Respiratory Compromise

Question 1

Define Hypoxemia (including normal ranges)

Answer 1

Reduced oxygenation of arterial blood and low arterial oxygen tension (PaO2)

• Normal range for PaO280-100 mmHg under 65 years
• Mild or relative 60-80 mmHg
• Moderate 40-60 mmHg
• Severe <40 mmHg

Question 2

What are the causes of hypoxemia?

Answer 2

1. Hypoventilation (ventilatory failure) - inadequate amount of oxygen entering alveoli for normal oxygen transfer into blood
   - Depression of the respiratory centre in the central nervous system (CNS) through a head injury or medications (e.g. drug overdose, anaesthesia)
   - Obstruction in the upper airways caused by blood, sputum, tumours or a foreign body
   - Chest wall movement may restrict lung movement (morbid obesity, acute and/or chronic pain, especially in post-operative patients - impairment to the chest wall due to trauma (e.g. fractured ribs)
   
   2. Impaired diffusion of gas - pathological changes in alveolar/capillary membrane may slow or prevent diffusion = poor O2transfer into arterial blood
      
      • Pulmonary oedema, asbestosis and asthma
   3. Intrapulmonary shunting - occurs despite being perfused by blood, the pulmonary region(s) are not ventilated by gas
      
      • contusions such as atelectasis, bronchospasm, consolidated pneumonia and acute respiratory distress syndrome (ARDS)
   4. Increased Dead space - portion of inspired O2and CO2that does not take part in gas exchange - inadequate blood perfusion to a lung region
      Pulmonary embolism or sepsis resulting from regions of lung that do not have a blood supply

Question 3

Describe Hypercapnia (including normal ranges)

Answer 3

Hypercapnia: abnormally elevated PaCO2 and high arterial CO2 tension
• Normal PaCO2around 35-45 mmHg
• CO2retention >50 mmHg
• Can impact multiple systems
• Rise in PaCO2= lowering of pH = patients become acidotic (pH <7.35) = vasodilation flushing and increase WOB
• Results typically from disease processes that cause bronchial airway narrowing and, therefore, trapping of gas in alveoli (e.g. asthma, COPD)
Tx: decrease WOB and improving ventilation (V) and perfusion (Q)

Question 4

Why can giving Oxygen to a COPD patient considered a double edged sword?

Answer 4

• Loss of Protective Hypoxic Vasoconstriction: supplemental O2can cause these capillaries to dilate + CO2 it not removed because of area is not well ventilated = increase CO2 in the blood
• Haldane Effect: the more desaturated the haemoglobin, the more CO2it can carry. If we provide excessive oxygen, we increase the proportion of oxyHb and prevent it from transporting CO2effectively. In COPD patients, for example, we need to titrate their oxygen saturation to between 88-92% to ensure effective CO2removal

Question 5

What is hypoxia?

What are the clinical manifestations of hypoxia?

Answer 5

educed oxygenation of cells in tissues with low CO2, low hemoglobulin, hypoxaemia. Patient becomes acidotic (pH <7.35) and cellular destruction

(depends on acute or chronic changes): headache, flushing, confusion, lethargy, PaCO2 > 100mmHg in acute elevations
• Can cause seizures (convulsions), coma, cardiovascular collapse

Question 6

What is acute respiratory failure (ARF)?

What are the classifications of ARF?

Answer 6

occurs because of acute or chronic impairment of gas exchange between the lungs and the blood causing hypoxia with or without hypercapnia - failure in gas exchange is due to heart or lung failure or both. *Clinically defined as hypoxaemia and/or hypercapnia at rest and at sea level or:
• PaO2below 60 mmHg (should be 80-100 mmHg)
PaCO2above 50 mmHg (should be 35-45 mmHg)

Type I respiratory failure presents as hypoxaemia with normal CO2
Type II respiratory failure presents as hypoxaemia and hypercapnia

Question 7

What is pulmonary Oedema (PO)?

Answer 7

Excess fluid in the lungs
Lungs normally contain very little fluid and are kept “dry” by lymphatic drainage and a balance of:
- capillary hydrostatic pressure
- capillary oncotic pressure
- capillary permeability

Question 8

What are the causes of PO?

Answer 8

• Cardiogenic:
○ Associated with an increase in left atrial pressure (LAP) due to valvular dysfunction + left ventricular failure = decreased stroke volume and cardiac output
○ Increased pulmonary capillary hydrostatic pressure = drags fluid from the interstitial space (exceeds lymphatic system capacity) = pooling in the lungs
• Non-Cardiogenic:
○ Injury to capillary endothelium = increase pulmonary micro-vascular permeability (e.g. noxious gas) = increase capillary permeability causes a disruption of surfactant production by alveoli = movement of fluid and plasma proteins into the interstitial space and alveoli
○ Compression of lymphatic vessels by tumours or trauma = obstruction of lymphatics = loss of ability to remove excess fluid from the interstitial space = accumulation of fluid in the interstitial space

Question 9

What are the clinical manifestations of PO?

Answer 9

respiratory distress - dyspnoea, orthopnoea, tachypnoea, hypoxaemia, increased WOB

Question 10

How do you diagnose PO?

Answer 10

• Physical Examination:
○ Bronchial wheezing, crackles (rales), cyanotic, productive cough with pink/frothy sputum and skin maybe cool and clammy. The patient may appear anxious, confused, have extra heart sounds (galloping rhythm S3), be in a coma or dead.
○ Hypotension/tachycardia (possibly from MI or HF), low SpO2, increased PaCO2, acidosis
• Diagnostics:
○ Chest X-ray: consolidation in the lungs, ventricular dilation, cardiomegaly
○ ECG: cardiac failure
ABG: how compromised the patient is

Question 11

Management of PO

Answer 11

aimed at removing offending agent or supportive like O2 therapy to maintain adequate ventilation and circulation. *Caution for O2 toxicity.

Question 12

What does management of PO depend on?

Answer 12

Cardiogenic: pharmacological agents: diuretics, vasodilators, improve contraction of heart (dopamine, dobutamine, adrenaline)
Non-cardiogenic: supportive measures: mechanical ventilation, hemodynamic and cardiovascular monitoring with pharmacological agents

Question 13

4 pharmacological treatments to PO

Answer 13

• Potassium sparing diuretic (spironolactone): aldosterone antagonist - inhibits sodium absorption in the distal tubule by blocking Na channels and aldosterone = increase sodium excretion and thus fluid. Adverse effects of hyperkalaemia, ACE inhibitors, gynaecomastia in men and post-menopausal bleeding
• Frusemide: diuresis by inhibiting Na and Cl reabsorption in the ascending LOH. Short acting and rapidly reduces fluid volume. Adverse effects are dose related and electrolyte disturbances (hyponatraemia, hypokalaemia, syncope, dehydration, orthostatic hypotension)
• Vasodilators (GTN): sublingual or IV - dilated BV addressing the workload on the heart. Adverse effects of tachycardia, hypotension, flushing, and headache
Sympathomimetics (Dopamine and dobutamine): increase cardiac output. Both vasodilators (dopamine vasoconstrictor @ higher dose). Adverse effects of tachycardia, ventricular ectopic beats

Question 14

What is atelectasis?

When does atelectasis occur?

Answer 14

loss of lung volume due to a collapse of tissue

Common after surgery but can be caused by chest pressure, blocked airway, lung cancer, pneumonia, pleural effusions and respiratory distress syndrome (RDS)

Question 15

What are the classes of atelectasis?

Answer 15

• Obstructive: physical blockage of the airway
• Non-obstructive
• Contraction, resorption, compression

Question 16

What are the clinical manifestations of atelectasis?

Answer 16

dyspnoea, tachypnoea, fever, cough, hypoxemia, leucocytosis, cyanosis, absence of breath sounds and diminished chest expansion

Question 17

How do you diagnose atelectasis?

Answer 17

Signs and symptoms

Chest X-ray - lack of air in lungs

Question 18

What is the treatment for atelectasis?

Answer 18

ambulation/position changes, deep breathing and oxygen administration

Question 19

ARDS is secondary to what conditions?

Answer 19

gastric content aspiration, trauma and sepsis, which is secondary to pulmonary or non-pulmonary infections, acute pancreatitis, hematologic disorders, reactions to drugs and toxins

Question 20

What occurs in ARDS and what is the pathophysiology?

Answer 20

Primary damage to alveolar/capillary membrane resulting in leakage of fluid into alveolar space and subsequent propitiatory failure. As the disease progresses, the work of breathing becomes increased and the lung stiffens and becomes more difficult to inflate

Pathophysiology: causes a massive inflammatory response (synthesis and release of neutrophils, macrophages, complement endotoxin, IL-1, tumour necrosis factor, proteolytic enzymes; ROS, prostaglandins and leukotrienes = further damage the capillary endothelium and alveolar epithelium = PO and haemorrhage = reducing lung compliance and impairing alveolar ventilation = pulmonary vasoconstriction, surfactant inactivation and fibrosis

Question 21

What are the clinical manifestations of ARDS?

Answer 21

ARDS is progressive and life threatening
• Rapid onset (12-18 hours)
• Characterised by an increased respiratory rate = respiratory alkalosis, dyspnoea, refractory hypoxemia and oxygen therapy
• Decrease in lung compliance increases the WOB = metabolic acidosis and plasma pH drops = reduce O2affinity for Hb = hypoxemia = hypotension and decreased CO
• If left untreated, ARDS will cause multiple organ failure and death.

Question 22

How do you diagnose ARDS?

Answer 22

a physical and radiological examination is required to confirm ARDS
• Initially fine crackles on auscultation
• Chest X-ray - clear or few infiltrates
• As ARDS develops into refractory hypoxemia, a chest X-ray will demonstrate bilateral infiltrates and exclusion of cardiogenic PO
Further tests may be required such as a chest computed tomography (CT) and bronchoscopy

Question 23

What is the treatment of ARDS?

Answer 23

• Essential to detect ARDS early and commence supportive therapy provision and prevention of complications such as oxygen
• May require mechanical ventilation in ICU with sedation and may be employed to decease O2consumption
Drugs can be administered to increase cardiac output

Question 24

What are the common causes of respiratory failure in children?

Answer 24

RDS and Croup

Question 25

What is RDS?

Answer 25

Respiratory distress syndrome:
• Lack of surfactant = alveolar collapse
• Most common cause of respiratory failure in premature infants
*Usually treated with corticosteroids to accelerate formation of surfactant or a post-natal surfactant (e.g. beractant) into the trachea

Question 26

What is Croup?

Answer 26

Laryngotracheobronchitis:
• Acute upper airway infection usually affecting infants and small children (aged 3 months – 5 years)
• Classified as viral (most common) or spasmodic

Question 27

What is viral croup caused by and what is the treatment ?

Answer 27

Caused by viruses (influenza, measles) and is usually preceded by an upper respiratory infection
• Airway obstruction may progress in some children which presents as excessive crying or cyanosis
• Not possible to treat with antibiotics, mucolytics or bronchodilators however corticosteroids may help is most cases
Treatment is primarily with supportive measures including oxygen, antipyretics and increased fluid intake with careful monitoring

Question 28

What is spasmodic croup and what is the treatment?

Answer 28

symptoms similar to viral croup but child is afebrile
• Thought to have an allergic origin and commonly occurs at night
In mild cases, it can be managed at home by taking the child into a bathroom with a warm, running shower to decrease irritation