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Hugh's MD1 Respiratory > Lou's Pathophysiology > Flashcards

Lou's Pathophysiology Flashcards

1
Q

Does ventilatory capacity limit healthy people during exercise?

A

No, HR does

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1
Q

What are the mechanical changes that occur due to pulmonary oedema?

A

Decrease lung compliance - fluid makes the increases the elastic work of breathing

Decrease lung volume - lungs are harder to expand

Increased airway resistance - due to fluid in the airways

Increased work of breathing (elastic and resistive)

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1
Q

What is the clinical presentation of abestosis?

A

Progressive breathlessness and cough

Crepitations (the type due to opening of alveolar during inspiration)

Clubbing

+/- Cyanosis

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2
Q

Why is systolic BP lower during inspiration

A

Negative interthoracic pressure > expands the compliance of pulmonary vasculature > blood pools there > reduces pulmonary return > SV is lower > BP is lower (the body response by increase HR).

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2
Q

What are some causes of increase pulmonary hydrostatic pressure?

A

Left ventricular failure,

mitral stenosis

fluid overload

pulmonary veno-occlusive disease

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2
Q

What causes pulmonary hypertension?

A
  1. Increase LA pressure - eg mitral stenosis, left heart failure
  2. Increased pulmonary blood flow - eg excess central volume
  3. Increased pulmonary vascular resistance - eg vasocontriction,

vasculature damage (emphysema), obstruction (PE)

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3
Q

What are 5 causes of hypoventilation?

A

Motor centre depression

Neuromuscular disease

Chest wall deformities

Obesity

Sleeping disordered breathing

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3
Q

What is MUD?

A

Medically undiagnosed dyspnoea

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4
Q

Why does obstruction occur during sleep?

A
  1. Muscles relax
  2. Airway is already narrowed (obesity, tonsils)
  3. Tongue falls back (esp if suprine)
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5
Q

What happens to residual volume with gas trapping?

A

It increases

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6
Q

Why is a low V/Q match bad?

A

Hb arrives at alveolar-capillary but isn’t filled with O2 > reduces PaO2 > hypoxaemia

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7
Q

What levels of PaCO2 occur during respiratory failure?

A

>60mmHg

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7
Q

How thick is the A-C membrane?

A

0.5 microns

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8
Q

When does diffusion limitation of CO2 occur?

A

Only if there is very severe diffusion impairment, inadequate ventilation is the primary cause

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8
Q

Generally, conditions that effect the alveolar membrane make the lungs …

A

Stiffer - increasing the elastic work of breathing

Except in Emphysema

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10
Q

How does metabolic acidiosis occurs due to pulmonary oedema?

A

Pulmonary oedema (=low gas exchange) therefore tissue hypoxia - anaerobic resp. - lactic acid - metabolic acidosis.

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11
Q

What physiological differences are present when breathing with an obstruction?

A

Active exhalation

Slower inhalation and exhalation

Reduction in maximum ventilation

Increased work of breathing/use of respiratory muscles

Increased sensation of breathing

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11
Q

What does anxiety do to the respiratory equilibrium?

A

Anxiety > hyperventilation > PaCO2 drop > pH Increases = Respiratory alkalosis

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12
Q

What diseases can disrupt the A-C membrane?

A

Infections - TB, pneumonia

Pneumonitis (inflammation of the alveoli) eg drug induced

Pulmonary fibrosis

Emphysema

Oedema

Lymphangitis

Carcinomatosis

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12
Q

What happens to maximum ventilation in restrictive lung disease?

A

It decreases

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13
Q

What is type I respiratory failure characterized by?

A

Low PaO2

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14
Q

What is type II respiratory failure characterised by?

A

PaCO2 >50mmHg and PaO2 low to normal

due to failure of ventilation

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15
Q

What is the normal lymphatic flow rate in the lung?

A

20ml/hour

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16
Q

What factors determine the compliance of the lungs?

A

Tissue composition

Surfactant

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17
Q

True or false, ventilation rate is higher dependent of PaO2?

A

False, PaO2 must drop below 60 before there is a response

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18
Q

What are the gas exchange changes that occur due to pulmonary oedema?

A

hypoxaemia due to shunt

Low V/Q units

Diffusion impairment

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18
Q

What makes up the alveolar-capillary membrane?

A

Layer of surfactant

Type I alveolar cell

Basement membrane

Endothelial cell

19
Q

What is breathlessness?

A

Breathlessness arises when there is a recognition by the subject of an inappropriate relationship between respiratory work and total body work

21
Q

What is a negative consequence of the vasocontrictory compensation of V/Q mismatch?

A

Increases pulmonary pressure if V/Q mismatch is wide spread

23
Q

Which occurs more readily interstitial or alveolar oedema?

A

Interstitial as capillary endothelium is more permeable to water cf to alveolar wall (and water enters the interstitium first)

25
Q

Does the pulmonary arterial pressure increase during exercise?

A

No, due to dilation and recruitment of extra pulmonary vessels

27
Q

What is acute respiratory failure defined as?

A

The failure of the respiratory system to provide adequent ventilation, oxygenation or metabolic requirements of the patient

28
Q

What is the problem with giving O2 to people with chronic hypercapnoea?

A

Their resp centre responds to PaO2 so if it is increased too much that can stimulate hypoventilation > further hypercapnoea

30
Q

What is the normal range of A-a gradients?

A

15-30

31
Q

What are the consequences of obstructive lung disease?

A

Recruitment of accessory muscles

Increase consumption of O2 by respiratory muscles

Possible fatigue of respiratory muscles

33
Q

What is the A-a gradient a measure of?

A

Alveolar/capillary gas exchange across all A-C units

34
Q

What are the mechanical effects of restrictive lung disease?

A

Breathlessness

Increase elastic work of breathing

Reduced lung volume

Shorter, faster breaths

Reduced maximum volume

  • Increase use of inspiratory muscle and O2 comsuption by them
35
Q

What are the pulmonary artery pressures during systole and diastole

A

25/8, mean=15mmHg

36
Q

What occurs during sleep apnoea?

A

Fall asleep >

Muscle relaxation >

Complete Obstruction >

Fall in PaO2 and increase in PaCO2 >

Brains wakes >

Muscle contract, airway re-opens >

Fall into deep sleep again

37
Q

What is lung compliance?

A

Change in V / Change in P

37
Q

What is the consequence of chronic sleep disorders?

A

Physiological change occurs to facilitate sleep > Re-set the resp centre to be able to tolerate a higher PaCO2 so that sleeping can occur > chronic hypercapnoea > PaO2 becomes the driver for ventilation

39
Q

What are the possible causes of high PaCO2

A

Predominately low ventilation

39
Q

What are some symptoms of sleep apnoea?

A

Snoring

Arousals

Choking

Excessive daytime sleeping, lTethargy, reduced libido, mood change, poor memory

Difficult to treat hypertension and unexplain resp failure

40
Q

What is gas trapping?

A

The obstruction of exhalation of gas due to a severe obstruction. Air is inhaled but can’t be exhaled

41
Q

What is Fick’s law?

A

Determines the rate of diffusion of a gas

42
Q

What is pulsus paradoxus?

A

When the difference in systolic BP between inspiration and expiration is greater.

43
Q

What is the equation for A-a gradient?

A

PAO2 = PiO2 - PACO2/RQ

followed up PAO2 - PaO2

Where

RQ is a constant = 0.8

PiO2 (partial pressure of inspired air) for room temp and sea level = 150

PACO2 is assumed to equal PaCO2 which is measured in arterial blood gas

And PaO2 is also measured in arterial blood gases

45
Q

What happens to perfusion if ventilation drops in a local area?

A

Compensatory drop due to divertion of blood flow in capillaries

46
Q

What are some management strategies for sleep apnoea?

A

Nasal CPAP (continue positive airway pressure)

Manibular advancement splint

Surgery

Lie on side

48
Q

What percentage of FVC (forced vital capacity) is expelled in a normal FEV1

A

80%

49
Q

What some possible causes of MUD?

A

Psychologenic

Deconditioned (got fat)

New clinical disease

Maximal effort

50
Q

What causes wheezing?

A

Airway obstruction

51
Q

When does diffusion limitation of O2 occur?

A

In heathly people: Never

People with mild diffusion impairment: during exercise

People with a severe diffusion impairment: at rest and during exercise

52
Q

What percentage of total O2 usage is required for the WOB at rest?

A

3%

53
Q

Which has a greater impact on lung mechanic and gas exchange, fluid in the alveoli or interstitial space?

A

Alveoli!

54
Q

What is the mechanism of asbestosis?

A

Chronic inflammation > progressive fibrosis > disruption and destruction to A-C membrane > Mechanical and gas exchange defect = Decrease PaO2, Increase A-a gradient, Reduced lung volume, reduced compliance, Increased work of breathing

56
Q

When is breathlessnees a symptom not a sensation?

A

When it occurs when it shouldn’t normally, when it doesn’t usually occur for that level of exertion.

57
Q

What does surfactant do?

A

It lower surface tension in alveoli to prevent them from collapsing, increases the compliance of the lung and keeps the alveoli dry.

58
Q

The respiratory centre sends the majority of its output via which nerve?

A

Phrenic

60
Q

What are the possible causes of low PaO2?

A

Low PiO2

Low Ventilation

Gas exchange abnormality - V/Q mismatch, shunt, A-C membrane problem

61
Q

What type of lung disease is asbestosis?

A

Restrictive

62
Q

What is the consequence of high V/Q mismatch?

A

Physiological dead space with little effect on PaO2

63
Q

Where in the brain is the respiratory centre located?

A

The pons and medulla

64
Q

How does airway obstruction increase the WOB?

A

It increases the resistive WOB, ie the work required to overcome the friction of airflow. (As opposed to an increase elastic work of breathing that occurs with restrictive lung disease)

65
Q

What are some causes of increase pulmonary capillary permeability?

A

Toxins, sepsis, multiple trauma

66
Q

What happens to total lung capacity with gas trapping?

A

It increases

Hugh's MD1 Respiratory (15 decks)

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