Airway Flashcards
What are the types of tracheostomy?
- Upper airway absent
–> End stoma formed when pt has had laryngeal resection. There is no upper airway connection to the lungs. - Upper airway present
–> surgical tracheostomy: performed under direct vision, surgical cut is made in trachea
–> Percutaneous dilatational tracheostomy: seldinger technique used to dilate needled hole
Most important difference is between laryngeal stoma, in which case there is no remaining upper airway connection with the lungs, and those forms of tracheostomy that allow management of upper airway if problems arise
Indications for tracheostomy
Upper airway obstruction
Post laryngeal/upper airway surgery
MSK disorders affecting ventilation (muscular dystrophy, spinal cord injury, motor neurone disease, post traumatic brain injury)
To assist weaning from ventilation on critical care
–> Reduced airway resistance
–> Improved airway toilet
–> Allows reduction in sedation as better tolerated than oral tube
Incompetent swallow/impaired upper airway reflexes
What are the types of tracheostomy tubes?
Cuffed: used if airway seal is required (e.g. for intermittent ventilation in critical care)
Uncuffed: if long term tracheostomy as less likely to cause trauma (which is usually due to cuff pressure)
Unfenestrated: Usually used in association with cuffed tracheostomy tube when intermittent ventilation is required, e.g. in surgical patients
Fenestrated: allow upper airway flow for phonation, designed for medium to long term use
What are the most common problems with tracheostomies?
-Displacement
-Obstruction
-Haemorrhage
DOH!
How can you determine the chronicity of type 2 respiratory failure?
Chronic type 2 resp failure (e.g. copd) patients will have high bicarb
What are the causes of respiratory failure in the surgical patient?
- Acute fall in functional residual capacity (FRC) without pulmonary vascular dysfunction:
–> Failure of chest mechanics after trauma or other processes which render lungs stiff/non compliant
–> Post op atelectasis, sputum retention, pneumonia, pharmacological respiratory depression (analgesia, sedatives, neuromuscular blocking drugs) - Acute fall in FRC with pulmonary vascular dysfunction
–> PE, ARDS, LVF - Airflow obstruction
–> asthma, COPD
What factors increase risk of respiratory problems?
-Hx asthma/copd
-Smoking
-Obesity
-Thoracic surgery
-upper abdominal surgery
-Older age
How to prevent respiratory compromise following surgery
-Identify those at risk
-Encourage early mobilisation
-Provide adequate analgesia
-Chest physio
-Nebulised salien
-Humidified oxygen at titrated dose
-Sputum culture
System for interpreting chest XR
Soft tissues (emphysema, foreign body)
Bones (ribs, sternum, clavicle)
Lung markings (does it extend all the way to edge)
Opacifications
Costophrenic angle
Abdominal abnormality: air under diaphragm, dilated bowel loops
Heart size/position/trachea
Increasing escalation of respiratory support
Mask oxygen therapy –> mask/tracheal CPAP –> NIV –> Intubation and ventilation –> PEEP and recruitment –> adjunctive therapies
When would CPAP be helpful? What is its mechanism?
-Type 1 respiratory failure
-During ventilation, airway pressure cannot drop below pressure indicated on the valve
This leads to:
–> recruitment of underventilated alveolae
–> increased FRC
–> Decreased intrapulmonary shunt (when blood passes through lungs but fails to take part in gas exchange)
–> decreased work of breathing
Patient selection for CPAP
-Must have reasonable resp rate and tidal volume
-Must be in control of airway
-Must be able to cooperate
When would NIV be used?What is it?
-Type 2 respiratory failure
-Two different pressures applied to pt via a facemask: higher pressure during inhalation, lower pressure during exhalation
-This is bilevel positive airway pressure mask ventilation (BIPAP)
-Ventilation is predominantly provided by iPAP, whereas ePAP provides recruitment of underutilised alveoli allowing for gas exchange and removal of exhaled gas
https://geekymedics.com/cpap-vs-niv-bipap/
Which patients would not be suitable for NIV?
-cardiovascularly unstable
-Decreased level of conciousness
-Severe metabolic acidosis
-Poor respiratory rate
-Must be in control of own airway
-Must be able to cooperate
What is minute volume in ventilation?
-Volume of gas inhaled or exhaled from person’s lungs per minute
How can minute volume be altered?
-Altering tidal volume or rate of respirations
-The greater the minute volume, the greater the removal of carbon dioxide
-However if tidal volume is too high, barotrauma may result
-Low tidal volume approach delivers best outcomes
What is high flow nasal oxygen?
-Can deliver up to 100% o2 with high flows and high humidity
-Positive airway pressure comparative to low pressure CPAP is delivered which helps work of breathing
-Generally well tolerated, allows communication and oral nutrition
-Usually used for type 1 respiratory failure in surgical patients
What is synchronised intermittent mandatory ventilation? What is controlled mandatory ventilation?
-SIMV preserves some of patients respiratory muscle activity by synchronising ventilation around the patient’s own respiratory effort
-Controlled mandatory ventilation: requires full sedation due to compulsory positive-pressure breaths from ventilator. Allows pt to play no part in breathing and is rarely used
What is PEEP?
-Pressure is administered during expiration to prevent airway collapse and recruit underventilated alveoli
When can ventilatory weaning be attempted?
-When original cause of respiratory failure has been treated successfully
-Sedative drugs have been reduced to a level at which they will not depress respiration
-Low inspired oxygen concentration maintains normal paO2
-CO2 elimination is no longer a problem
-Sputum production is minimial
-Nutritional status, minerals, trace elements are normal
-Neuromuscular function of diaphragm and intercostals are adequate
-Pt is reasonably cooperative
However baseline function must be considered
What is atelectasis? What causes it?
-Absence of gas from all or part of lung
-Commonly seen following abdominal and thoracic procedures
Casued by:
-Reduced lung expansion from pain and splinting of diaphragm (reduced contraction to avoid pain)
-Leads to retention of secretions, distal airway collapse
-Exacerbated in the elderly/overweight/smokers/those with pre-existing lung disease
How is atelectasis treated?
-Physiotherapy
-Mobilisation
-Incentive spirometer
-High flow o2 if available
What are the most common organisms for hospital acquired pneumonia?
-MRSA
-Pseudomonas
-Enterobacter
-Serratia
How is PE treated?
-usually LMWH initially then NOAC
-UFH infusion if moderate risk of bleeding
-In very high risk patients, IVC filter
-D/w haematology if unsure
Normal ranges for ABG components:
-pH: 7.35-7.45
-PaCO2: 4.5-6 kpa
-Hco3-: 24-28 mmol/L
-Base deficit/base excess: normal range +2 to -2
-PaO2: 10-14
-Serum lactate: <1.2
-Anion gap: 10-15
What is the anion gap?
–> AG = ([Na+] + [K+]) - ([Cl-] + [HCO3-])
Raised anion gap:
–> increase in unmeasured anions (e.g. lactate and ketones)
Normal anion gap
–> total concentration measured anions are unchanged
–> most commonly following overuse of NAcl, also seen after bladder surgery and ileal conduit formatoion
How are hydrogen ions produced?
-As a result of production of CO2 (excreted by lung-controlled by chemoreceptors in medulla)
-Small amount produced as products of metabolism: excreted by kidney
-Therefore 2 methods of H+ ion homeostasis: renal and respiratory
Describe the respiratory control mechanism of pH
-Rapid response system that requires normal CNS function (central pH chemoreceptors) and lung function to allow CO2 to be transferred from pulmonary venous blood to alveolar gas and excreted in expired gas
-Dysfunction of mechanics/control of respiration causes retention of CO2 and rise in H+ ion concentration (respiratory acidosis) or overexcretion and fall in H+ concentration (respiratory alkalosis)
Describe the renal control mechanism of pH
-Slower responding system that depends on excretion of H+ ions in urine by distal nephron
Conditions that impair renal function will prevent H+ excretion resulting in metabolic acidosis
e.g.
–> obstructive uropathy
–> circulating volume depletion
Describe the acid buffer equation
Left side volatile (respiratory) right side non volatile (renal)
Describe respiratory acidosis
-Retention of CO2 causes rise in H+ by driving acid-base equation to the right
-Kidney responds slowly over 48 hrs to compensate by increasing H+ excretion in distal nephron, returning H+ towards normal, although normality cannot be achieved
Describe metabolic acidosis
Inability of kidney to excrete non-volatile H+ ion or sudden increase in non-volatile acid load (e.g. in sepsis) will drive equation to the right and resp function will rapidly respond by increasing minute volume, reducing CO2 and cause H+ to return to normal
Describe respiratory alkalosis
-Results when minute ventilation is higher than required to maintain appropriate PaCO2
-PaCO2 is driven down and H+ falls (pH rises)
Causes
-This is usually caused by increased central respiratory drive commonly caused by fever, hepatic disease, aspirin toxicity or CNS dysfunction
Metabolic alkalosis
-Abnormal retention of bicarb (loop directics, chronic hypokalaemia)
-Loss of H+ (GOO, chronic nasogastric aspiration
What are the causes of metabolic acidosis?
-Impaired tissue perfusion (tx cause, improve circulation)
-Renal failure (tx cause, ? need for bicarb/RRT)
-Hepatic failure (? for transplant)
What are the causes of respiratory acidosis?
-Head/spinal injury - ventilation
-Drug overdose: antidote +/- ventilation
-Chest wall deformity/injury - ventilation if indicated, surgery for flail chest/multiple rib #
-Myopathy/peripheral neuropathy - ventilation if indicated
-Pulmonary disease: tx disease, respiratory support and ventilation if indicated
-Massive PE: re-establish perfusion of ventilated lung
