WEEK 1 - Respiratory Failure Flashcards
Define acute lung failure (ALF)
A clinical condition where the pulmonary system fails to maintain adequate gas exchange.
I.e. hypoxaemia, hypercapnia or combination of both.
Most common type of organ failure in critical care.
What is the aetiology of ALF?
Virtually every respiratory disorder can/may result in respiratory failure
Eg. Atelectasis, alveolar consolidation (pneumonia), increased alveolar capillary membrane thickness, excessive bronchial secretions, bronchospasm, distal airway and alveolar weakening.
Classify extrapulmonary ALF
Disorders that affect the brain, spinal cord, neuromuscular system, thorax, pleura and upper airways
Classify intrapulmonary ALF
Disorders that affect the lower airways and alveoli, pulmonary circulation and the alveolar-capillary membrane.
What is hypoxaemia?
PaO2 less than or equal to 50mmHg
I.e. failure to oxygenate
Problem: inadequate oxygenation exchange between the alveoli and the pulmonary capillary system.
Reduced oxygenation of arterial blood.
What is hypercapnia?
PaCO2 greater than or equal to 50mmHg with a pH less than or equal to 7.25
Failure to ventilate
Problem: alveolar hypoventilation which results in increased PaCO2 and decreased PaO2. Results in increased CO2 in arterial blood.
What are the goals of Rx for ALF?
Maintain a patent airway, optimising O2 delivery, minimising O2 demand, treating the cause and preventing complications.
What is hypoxaemic respiratory failure?
Oxygenation failure
A patient who’s primary problem is inadequate oxygenation
Hypoxaemia - a low PaO2 and a normal or low PaCO2
The low PaCO2 is attributed to the alveolar hyperventilation associated with hypoxaemia
What are signs and symptoms of hypoxaemia?
Dyspnoea Tachypnoea Accessory muscle use Decreased SpO2 Unable to speak in sentences Prolonged expiration Agitation, disorientation, delirium Restless Confusion, ALOC Tachycardia, hypertension Cool clammy skin, diaphoretic Fatigue
What are the late signs and symptoms of hypoxaemia?
Cyanosis
Coma
Arrhythmia
Hypotension
What are the major mechanisms of hypoxaemia?
- Alveolar hypoventilation
- Intrapulmonary shunting
- Ventilation perfusion mismatch
- Diffusion deficits
- Decreases barometric pressure
What is ventilation-perfusion mismatch?
Occurs when ventilation and blood flow are mismatched.
Blood passes through the alveoli that are under ventilated for the given amount of perfusion. Blood leaves with lower than normal amount of oxygen.
Most common cause of hypoxaemia.
Can be due to alveoli that are partially collapsed or partially filled with fluid.
What is alveolar hypoventilation?
The amount of gas that enters the alveoli per minute.
Occurs when the amount of O2 being brought into the alveoli is insufficient to meet metabolic needs of the body.
Hypoventilation also produces an increase in alveoli CO2, as CO2 is still being produced by the body but is not being released.
What homeostatic mechanisms occur during hypoventilation? (i.e. the flow chart with homer’s face on it)
- decrease in ventilation
- increase in blood PaCO2
- increase in CSF CO2
- increase in CSF H+
- decrease in CSF pH
- H+ stimulates central chemoreceptors
- medullary respiration centre increases ventilator rate
What is intrapulmonary shunt?
Extreme form of V/Q mismatch (anatomical and intrapulmonary).
Blood reaches arterial system without participating in gas exchange.
Alveolar collapse secondary to atelectasis.
Alveolar flooding with pus, blood or fluid
What happens to metabolism when there’s a low cardiac output?
Aerobic metabolism changes to anaerobic metabolism which leads to lactic acid build up and further depresses myocardium function and lowers cardiac output.
What is PaCO2 used for ?
To evaluate ventilation
What happens to PaCO2 when ventilation is reduced?
PaCO2 is increased
What happens to PaCO2 when ventilation is increased?
PaCO2 is reduced
What are the signs and symptoms of hypercapnia?
Dyspnoea Rapid respiration, shallow breaths Decreased tidal volume Decreased minute volume Pursed lip breathing, tripod position Muscle weakness Disorientation Seizures, coma Arrhythmias Hypertension Bounding pulse
What are some causes of hypercapnia?
Depression of respiratory centre by drugs.
Disease of the medulla.
Abnormalities of the spinal conducting pathways.
Diseases of the NMJ or respiratory muscles themselves.
Thoracic cage abnormalities.
Large airway obstruction.
Increased work of breathing or physiological dead space.
What are some airway and alveoli abnormalities causing ventilation failure?
Asthma, COPD, CF
Airway obstruction
Respiratory muscle fatigue and ventilatory failure occur due to additional work requirements to inspire adequate tidal volume against increased airway resistance and air trapped within the alveoli.
What are some central nervous system abnormalities causing ventilation failure?
Drug overdose: suppress the drive to breath, decrease CO2 reactivity in the brainstem which allows PaCO2 to rise.
Head injury: ALOC may interfere with the pt ability to manage secretions or adequately protect the airway. Medulla doesn’t alter the RR in response to a change in PaCO2.
High spinal injury: limit nerve supply to the respiratory muscle of the chest wall and diaphragm.
What are some chest wall abnormalities causing ventilation failure?
Flail chest, fractured ribs, severe obesity (BMI 40+)
Limits the normal movement of the chest wall, limit expansion/diaphragmatic movement and consequently gas exchange.
What are the predisposing factors of pulmonary embolisms?
Clinical prediction rules (Well's score) and Virchow Triad: - venous stasis - injury to vascular endothelium - hypercoagulability
What are precipitating conditions for pulmonary embolism?
previous pulmonary emboli CV disease surgery cancer trauma gynaecologic conditions
What are the 3 main symptoms of PE that prompt further inquiry ?
Dyspnoea, especially if unexplained.
Chest pain especially pleuritic/aggravated by inspiration.
Haemoptysis.
What are the PE rule out criteria?
Age >50 Pulse <100 SaO2 >94% No unilateral leg swelling No haemoptysis No recent trauma or surgery No prior DVT or PE No oral hormone use
What changes occur with PE?
Increased dead space
Bronchoconstriction
Compensatory shunting
Haemodynamic consequences (pulmonary hypertension, increased workload of RV, RV failure)
Wtf is the d-dimer?
D-dimer levels are elevated in plasma in the presence of acute thrombosis becoz of simultaneous activation of coagulation and fibrinolysis.
Normal d-dimer level = acute PE or DVT is unlikely.
Not useful for determining PE coz high chance of false positives.
How can you identify PE on an ECG?
Sinus tachycardia New-onset atrial arrhythmias New R) bundle branch block (complete or incomplete) QR pattern in V1 S1Q3T3 T wave inversion in V1 through V4 ST segment migration in V1 through V4 Q wave should never be more than 25% the height of he RS wave
How do you manage PE?
The best management is prevention.
Assess on admission and review daily.
Prophylaxis : anticoags, heparin, LMWH, TED stockings
Treatment: prevent recurring PE, facilitate clot dissolution, reverse effect of pulmonary hypertension, promote gas exchange, prevent complications
How do you prevent PE from recurring?
Administer unfractionated LMWH and warfarin
Heparin is administered to prevent further clots from forming has NO EFFECT on existing clots.
How do you dissolute a clot?
Administer fibrinolytic agents (limited success)
Pulmonary embolectomy (bypass)
Catheter embolectomy
Venous filters
What is the anatomic alteration that occurs with flail chest?
Double fractures of at least 3 or more adjacent ribs.
The affected ribs cave in (flail) during inspiration as a result of the generated subatmospheric pressure.
Compresses and restricts the underlying lung.
What is paradoxical chest wall movement in flail chest?
During inspiration the fractured ribs are pushed inward by the atmospheric pressure surrounding the chest and negative intrapleural pressure.
During exhalation the flail area bulges outwards when the intrapleural pressure becomes greater than the atmospheric pressure.
What are signs/symptoms of flail chest in your assessment?
Tachypnoea Increased HR & BP Hypoxaemia, pain, anxiety, cyanosis Diminished breath sounds Boney crepitus Paradoxical chest wall movements of affected segment
How do you manage a flail chest?
Protect the underlying lung and allow adequate oxygenation, ventilation and pulmonary toilet:
Administer supplementary O2.
Provide analgesia.
Aggressive physiotherapy.
Endotracheal intubation & positive pressure ventilation (PEEP).
Surgical fixation.
What is a simple closed pneumothorax?
When gas accumulates in the pleural space, separating the visceral and parietal pleura.
Enhances the natural tendency of the lung to recoil or collapse & the natural tendency of the chest wall to move outward or expand.
As the lung collapses the alveoli are compressed & atelectasis ensues.
In severe cases, great veins may be compressed & cause venous return to the heart to diminish.
What is a tension pneumothorax?
Air from a laceration in the lung tissue or via an open chest wall injury enters the intrapleural space with each breath but cannot escape.
Progressive increase ni volume of trapped air will compress the adjacent lung, limiting lung expansion leading initially to respiratory distress & hypoxaemia.
As intrathoracic pressure increases, the mediastinal structures (vena cava, trachea, heart) are compressed & displaced AWAY from the affected side.
Results in decreased venous return with a drop in cardiac preload.
Severely compromised CO which progresses rapidly to cardiogenic shock & cardiac arrest.
What is a haemothorax?
Collection of blood within the pleural space.
Bleeding from # ribs, lacerated intercostal arteries, pulmonary parenchyma, ruptures or lacerated intrathoracic blood vessels, injury to cardiac chamber etc.
Diminished or absent breath sounds.
Shock etc
What is an open pneumothorax?
“sucking chest wound”
Loss of negative pressure & the lung collapses, +/- air leaks & associated haemorrhage.
Profound respiratory distress, hypoxaemia & shock may progress to death.
