Respiratory failure Flashcards
What is respiratory failure?
- PaO2 < 8kPa
- subdivided into 2 main types according to PaCO2 level
- occurs when gas exchange is inadequate, resulting in hypoxia
What are the different types of respiratory failure?
- type I hypoxaemic
- type II hypercapnic
- type III perioperative - generally a subset of type I failure but is sometimes considered separately bc it is so common
- type IV - secondary to cardiovascular instability
What is type 1 respiratory failure?
- hypoxia
- PaO2 < 8kPa
- normal or low PaCO2
- ABG may reveal respiratory alkalosis
What is type 2 respiratory failure?
- ventilatory failure
- hypoxia (PaO2 < 8kPa)
- hypercapnia (PaCO2 > 6.5 kPa)
- ABG may reveal a respiratory acidosis or partially corrected resp acidosis if longstanding (eg. COPD)
What is type 3 (peri-operative) respiratory failure?
Residual anaesthesia effects, post-operative pain and abnormal abdominal mechanics contribute to decreasing functional residual capacity (FRC) and progressive collapse of dependant lung units (alveoli)
Causes of post-operative atelectasis incude;
- reduced FRC
- supine / obese / ascites
- anaesthesia
- upper abdominal incision
- airway secretions
What is type 4 (IV) (shock) respiratory failure?
Patients who are intubated and ventilated and in the process of resucitation for shock:
- cardiogenic
- hypovolaemic
- septic
In the normal lung, what is the ventilation: perfusion (V/Q) ratio?
- 1
- however, slightly lower at base of lung (where more perfusion than ventilation), and higher towards apex of lung (ventilation > perfusion)
- pulmonary system can adapt to small V/Q mismatches, eg. if a section of lung not ventilated -> hypoxic -> pulm vasculature constricts diverting blood to areas that are ventilated
- however, this can only partially overcome poor ventilation
- in global hypoxia eg. persistent alveolar hypoventilation, all the pulm vasculature will contract -> leads to pulm hypertension and -> cor pulmonale
What is an area with no ventilation (and thus a V/Q of 0) termed?
shunt
What is an area with no perfusion (and thus a V/Q of infinity) termed?
dead space
It is difficult to increase oxygen content by increasing blood flow, due to its non-linear saturation curve and poor solubility. It is easy to get rid of carbon dioxide due to its linear solution curve (does not become saturated).
What are the pathophysiological mechanisms that can lead to hypoxaemia?
What is the difference between acute and chronic respiratory failure?
- Acute respiratory failure is characterised by life-threatening derangements in ABGs and acid-base status. It develops over minutes to hours and pH is therefore more likely to be affected
- Chronic respiratory failure develops over several days or longer. It allows more time for renal compensation resulting in a greater increase in bicarb concentration. pH may only be slightly reduced as a consequence w/ manifestations that are less severe and not be as readily apparent
Describe the normal process of mechanical ventilation
- lungs have inherent elastic properties that cause them to collapse away from chest wall
- this generates a negative intrapleural pressure -> increases the more the lungs are stretched
- alveolar pressure = recoil + intrapleural pressure
- there is only flow of air if a pressure difference is present
- in inspiration, contraction of diaphragm decreases the IP pressure, transmitted to the alveoli. Palv is less than atmospheric -> air moves into lungs
- in expiration, resp muscles relax (IP pressure less negative), but recoil remains positive so Palv becomes positive -> air forced out of lung
- during quiet inspiration, the main muscle used = diaphragm
- during more vigorous respiration, intercostal and accessory muscles are utilised
- quiet expiration is passive + relies on recoil
- during forced expiration, abdominal muscles are used to help push the diaphragm back to its resting position
Describe the physiological control of breathing
- peripheral chemoreceptors respond to reduced PaO2, increased PaCO2 and increased [H<span>+</span>]
- they are located in carotid and aortic bodies, although carotid is most important in influencing ventilation
- innervated by CN IX, stimulated by PaO2 <8kPa
- central chemoreceptors respond to changes in [H+] in the CSF, which closely reflects PaCO2
- does not respond to peripheral increased [H+] as these ions cannot cross BBB
- PaCO2 is the most important determinant of ventilation, 75% of increased ventilation response to hypercapnia is due to central chemoreceptor activity
- O2 and CO2 control can alter the responses to changes in each other, eg. hypoxia reduces sensitivity to CO2
- in COPD, sensitivity to [H+] in the CSF may be lost, in these pts the resp drive may be lost; O2 treatment may therefore reduce respiratory drive
What are the acute causes of type 1 respiratory failure?
- asthma
- PE
- pneumonia
- parenchymal disease
- pulmonary oedema
- ARDS
- diseases of right-left shunt
What are the chronic causes of type I respiratory failure?
- emphysema
- kyphoscoliosis
- pulmonary alveolar fibrosis