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Medical Studies 1 > Resp Week 6 > Flashcards

Resp Week 6 Flashcards

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USMLE® Step 1 flashcards
1
Q

what are the two states of normal human sleep

A

REM

non-REM

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2
Q

what is clinical sleep staging based on

A

EEG

EOG

EMG

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3
Q

what are the subdivisions of NREM sleep

A

N1, N2, N3 (going from lighter to deeper sleep )

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4
Q

describe EEG waves, percentage of time, and function during the different stages of sleep

A

stage W (awake but resting) = alpha waves, 5%, normal bodily activity

stage N1 = theta waves, 5%, cardiovascular rest

stage N2 = sleep spindles and K complexes, 50%, cardiovascular rest

stage N3 = delta waves, 15%, cardiovascular rest

stage REM = sawtooth waves, 25%, cardiovascular activation

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5
Q

describe the normal changes in ventilation during sleep

A

drive to breathe is reduced during sleep

upper airway resistance increases during sleep, therefore reduced breathing capacity

metabolic rate decreases by 10-15% during sleep, decreasing breathing drive

PCO2 increases and PO2 decreases

as a result, hypoventilation occurs during sleep

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6
Q

describe obstructive sleep apnoea

A

disordered breathing during sleep in which the airway is mechanically obstructed, leading to a cessation of airflow, resulting in intermittent hypoxia and fragmented sleep

has CV and cerebrovascular impacts

several risk factors e.g obesity, alcohol use, upper airway abnormalities

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7
Q

what are 10 clinical features of OSA

A

daytime somnolence

nocturia

cognitive impairment

dry mouth

large neck

witnessed apnoeas

insomnia

morning headaches

high BMI

crowded oropharynx

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8
Q

what is the mallampati score

A

clinical assessment tool used to evaluate the visibility of the oral structures and predict the difficulty of intubation

determined by having patient sit upright with their mouth open and tongue protruded

score is based on visualisation of oropharynx

a higher score indicates a higher likelihood of difficult intubation

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9
Q

what are the 4 classes of the mallampati score and what can be seen in each

A

class 1 - full visibility of uvula, soft palate and fauces

class 2 - visibility of soft palate and part of uvula

class 3 - only soft palate seen

class 4 - only shows hard palate

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10
Q

what are 3 diagnostic methods of OSA

A

polysomnography

blood O2

home sleep apnoea testing

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11
Q

describe polysomnography

A

comprehensive overnight sleep study recording multiple physiological parameters

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12
Q

what are 9 measurements taken during polysomnography

A

pulse ox - O2 in blood

EEG - brain electrical activity

EOG - tracks eye movement

EMG - monitors muscle activity

ECG - heart electrical activity

nasal pressure cannula - measure airflow through nostrils

thermocouple - measures airflow by detecting temp changes

microphone - records sounds like snoring during sleep

thoraco-abdominal bands - monitor chest/ab mvmt to assess breathing

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13
Q

describe home sleep apnoea testing

A

portable assessment for detecting sleep-disordered breathing at home

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14
Q

what is the difference between obstructive and central apnoea

A

obstructive apnoea is complete cessation of airflow due to upper airway resistance and obstruction, whereas central apnoea is complete cessation of airflow due to lack of control from brainstem respiratory centres

central apnoea is much less common than obstructive (10:1)

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15
Q

what is mixed apnoea

A

combination of central and obstructive apnoea

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16
Q

what is hypopnea

A

significant reduction in airflow, associated arousal during sleep, or oxygen desaturation

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17
Q

what is the respiratory disturbance index (RDI)

A

number of apnoeas, hypopneas, and ‘unsures’ (reduction in airflow not reaching any of the criteria) per hour

this info forms basis of RDI

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18
Q

what are 4 acute complications of sleep disorder breathing

A

excessive somnolence

inappropriate falling asleep

psychosocial consequences

snoring

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19
Q

what are 4 chronic complications of sleep disordered breathing

A

pulmonary HTN

CVD

cerebrovascular accident

uncontrolled HTN

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20
Q

what is the importance of early referral

A

indicated for individuals w cerebrovascular co-morbidities or risk factors, patients who are drowsy driving, and patients who operate heavy machinery

OSA must be reported to the DMV in all instances

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21
Q

what are 5 Rx options for sleep apnoea

A

CPAP

mandibular splint

surgery

lifestyle modification

sleeping on side

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22
Q

describe CPAP as a Rx for sleep apnoea

A

high efficacy

low risk

pressure is set based on body habitus

blows air into nose/mouth to splint open upper airway

provides major benefit

23
Q

describe mandibular splint as a Rx for sleep apnoea

A

moulded mouthpiece that pries open the airway

not effective for obese patients

24
Q

describe surgery as a Rx for sleep apnoea

A

variable results

generally, this is a second-line option due to invasiveness and associated costs

25
Q

describe lifestyle modification as a Rx for sleep apnoea

A

reduced EtOH, sedatives, cigarettes, weight loss

has implications for other body systems e.g CV and GI

26
Q

describe sleeping on side as a Rx for sleep apnoea

A

positional changes may be sufficient to provide symptomatic relief

easy method

27
Q

what are 6 reasons for non-compliance with CPAP as a Rx for sleep apnoea

A

comfort - can be tight

xanthostoma - dry mouth due to airflow

aesthetic - may appear unattractive

claustrophobia - mask can be restricting in nature

cost - it is expensive

lack of symptomatic response - no immediate response, meaning less inclined to keep using

28
Q

what is type 1 respiratory failure

A

lungs cannot move enough O2 into the blood, leading to hypoxaemia (PaO2 < 60mmHg)

29
Q

what is type 2 respiratory failure

A

lungs cannot remove enough CO2 from the blood, leading to hypercapnia (PaCO2 > 45mmHg; often coexists w hypoxaemia)

30
Q

compare and contrast pulse ox with ABG

A

pulse ox reflects tissue O2 supply by measuring the percentage of Hb saturated w O2 but does not measure blood CO2 or O2 level

whereas

arterial blood gas sample provides accurate assessment of hypoxaemia and hypercapnia, acid-base status, and extended parameters such as lactate

31
Q

what are 2 key mechanisms of respiratory failure

A

failure of pulmonary ventilation

failure of pulmonary gas exchange

32
Q

describe failure of pulmonary ventilation in regards to respiratory failure

define, cause, impact

A

this is the failure to physically move air in and out of lungs, resulting in alveolar hypoventilation (smaller, slower breathing)

caused by extrapulmonary factors such as CNS depression and respiratory pump failure

this leads to hypercapnia and hypoxaemia

33
Q

what are 3 things that can lead to CNS depression (extrapulmonary cause of failure of pulmonary ventilation)

A

drugs e.g opioids

structural abnormalities e.g stroke

raised ICP e.g tumour

34
Q

what are 3 things that can lead to respiratory pump failure (extrapulmonary cause of failure of pulmonary ventilation)

A

phrenic nerve dysfunction e.g due to direct damage

neuromuscular weakness e.g diseases such as MND

chest cage restriction e.g kyphoscoliosis

35
Q

describe failure of pulmonary gas exchange in regards to respiratory failure

cause, impact

A

caused by pulmonary factors such as problems with the lungs or blood vessels

results in reduced O2 delivery from lung to blood

it does not usually cause CO2 retention except for in severe COPD where there is severely reduced lung reserve

36
Q

what are 4 causes of pulmonary gas exchange failure and name one dominant mechanism for each with an example

A

diffusion limitation = thickened interstitium and alveolar-capillary membrane e.g interstitial lung disease

ventilatory defect (intrapulmonary shunt) = alveolar collapse e.g pneumothorax

perfusion defect (dead space) = pulmonary vascular narrowing or obstruction e.g PE

right to left anatomic shunt = de-O2 blood re-entering systemic circulation e.g intracardiac shunt

37
Q

what are 4 major consequences of hypoxaemia

A

damage to vital organs and tissues via cellular hypoxia

increased sympathetic discharge, leading to tachycardia and HTN

lactic acidosis

chronic effects, such as impaired cough reflex and depressed asthma symptom perception

38
Q

what are 4 major consequences of hypercapnia

A

cerebral autoregulation problems - there is an initial increase in inspiratory drive, but then due to an increase in cerebral blood flow there is increased ICP leading to headache, and decreased inspiratory drive, then there is CO2 narcosis and eventual seizure, coma or death

direct cardiorespiratory effects e.g arrthymia and cardioresp arrest

respiratory acidosis

physiologic responses e.g increase release of O2 to tissues

39
Q

what are implications of O2 induced hypercapnia

A

increased alveolar dead space - normal compensatory mechanisms in chronic severe COPD act to redistribute pulmonary blood flow to better ventilated areas of the lung, but excessive O2 therapy will reverse this protective effect which leads to reduced CO2 clearance

haldane effect - excessive O2 will displace CO2 bound to Hb, thus raising blood CO2 retention

blunting of hypoxic ventilatory drive

40
Q

what are 3 general principles for O2 therapy

A

always treat primary/reversible problems e.g pneumonia, HF

O2 therapy is vital for T1RF

O2 therapy can correct hypoxaemia in T2RF but does not correct hypercapnia, and may in fact make it worse

41
Q

what are 5 treatment options for respiratory failure

A

high flow nasal O2 therapy (HFNOT)

continuous positive airway pressure (CPAP)

bi-level ventilation (BPAP)/non-invasive ventilation (NIV)

intubation and mechanical ventilation

extracorporeal membrane oxygenation (ECMO)

42
Q

what are 2 acid-base consequences of respiratory failure

A

lactic acidosis in severe hypoxaemia

primary respiratory acidosis in hypercapnic respiratory failure (T2RF)

43
Q

describe how lactic acidosis in severe hypoxaemia can occur due to respiratory failure

A

tissue hypoxia leads to an increased in anaerobic respiration, which produces lactic acid as a byproduct

this is compensated for by an increased respiratory drive in an attempt to blow off CO2 to normalise pH

44
Q

describe how primary respiratory acidosis in hypercapnic respiratory failure can occur

A

an excess CO2 results in increased renal retention of bicarbonate ion to buffer in order to attempt to normalise pH

for metabolic compensation to occur to oppose this, you need to have normally functioning kidneys

45
Q

what are 4 assessments that can be made by measuring ABG

A

pulmonary gas exchange

acid-base balance

lactate

co-oximetry

46
Q

what is the normal range of PaO2

A

75-100mmHg, depending on age

47
Q

what is normal range of pH

A

7.35-7.45

48
Q

what is normal range of PaCO2

A

35-45mmHg

49
Q

what is normal range of bicarbonate ion

A

22-28mmol/L

50
Q

what is normal range of lactate

A

0.2-2.0mmol/L

51
Q

what is the difference between hyperlactatemia and lactic acidosis

A

lactate >2mmol/L is hyperlactatemia

lactate >4mmol/L is lactic acidosis

52
Q

what is type A lactic acidosis

A

severe tissue hypoxia or hypoperfusion eg hypovolemia or cardiac failure

53
Q

what is type B lactic acidosis

A

impaired cellular metabolism or regional ischemia without severe hypoxia or hypoperfusion e.g high dose inhaled beta antagonists such as salbutamol

Medical Studies 1 (11 decks)

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