinase level with a normal troponin I level may indicate myositis, which occasionally can cause respiratory failure.
In chronic hypercapnic respiratory failure, serum levels of thyroid-stimulating hormone (TSH) should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure

Respiratory Failure: Management

ABC’ s
Ensure airway is adequate
Ensure adequate supplemental oxygen and assisted ventilation, if indicated
Support circulation as needed

Respiratory Failure: Management

Treatment Goals;
O2 therapy
Mobilization of secretions
Positive pressure ventilation(PPV).
If secondary to V/Q mismatch- 1-3Ln/c or 24%-32% by mask
If secondary to intrapulmonary shunt- positive pressure ventilation-PPV.
May be via ETtube, Tight fitting mask
Goal is PaO2 of 55-60 with SaO2 at 90% or more at lowest O2 concentration possible.
O2 at high concentrations for longer than 48 hours causes O2 toxicity


Respiratory Failure: Management
Treatment of a specific cause when possible Infection
Antimicrobials, source control
Airway obstruction;Bronchodilators, glucocorticoids
Improve cardiac function;
Positive airway pressure, diuretics, vasodilators,
morphine, inotropy, revascularization

Respiratory Failure: Management

Mechanical ventilation
Non-invasive (if patient can protect airway and is
hemodynamically stable)
Mask: usually orofacial to start Invasive,Endotracheal tube (ETT).
Tracheostomy – if upper airway is obstructed

Indications for Mechanical Ventilation

Cardiac or respiratory arrest
Tachypnea or bradypnea with respiratory fatigue or
impending arrest
Acute respiratory acidosis;
Refractory hypoxemia (when the P aO 2 could not be
maintained above 60 mm Hg with inspired O 2 fraction
(F I O 2 )>1.0)
Inability to protect the airway associated with depressed levels of consciousness


Indications forMechanical Ventilation
Shock associated with excessive respiratory work
Inability to clear secretions with impaired gas exchange or excessive respiratory work.
Newly diagnosed neuromuscular disease with a vital capacity <10-15 mL/kg.
Short term adjunct in management of acutely increased intracranial pressure (ICP)

Invasive vs. Non- invasive Ventilation

Consider non- invasive ventilation particularly
in the following settings:COPD exacerbation.
Cardiogenic pulmonary edema Obesity hypoventilation syndrome.
Noninvasive ventilation may be tried in selected.
patients with asthma or non-cardiogenic hypoxemic
respiratory failure.