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Clin Med II > Bronchiectasis and Critical Care > Flashcards

Bronchiectasis and Critical Care Flashcards

1
Q

bronchiectasis

A
  • permanent, abnormal dilation and destruction of bronchial walls
  • inflamed and easily collapsible airways -> airflow obstruction
  • chronic cough and viscid sputum
  • may be caused by recurrent inflammation or infection
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2
Q

what disease is highly associated with bronchiectasis

A
  • cystic fibrosis
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3
Q

cystic fibrosis

A
  • abnormal transport of chloride and sodium across epithelium
  • causes thick viscus secretions
  • usually dx in childhood
  • pseudomonas infections common
  • dx with sweat chloride test
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4
Q

clinical features of bronchiectasis

A
  • cough with mucopurulent sputum
  • hx of repeated RTI
  • dyspnea
  • rhinosinusitis
  • hemoptysis
  • recurrent pleurisy
  • fatigue
  • stress incontinence
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5
Q

PE findings for bronchiectasis

A
  • chronic pulmonary crackles
  • wheezing
  • rarely digital clubbing
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6
Q

treatment of bronchiectasis

A
  • treat underlying disease
  • prevent aspiration
  • immunizations
  • abx
  • nebulized hypertonic saline- thin secretions
  • chest PT
  • oscillatory positive expiratory pressure
  • pulm rehab
  • bronchodilators- may thin secretions
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7
Q

purpose of pulmonary rehab

A
  • reduce sx
  • optimize functional status
  • increased participation
  • reduce health care costs
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8
Q

features of pulmonary rehab

A
  • pt assessment and education
  • exs training
  • nutritional support
  • psychosocial support
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9
Q

outcomes of pulmonary rehab

A
  • improved QOL and exs capacity
  • reduced number of severe exacerbations
  • reduced health care utilization
  • improves pt survival
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10
Q

components of pulmonary rehab

A
  • edu about disease, functional status, and habit patterns to promote self care
  • smoking cessation
  • breathing retraining
  • chest PT
  • exercise
  • nutritional support
  • psychosocial support
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11
Q

when to initiate mechanical ventilation

A
  • hypoxemic
  • hypercarbic
  • do not wait until it is an emergency
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12
Q

hypoxemia definition

A
  • SaO2 < 90% on FiO2 > 60%

- pneumonia, pulmonary edema, V/Q mismatch

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13
Q

hypercarbic definition

A
  • pCO2 > 50 mmHg and pH < 7.3

- obstructive lung disease, muscle fatigue, neuromuscular diseases

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14
Q

what is the most common type of mechanical ventilation

A
  • endotrachial intubation through mouth

- ET diameter of 7-8 mm

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15
Q

what drugs should be used during initiation of mechanical ventilation

A
  • paralytic + anesthetic
  • succinylcholine or rocuronium
  • propafol or etomidate
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16
Q

where should ET be if placed correctly

A
  • 3-5 cm above carina

- confirm placement with CXR

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17
Q

complications of mechanical ventilation

A
  • R main stem intubation
  • trachea- esophageal fistula
  • ET tube migration
  • laryngeal damage- ulcers, vocal cord paresis
  • dental trauma
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18
Q

FiO2

A
  • fractioned of inspired oxygen

- amount of oxygen the vent is delivering to pt

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19
Q

PEEP

A
  • positive end expiratory pressure

- det amount of pressure that is in pts airways at the end of each breath

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20
Q

TV

A
  • tidal volume

- size of breath

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21
Q

pressure support

A
  • amount of support the vent gives pt when initiating own breath
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22
Q

benefits of PEEP

A
  • used to prevent alveolar collapse
  • recruits alveoli that have collapsed -> increased surface area for gas exchange
  • reduced FiO2 requirement
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23
Q

harm of PEEP

A
  • reduced CO by decreasing venous return and external constrain of RV
  • may be exaggerated in hypovolemic pts
  • decreased CO -> impaired perfusion
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24
Q

misuse of PEEP

A
  • often used for atelectasis and pulmonary edema- no data to back these practices up
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25
Q

volume control

A
  • pt receives a set volume of air X number of times per min
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26
Q

synchronized intermittent mandatory vent (SIMV)

A
  • set RR but pt can initiate breath on their own
  • good to wean pts off
  • can cause dyssynchrony during tachypnea
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27
Q

assist control (AC)

A
  • good “set it and forget it” mode
  • good for newly intubated pts or sedated pts
  • can cause auto-peep during tachypnea- avoid this setting in awake pts
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28
Q

auto-PEEP

A
  • vent is trying to exhale but pt breaths in -> vent puts high pressure in airways -> barotrauma
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29
Q

pressure control (PC)

A
  • each breath associated with a set amount of pressure given through the vent
  • TV depends on driving pressure
  • gives good airway control
  • not a weaning mode and requires sedation
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30
Q

pressure support ventilation (PSV)

A
  • ideal for weaning pts
  • pts TV and RR are not pre-set
  • pt receives assistance with each breath or sometimes no assistance
  • TV and minute volume must be monitored- possible hypoventilation
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31
Q

determining if pt is ready for extubation

A
  • reversible cause must be reversed
  • hemodynamically stable
  • awake, alert, and following commands
  • PaO2 > 60 on an FiO2 40-50%
  • PEEP < 10
32
Q

steps for extubation

A
  • det if pt is ready
  • pass spontaneous breathing trial
  • rapid shallow breathing index (RSBI) < 100
  • try extubation if pass all these
  • if they fail det why they failed and try again later
33
Q

what is the rapid shallow breathing index

A
  • ration of RR to TV
34
Q

non-invasive ventilation

A
  • used in pts with respiratory failure
  • uses a face mask
  • good for acute onset issues i.e. CHF flash pulmonary edema
  • uses BiPAP to provide assistance with hypercarbic and hypoxic respiratory failure
35
Q

what is BiPAP

A
  • bilevel positive airway pressure
36
Q

tracheostomy

A
  • preferred in pts with low likelihood of extubation in 5-7 days
  • more comfortable, less sedation
37
Q

tracheostomy complications

A
  • tracheal stenosis in first 6 mo after removal
  • accidental decannulation
  • aspiration
  • cuff leaks -> possible aspiration
38
Q

what is A-a gradient

A
  • alveolar arterial O2 gradient
  • A= alveolar O2
  • a= arterial O2
39
Q

what does A-a gradient measure

A
  • measures how effective gas exchange is occurring
  • indicates how much oxygen is getting into blood stream
  • impt measure for treatment of hypoxemia
40
Q

what does it mean if A-a gradient corrects with O2

A
  • V/Q mismatch
  • i.e. large PE, COPD
  • increasing O2 means functioning parts of lungs take up O2
41
Q

what does it mean if A-a gradient does not correct with O2

A
  • there is a shunt- problem at the alveolar membrane

- common in severe atelectasis

42
Q

ARDS

A
  • syndrome that includes:
  • bilateral infiltrates
  • progressive respiratory failure
  • hypoxemia not responsive to increased FiO2
  • not a dx on its own, must treat underlying cause
43
Q

majority of causes of ARDS

A
  • sepsis
  • pneumonia
  • trauma
  • multiple transfusions
  • aspiration of gastric contents
44
Q

phases of ARDS

A
  • exudative
  • proliferative
  • fibrotic
45
Q

exudative phase of ARDS

A
  • alveolar edema
  • high concentration of inflammatory cytokines -> leukocyte recruitment
  • usually occurs in first 7 days
  • assoc with bilateral infiltrates
46
Q

proliferative phase of ARDS

A
  • next 7-21 days
  • assoc with recovery
  • pts will hopefully be extubated but may have sx
  • fibrotic changes may occur
47
Q

fibrotic phase of ARDS

A
  • not all pts reach this phase
  • interstitial fibrosis, emphysema like changes
  • poor prognosis- higher mortality
48
Q

ARDS treatment

A
  • treat underlying problem
  • hypoxemia- use lowest vent settings to achieve PaO2 of 55 mmHg
  • pH > 7.3 at lowest possible TV and RR
  • fluid management
  • close supportive care
  • TV of 6-8 and always look for plateau pressures to protect lungs
49
Q

prognosis of ARDS

A
  • 30% mortality
  • higher rates of mortality seen in elderly
  • over ventilation and barotrauma associated with higher mortality
50
Q

benefits of central lines

A
  • good for longer use
  • more durable
  • safer access
  • may be used for dialysis catheters and temp pacing wires
51
Q

internal jugular v central line placement

A
  • easily accessible via US
  • provides straight shot to RA for pacing wires
  • confirmed with CXR
52
Q

femoral v central line placement

A
  • large vein easily accessible in emergencies
  • high rates thrombosis
  • limited mobility
  • possible increased infection risk
  • confirmed with blood gas or gravity test
53
Q

subclavian v central line placement

A
  • ideal vein but requires some skill
  • theoretical increased risk bleeding and pneumothorax
  • not as easily viewed with US- use landmarks
  • confirm with CXR
54
Q

central line data

A
  • central venous pressure- measured via IJV or SCV

- can help determine fluid status

55
Q

what is normal central venous pressure

A
  • 0-20 mmHg
56
Q

complications of central lines

A
  • venous air embolism- place in trandelenburg position
  • pneumothorax
  • catheter tip malposition
  • thrombotic occlusion later
  • venous thrombosis later
  • infection
57
Q

common causes of central line infections

A
  • coag neg staph
  • GNR- pseudomonas
  • staph aureus
58
Q

arterial lines

A
  • indicated in unstable pts who require vasopressor support or severe HTN
  • measurements prone to error
59
Q

radial artery line

A
  • less invasive, smaller artery
  • pt can remain mobile
  • good for short term use
60
Q

femoral artery line

A
  • easy to access but risk of vessel injury
  • limited mobility
  • good for emergency
61
Q

axillary arter line

A
  • most difficult to place
  • risk of vascular injury but very durable
  • doesnt impact mobility
  • good if pt will need line in for an extended period of time
62
Q

how do you place arterial lines

A
  • palpate for pulse

- US is not necessary like central lines

63
Q

arterial line complications

A
  • infection
  • arterial occlusion
  • limited mobility
64
Q

swan- ganz catheters measurements

A
  • placed directly into pulmonary artery
  • direct measurement of right heart filling pressures
  • indirect measurement of PCWP
  • measure CO
  • measure of mixed venous O2 sat
65
Q

how CO measured via swan ganz catheters

A
  • measured via thermo-dilution
66
Q

swan ganz complications

A
  • pulmonary artery injury
  • ventricular arrhythmias- esp if catheter left in RV
  • infection
67
Q

how are vasopressors administered

A
  • admin through central line

- monitored with arterial lines

68
Q

vasopressin

A
  • antidiuretic hormone
  • acts on V1 -> vasoconstriction
  • used for severe septic shock, vasoplegic states
  • caution in CAD
  • longer half life
  • vasopressor
69
Q

phenylephrine

A
  • most commonly used pressor
  • alpha 1 agonist -> arterial vasoconstriction
  • limited cardiac activity so not good for cardiogenic shock
  • quick on off
  • good for hypotension from altered vascular resistance
  • vasopressor
70
Q

norepinephrine

A
  • alpha 1 and beta 1 agonist
  • predominantly acts on alpha 1 -> increased SVR
  • rapid on off
  • good for refractory septic shock
  • vasopressor
71
Q

dobutamine

A
  • Beta 1 agonist, limited beta 2
  • increases CO
  • less reflex hypotension
  • used for decomp HF without shock
  • will increase myocardial O2 consumption and can cause ventricular arrhythmias
  • inotrope
72
Q

milrinone

A
  • PDE III inhibitor that increases SV by increasing cAMP via vasodilation
  • slow onset
  • usually requires bolus
  • used with other inotropes
  • hypotension is major downside
  • inotrope
73
Q

dopamine

A
  • effect varies with dose
  • intermed- stimulates beta receptors -> increased HR and CO
  • high- alpha stimulation -> increased SVR
  • causes arrhythmias
  • inotrope
74
Q

what is the main purpose of nutrition in the ICU

A
  • feeding gut prevents atrophy of intestinal lining

- acts as barrier to infection

75
Q

how is nutrition administered in ICU

A
  • standard NG tube
  • dobhoff feeding tube (smaller and more comfortable)
  • TPN last line- high complication risk, doesn’t prevent atrophy
76
Q

when is feeding contraindicated

A
  • shock
  • bowel obstruction
  • intestinal ischemia
77
Q

complications of feeding

A
  • aspiration

- diarrhea from sorbitol content

Clin Med II (16 decks)

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