1
4th stage
Medicine
Lec-13
د. ظاهر1/1/2016
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.
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.
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.
Pathophysiology:
Respiratory failure can arise from an abnormality in any of the components of the
respiratory system;
Airways,
2
Alveoli,
Central nervous system (CNS),
Peripheral nervous system,
Respiratory muscles,
Chest wall
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
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
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.
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.
3
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.
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.
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.
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 wi
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
4
HYPOXEMIC RESPIRATORY FAILURE
CAUSES OF ARTERIAL HYPOXEMIA
1.
↓FiO2
2.
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
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
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.
5
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.
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
Management
ABC’ s
Ensure airway is adequate
Ensure adequate supplemental oxygen and assisted ventilation, if indicated
Support circulation as needed
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.
6
O2 at high concentrations for longer than 48 hours causes O2 toxicity
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
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
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.