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CCP S2 > Mech Vent > Flashcards

Mech Vent Flashcards

1
Q

What is compliance

A

ease with which a structure distends

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2
Q

What is elastane

A

inverse of compliance

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3
Q

what is normal resistance in an intubated pt

A

approx 6cmH20 ( will increase with smaller ET tubes)

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4
Q

what is normal resistance in an unintubaned pt

A

0.6-2.4cmH2O

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5
Q

Effects of PEEP

A

resp:
-increased FRC
-improved oxygenation (decreasing shunt)
-decreases hypoxic vasoconstriction
-decreases WOB
-improves V/Q
-reduces biotrauma (opening/closing)
-increases dead space ventilation which may lead to volumtrauma
cardiac:
-decreased LV afterload by decreasing transmural pressure
-increases RV preload by increasing pulmonary vascular resistance
-decreases LV preload through reduction of RV output

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6
Q

Indications for NIPPV

A
  • AECOPD
  • ACPE
  • ARDS
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7
Q

Predictors of difficult intubation

A 
L- look externally
E- evaluate 3-3-2
M- mallanpati
O- obstruction
N- neck mobility
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8
Q

contraindications for a SGA

A

R- restricted mouth opening
O- obstruction
D- distorted airway
S stiff lungs

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9
Q

predictors of a difficult BVM

A 
M- mask seal
O- obstruction
A- age
N -no teeth
S- stiff lungs
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10
Q

Predictors of difficult FONA

A 
S- surgery
H- hematoma
O - obese
R- radiation
T- tumour
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11
Q

Benefits of prone positioning

A
  • optimizes V/Q matching (increase blood delivery to dependant lungs)
  • reduces atelectasis
  • facilitates secretion drainage
  • less lung deformity
  • increases FRC
  • decreases transpulmonary pressure
  • increases uniform alveolar ventilation
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12
Q

examples of V/Q mismatch

A
  • COPD
  • Asthma
  • pulmonary vascular disease
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13
Q

examples of Shunt

A
  • Alveolar edema
  • Atelectasis
  • Intrapulmonary shunt
  • Intracardiac shunt
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14
Q

Causes of hypercapnic respiratory failure

A

CNS: drugs, stroke, central apnea
Anterior Horn cell: C-spine, asia A, ALS
Motor neuron: GBS, tick syndrome
NMJ: mysethenia gratis, eaton lambert
Muscular: muscular dystrophy, drugs, central illness
Airway/alveoli: COPD, Asthma, pulmonary fibrosis, pulmonary edema

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15
Q

Risk factors for ARDS

A

pneumonia, gastric content aspiration, pulmonary contusion, inhalation injury, near drowning, sepsis, non thoracic trauma or hemorrhagic shock, pancreatitis, major burns, drug OD, blood transfusion, cardiopulmonary bypass, repurfusion edema after lung transplant or embolectomy

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16
Q

Cause of elevated PIP + Plat

A
  • ARDS
  • Pulmonary fibrosis
  • Abdominal distension
  • pneumonia
  • Pleural effusion
  • pneumthorax
  • atelectasis
  • bronchial intubation
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17
Q

Cause of elevated PIP

A
  • Asthma
  • Obstruction or kink
  • Excessive secretions
  • clogged HME
  • small ET tube
  • high flow rate
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18
Q

How to reduce plateau pressure

A

decrease vT (volume or pressure) or PEEP

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19
Q

how to reduce PIP

A

reduce flow…..increase TI or lower vT

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20
Q

how do you manipulate vcalc

A

Ti or vT

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21
Q

obstructive lung disease

A
  • (COPD), which encompasses emphysema and chronic bronchitis
  • Asthma
  • Bronchiectasis
  • Cystic Fibrosis
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22
Q

Restrictive lung disease

A
  • Interstitial lung disease
  • Sarcoidosis
  • Neuromuscular disease, such as amyotrophic lateral sclerosis (ALS)
  • Pulmonary fibrosis
  • Asbestosis
  • Silicosis
23
Q

type 1 respiratory failure

A

hypoxemic

examples: v/q, shunt, impaired diffusion, hypoventilation and, decrease fio2

24
Q

type 2 respiratory failure

A

hypercapneic

25
Q

type 3 respiratory failure

A

peri-operative

26
Q

type 4 respiratory failure

A

Shock

examples: hypovolemia, sepsis, cardiogenic

27
Q

Indications for intubation

A
  • oxygenation
  • ventilation
  • protection
  • clinical course
  • undifferentiated shock
  • severe metabolic acidosis
28
Q

explain volume cycled ventilation

A

trigger: pt or time
limit: flow
cycle: volume
PIP: variable
vT:constant
advantages: guaranteed minute ventilation
disadvantages: flow may not meet pt’s demand, airway pressure varies depending on resistance and compliance

29
Q

explain pressure cycled ventilation

A

trigger: pt or time
limit: pressure
cycl: Ti
PIP: constant
vT: variable depending on resistance and compliance
advantages: limits airway pressure, may improve gas exchange
disadvantages:vT varies with changes in compliance and resistance

30
Q

ARDSnet lung protective strategy

A
  • start with 6ml/kg, reduce by 1ml/kg to achieve a pPlat <30cmH20
  • If Pplat <25cmh20, increase vT by 1ml/kg until Pplat> 25

-min vT 4ml/kg
-max vT 8ml/kg
minimum arterial PH 7.15

31
Q

how do you optimize PEEP in ARDS management

A

-follow PEEP/FiO2 table from ARDSnet
-maintain PEEP above lower inflection point of pressure volume curve
-respiratory system compliance optimization
-driving pressure below 15cmH20
stress index <1
-end expiratory pPlat > 0
-imaging techniques

32
Q

signs of hyperinflation

A
  • failure of expiratory flow to return to 0 prior to next breath
  • increasing PIP and pPlat with each breath (volume cycled
  • decreasing vT (pressure cycled)
  • inspiratory volume>expiratory volume
  • high auto-peep
  • trigger dyssyncrony
33
Q

Mech vent strategy for COPD AC volume

A
  • low RR (approx 10 bpm)
  • vT: 5-8 ml/kg PBW
  • inspiratory pause: .5-.8 sec
  • low I:E (1:4 or less)
  • increase external PEEP stepwise to match auto-peep (is pPlat decreases with increase in external PEEP= PEEP responsive)
34
Q

mech vent strategy for COPD PCV

A
  • driving pressure and Ti to achieve vT of 5-8ml/kg PBW-
  • raise external PEEP to pPlat constant

…..if in PSV, try to match pt’s rate ie higher

35
Q

mech vent strategy for Asthma AC volume

A

-RR 6-10 bpm
-PEEP: 0-5cmh20
-vT: 4-8ml/kg
-inspiratory flow: 80-100L/min
I:E: 1:4-5
expiratory time: 4-5sec
PIP: adjust to above airway pressure caution >50cmh2o

36
Q

What causes a rightward shift in oxygen hemoglobin dissociation curve

A

-increase PaCO2
-hyperthermia
-acidosis
-increase altitiude
-increase DPG
-sickle cell anemia
DECRESED AFFINITY

37
Q

What causes a leftward shift in oxygen hemoglobin dissociation curve

A

-decreased PaCO2
-hypothermia
-alkalosis
-fetal hemoglobin
-decreased DPG
-carbon-monoxide poisoning
INCREASED AFFINITY

38
Q

flow taget for asthma

A

80-100 L/min

39
Q

what is driving pressure

A

plat-peep aim from less than 15

40
Q

recruitment maneuver responder

A

oxygenation and compliance improves

41
Q

SaO2

A

Direct laboratory percentage of oxyhemoglobin of arterial blood

42
Q

PAO2

A

Disolved O2 in plasma 80-100 mmHg

43
Q

A-a gradient

A

Difference between alveoli vs pulmonary capillary. A=Alveolar(PAO2), a=Arterial oxygenation(PaO2). Normal adult, 3-10mmHg

PEDS, (age/4)+4

44
Q

PaO2/FiO2 ratio

A

measurement of oxygenation in ventilated patients. Normal 300-500mmHg, abnormal < 300mmHg, Severe < 200mmHg

45
Q

how much dead space is there with most mechanical ventilation? Why is this important?

A

150 mL **NORMAL PHYSIOLOGY
- If you are trying to improve ventilation by increasing RR, you may just increase deadspace ventilation (5% increase in VT is normally more efficient than a 5% in RR)

46
Q

what can a FiO2 > .6

A

Hyperoxemia causes the release of reactive oxygen intermediates (ROIs) =

  • absorbtive atelectasis
  • accentuation of hypercapnia
  • airway injury
  • bronchopulmonary dysplasia
  • parenchymal injury
  • extrapulmonary toxicity
47
Q

absorptive atelectasis

A

High FiO2 - O2 replaces nitrogen, surfactant inactivation or when less than normal levels of inhaled nitrogen ( nitrogen wash-out ) are present in the alveoli causing atalectasis

POSSIBLE CAUSES

●A low regional ventilation-perfusion ratio (where oxygen diffuses from alveoli to capillaries faster than it is replenished by inhaled oxygen), decreasing alveolar volume, may result in complete alveolar closure.

●Qualitative or quantitative surfactant abnormalities that promote alveolar collapse and further reduce the ventilation-perfusion ratio

●A high rate of oxygen uptake, due to an increase in metabolic demand

●An impaired pattern of respiration that fails to correct atelectasis (eg, ventilation at low tidal volumes and/or without intermittent sighs or “adequate” PEEP when using mechanical ventilation)

48
Q

how is absorptive atelectasis corrected

A

Not directly reversed by a reduction of FiO2, emphasizing the desirability of rapid titration of FiO2 to the lowest fraction necessary to maintain an arterial oxygen saturation (SaO2) >90 percent

49
Q

accentuation of hypercapnia

A

Phenomenon of increased partial pressure of arterial carbon dioxide (PaCO2) associated with increases in FiO2 predominantly described in individuals with chronic compensated respiratory acidosis; these patients have limited ability to increase alveolar ventilation to compensate for rising PaCO2 and falling pH.

50
Q

mechanisms that cause hyperoxic hypercapnia

A

● The Haldane effect. Rightward displacement of the CO2-hemoglobin dissociation curve in the presence of increased oxygen tension;

●Increased dead space (ie, “wasted”) ventilation. Worsening ventilation-perfusion matching and redistribution of blood flow from well-ventilated to poorly ventilated alveoli due to a reversal of hypoxic pulmonary vasoconstriction

●A modest decrease in minute ventilation, which also reduces alveolar ventilation, due to decreased stimuli from peripheral chemoreceptors to the central respiratory center

●The anxiolytic and anti-dyspneic effects of supplemental oxygen can promote sleep, This can result in progressive hypercarbia

51
Q

Permissive hypercapnia

A

PCO2 is maintained at a higher than normal level (>45 mm Hg)

Decreased Vt (protect agains baro/volutrauma)

Indicated for ARDS, status asthmaticus

52
Q

risks of permissive hypercapnia

A

Cardio- tachycardia or arrhythmia (sympathetic stimulation), hypotenion (increased SVR + tachycardia + myocyte depression due to acidosis), right heart failure (pulmonary vasoconstriction), coronary steal

Neuro- increased ICP (cerebral vasodilation), agitation or DLOC, decreased seizure threshold, cerebral vascular steal, IVH (neonates)

Resp: worsening hypoxemia or lung injury

53
Q

effects of mech vent on the body dystems

A

Pulm- barotrauma, VALI, auto-peep, V/Q (increase dead space, improve shunt), diaphragm atrophy

hemodynamics- reduced venous return (preload), reduced RV output (increase pulm vascular resistance), deduced LV output (increased PVR can push septum to left impairing filling)

GI- stress ulcers and GI bleeding, reduced splenic perfusion,

Renal- reduced perfusion and AKI due to decreased CO, interleukin-6and hormonal activation

neuro- increased ICP

CCP S2 (10 decks)

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