Respiratory failure Flashcards
1
Q
What is respiratory failure?
A
- PaO2 < 8kPa
- subdivided into 2 main types according to PaCO2 level
- occurs when gas exchange is inadequate, resulting in hypoxia
2
Q
What are the different types of respiratory failure?
A
- 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
3
Q
What is type 1 respiratory failure?
A
- hypoxia
- PaO2 < 8kPa
- normal or low PaCO2
- ABG may reveal respiratory alkalosis
4
Q
What is type 2 respiratory failure?
A
- 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)
5
Q
What is type 3 (peri-operative) respiratory failure?
A
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
6
Q
What is type 4 (IV) (shock) respiratory failure?
A
Patients who are intubated and ventilated and in the process of resucitation for shock:
- cardiogenic
- hypovolaemic
- septic
7
Q
In the normal lung, what is the ventilation: perfusion (V/Q) ratio?
A
- 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
8
Q
What is an area with no ventilation (and thus a V/Q of 0) termed?
A
shunt
9
Q
What is an area with no perfusion (and thus a V/Q of infinity) termed?
A
dead space
10
Q
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?
A
11
Q
What is the difference between acute and chronic respiratory failure?
A
- 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
12
Q
Describe the normal process of mechanical ventilation
A
- 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
13
Q
Describe the physiological control of breathing
A
- 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
14
Q
What are the acute causes of type 1 respiratory failure?
A
- asthma
- PE
- pneumonia
- parenchymal disease
- pulmonary oedema
- ARDS
- diseases of right-left shunt
15
Q
What are the chronic causes of type I respiratory failure?
A
- emphysema
- kyphoscoliosis
- pulmonary alveolar fibrosis
16
Q
What are clinical features of type 1 respiratory failure?
A
- features of underlying cause of the resp failure
- tachypnoea
- tachycardia
- sweating
- pulsus paradoxus
- use of accessory muscles of respiration
- intercostal recession
- inability to speak
- central cyanosis
if longstanding -> polycythaemia, pulmonary HTN, cor pulmonale
17
Q
What is the pathophysiology of type 1 respiratory failure?
A
There are 3 mechanisms by which hypoxia can occur in the presence of normal/low PaCO2:
- V/Q mismatch (most common) - where areas of low ventilation relative to perfusion (low V/Q) contribute to hypoxaemia.
- Shunt -> extreme V/Q mismatch
- Diffusion defect
Due to any disease that impairs gas transport across the alveolar-capillary interface. Levels of CO2 in the blood can remain normal or reduce as ventilation increases to compensate for lack of oxygen. The remaining normal lung is sufficient to excrete the carbon dioxide being produced by tissue metabolism as CO2 has such a high diffusion coefficient.
18
Q
Type 2 respiratory failure is caused by alveolar hypoventilation. What are the causes of this?
A
- pulmonary disease - LT asthma, COPD, pneumonia, pulm fibrosis, OSA
- reduced resp drive - sedative drugs, CNS tumour, trauma, raised ICP
- nerve - guillian-barre syndrome, motor neurone disease
- muscle - muscular dystrophy
- neuromuscular - cervical cord lesion, diaphragmatic paralysis, myaesthenia gravis
- other - fatigue due to tachypnoea in met acidosis, obesity, flail chest
19
Q
What are the clinical features of type 2 respiratory failure?
A
Clinical features include those of the underlying lung disease as well as the hypoxia symptoms mentioned for T1RF, and now hypercapnic features also:
- headache (cerebral artery vasodilatation + inc ICP)
- peripheral vasodilatation
- tachycardia
- bounding pulse
- asterixis
- papilloedema
- confusion
- droswiness
- coma
20
Q
What is the pathophysiology of type 2 respiratory failure?
A
- the conditions mentioned cause alveolar hypoventilation
- where alveolar ventilation is insufficient to excrete volume of CO2 being produced by tissue metabolism
- inadequate alveolar ventilation is due to:
- reduced ventilatory effort
- inability to overcome an increased resistance to ventilation
- failure to compensate for an increase in deadspace and/or CO2 production
- or a combination of these factors
- this results in decreased levels of oxygen and increased levels of carbon dioxide in the blood
- respiratory acidosis ensues
21
Q
What investigations can/should be done for respiratory failure?
A
- pulse oximetry
- bloods -> FBC, U+Es, CRP, ABG
- imaging -> CXR
- ECG
- pulm function tests
22
Q
Assess the RF according to ABC and treat the underlying cause.
What is the management of type 1 respiratory failure?
A
- give oxygen (35-60%) by facemask to correct hypoxia
- safe to administer as much oxygen as is required to return PaO2 to normal
- assisted ventilation if PaO2 still < 8 kPa, despite 60% oxygen
23
Q
What is the management of type 2 respiratory failure?
A
- treat underlying cause
- give controlled oxygen therapy -> start at 24%
- recheck ABG/PaCO2 after 20 mins, if PaCO2 is steady or lower then increase oxygen concentration to 28%
- if however, PaCO2 risen by >1.5 kPa + pt still hypoxic -> consider resp stimulant eg. doxapram or provide NIPPV
- if this fails, consider intubation and ventilation if appropriate
The brain may be relatively insensitive to CO2 and respiration if primarily driven by hypoxia; caution should be exercised when giving O2. If 100% oxygen given and pt relies on hypoxic drive for ventilation, patient will begin to hypoventilate as they are receiving the oxygen needed to satisfy the hypoxia. The hypoventilation exacerbates the hypercapnia.
Small increases in PaCO2 can be tolerated but not if pH falls dramatically. The pH should not be allowed to fall below 7.25; under such circumstances, increased ventilation must be achieved either by use of resp stimulant or artifical ventilation.
24
Q
What are the pathophysiological consequences of hypercapnia (and subsequent pH decrease)?
A
-
brain:
- alterations in brain biochem (GABA, glutamate, glutamine aspartate)
- increased cerebral blood flow
- raised ICP
-
circulation
- depression of cardiac contractility + fibrillation threshold
- coronary and systemic artery vasodilatation
25
What is positive airway pressure (PAP)?
* patients who are unable to breathe on their own will require **positive pressure** (above atmospheric) to move oxygen (air) into their lungs for gaseous exchange to take place
* PAP ventilation is often used for patients who have acute type 1 or 2 respiratory failure
* usually PAP ventilation will be reserved for the subset of patients for whom oxygen delivered via a face mask is deemed insufficient or deleterious to health
* patients on PAP will be **closely monitored** in either ICU, HDU, CCU or specialist resp unit
26
What are the most common conditions for which PAP ventilation is used in hospital?
* congestive cardiac failure
* acute exacerbation of COPD or asthma
It is not used in cases where the airway may be compromised or consciousness impaired
27
What is CPAP?
* delivers stream of compressed air via a hose to a nasal pillow or full-face mask
* splinting the airway (**keeping it open under air pressure**)
* so that unobstructed breathing becomes possible
* it is important to understand, however, that it is the **air pressure** and not the movement of air that prevents the airway collapse
* when machine turned on, but prior to mask being placed on head, a flow of air comes through mask
* after mask placed on head, it is sealed to the face and air stops flowing
* at this point, it is only the **air pressure** that accomplishes the desired result
* the CPAP machine blows air at a prescribed pressure (aka titrated pressure)
* a typical CPAP machine can deliver pressures between 4-20 cm/H2O
* CPAP is often used in patients with heart failure + OSA
28
The problem with a CPAP, however, was that the person had to exhale against the extra pressure. This made it unsuitable for certain people, including those suffering from neuromuscular diseases.
Therefore, **BiPAP** was developed - what is this?
* air delivered through mask set at one pressure for inhaling and another for **exhaling**
* this makes BiPAP much **easier** for users to adapt to
* also allows **neuromucular disease** sufferers to use the device
* bc of these dual settings, BiPAP allows people to get more air in and out of the lungs without the natural muscular effort needed to do so
* the two different pressures are:
* **inspiratory positive airway pressure (IPAP)**
* **expiratory positive airway pressure (EPAP)** - this is _lower_ than the IPAP, but still _greater_ than atm pressure
* this makes for easier exhalation which alternate at preset time intervals
* BiPAP combines pressure-controlled ventilation with unrestricted spontaneous breathing
* often used in pts w/ T2RF caused by **COPD**
29
What are the characteristics and usage of **nasal cannulae**, for oxygen therapy?
* used to deliver **low** concs of oxygen
* can deliver from **24-40%**
* at flow rate of 1-4 L /min
* used by pts who have _adequate_ ventilation and tidal volume but would **benefit** from oxygen therapy (hypoxic)
* these pts don't require oxygen to degree of wearing a non-rebreathe mask
* this device consists of plastic tube which fits behinds ears + set of two prongs which are placed in the nostrils
* the nasal cannula is connected to an oxygen tank, a portable oxygen generator or a wall connection in a hospital via a flowmeter
* rates **above 6 L/min** can result in discomfort to the patient, drying of the nasal passages and possibly nose bleeds (epistaxis)
* nasal cannulas are a good alternative to simple face masks as they allow the pt to continue to talk, eat and drink while receiving the therapy
30
Describe the use of **simple face oxygen masks**
* used to deliver moderate to high concs of O2
* can deliver **40-60%**
* at flow rate of **10-12 L/min**
* mask is a plastic device, contoured to fit over a pts nose + mouth
* used to deliver O2 as the pt breathes through either nose or mouth
* a simple oxygen mask has open side ports that allow room air to enter mask and **dilute** oxygen, as well as allowing **exhaled CO2** to leave
* also has narrow plastic tubing fixed to the bottom of the mask that is used to connect mask to an O2 source
* an adjustable elastic band is connected to each side of the mask and slides over the head and above the ears to hold the mask securely in place
* it isn't very **precise**, _avoid_ in hypercapnia + T2RF and in COPD as there is a risk of CO2 accumulation
31
What are venturi masks?
* deliver supplemental oxygen at **precise** concentration for _controlled_ oxygen therapy
* **_high-flow_** oxygen therapy devices
* tubing that connects to the oxygen source is larger than that of other masks
* the kits usually include **interchangeable adaptors** that widen or narrow the diameter of the flow through the tubing to allow settings of specific concentrations of oxygen through the mask
* these are colour coded for specific concentrations as follows;
* **blue 24%**
* **white 28%**
* **yellow 35%**
* **red 40%**
* **green 60%**
32
What are partial rebreather masks?
* partial rebreather mask used to deliver **high** conc of oxygen
* can deliver **60-90% oxygen**
* at a flow of **6-15L/min**
* mask similar to simple face mask however side ports are covered with **one-way discs** to prevent room air entering mask
* this mask is called a rebreather bc it has a soft plastic **reservoir bag** connected to the mask that conserves the first third of the patient't exhaled air while the rest escapes through side ports
* this is designed to make use of CO2 as a resp stimulant
33
What is a non-rebreathe mask?
* used to deliver **high-flow oxygen**
* can deliver 90-100% oxygen
* at a flow rate of 15L/min
* *also* similar to simple face mask but has multiple one-way valve sin side ports
* these valves prevent room air from entering mask but allow exhaled air to leave mask
* it has a reservoir bag like a partial rebreather mask but the reservoir bag has a one-way valve that prevents exhaled air from entering the reservoir
* when the patient exhales, **oxygen** fills the reservoir bag and when they inhale, oxygen from **both** the bag and from the supply source are inhaled
34
When are intubation and ventilation indicated?
* apnoea
* worsening acidosis and increased PaCO2
PaO2 \< 8 kPa despite an FiO2 \> 0.5 with or without CPAP
* GCS \< 8
* unable to clear pulmonary secretions by conventional methods
* patient is tiring (inc RR, tachycardia, abnormal resp patterns)
35
Patients with end-stage lung disease have complex health and social care needs so a multi-professional approach is essential in providing optimal care and support.
What are the clinical indicators of advanced lung disease?
* **cachexia**: low BMI, poor or deteriorating performance status
* **inc hosp admissions** for infective exacerbations or RF
* severe airways obstruction (**FEV1 \<30%**)
* severe **restrictive** defect (vital capacity \<60%, transfer factor \<40%)
* meets criteria for LTOT; **persistent hypoxia** (PaO2 \<7.3 kPa)
* persistent, severe symptoms despite optimal tolerated treatment
* **breathlessness** limiting daily activities between exacerbations, at rest or on minimal effort
* symptomatic **RHF**
36
What is the use of opioids and benzos in advanced lung disease?
* **opiods** - can improve persistent, severe breathlessness and cough
* **benzodiazepines** - may relieve anxiety/panic associated w/ severe breathlessness but are less effective than opioids for breathlessness and should be a 3rd line treatment for patients with symptoms unresponsive to non-pharm measures + opioids
