Mech Vent Flashcards
What is compliance
ease with which a structure distends
What is elastane
inverse of compliance
what is normal resistance in an intubated pt
approx 6cmH20 ( will increase with smaller ET tubes)
what is normal resistance in an unintubaned pt
0.6-2.4cmH2O
Effects of PEEP
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
Indications for NIPPV
- AECOPD
- ACPE
- ARDS
Predictors of difficult intubation
L- look externally E- evaluate 3-3-2 M- mallanpati O- obstruction N- neck mobility
contraindications for a SGA
R- restricted mouth opening
O- obstruction
D- distorted airway
S stiff lungs
predictors of a difficult BVM
M- mask seal O- obstruction A- age N -no teeth S- stiff lungs
Predictors of difficult FONA
S- surgery H- hematoma O - obese R- radiation T- tumour
Benefits of prone positioning
- 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
examples of V/Q mismatch
- COPD
- Asthma
- pulmonary vascular disease
examples of Shunt
- Alveolar edema
- Atelectasis
- Intrapulmonary shunt
- Intracardiac shunt
Causes of hypercapnic respiratory failure
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
Risk factors for ARDS
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
Cause of elevated PIP + Plat
- ARDS
- Pulmonary fibrosis
- Abdominal distension
- pneumonia
- Pleural effusion
- pneumthorax
- atelectasis
- bronchial intubation
Cause of elevated PIP
- Asthma
- Obstruction or kink
- Excessive secretions
- clogged HME
- small ET tube
- high flow rate
How to reduce plateau pressure
decrease vT (volume or pressure) or PEEP
how to reduce PIP
reduce flow…..increase TI or lower vT
how do you manipulate vcalc
Ti or vT
obstructive lung disease
- (COPD), which encompasses emphysema and chronic bronchitis
- Asthma
- Bronchiectasis
- Cystic Fibrosis
Restrictive lung disease
- Interstitial lung disease
- Sarcoidosis
- Neuromuscular disease, such as amyotrophic lateral sclerosis (ALS)
- Pulmonary fibrosis
- Asbestosis
- Silicosis
type 1 respiratory failure
hypoxemic
examples: v/q, shunt, impaired diffusion, hypoventilation and, decrease fio2
type 2 respiratory failure
hypercapneic
type 3 respiratory failure
peri-operative
type 4 respiratory failure
Shock
examples: hypovolemia, sepsis, cardiogenic
Indications for intubation
- oxygenation
- ventilation
- protection
- clinical course
- undifferentiated shock
- severe metabolic acidosis
explain volume cycled ventilation
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
explain pressure cycled ventilation
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
ARDSnet lung protective strategy
- 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
how do you optimize PEEP in ARDS management
-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
signs of hyperinflation
- 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
Mech vent strategy for COPD AC volume
- 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)
mech vent strategy for COPD PCV
- 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
mech vent strategy for Asthma AC volume
-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
What causes a rightward shift in oxygen hemoglobin dissociation curve
-increase PaCO2
-hyperthermia
-acidosis
-increase altitiude
-increase DPG
-sickle cell anemia
DECRESED AFFINITY
What causes a leftward shift in oxygen hemoglobin dissociation curve
-decreased PaCO2
-hypothermia
-alkalosis
-fetal hemoglobin
-decreased DPG
-carbon-monoxide poisoning
INCREASED AFFINITY
flow taget for asthma
80-100 L/min
what is driving pressure
plat-peep aim from less than 15
recruitment maneuver responder
oxygenation and compliance improves
SaO2
Direct laboratory percentage of oxyhemoglobin of arterial blood
PAO2
Disolved O2 in plasma 80-100 mmHg
A-a gradient
Difference between alveoli vs pulmonary capillary. A=Alveolar(PAO2), a=Arterial oxygenation(PaO2). Normal adult, 3-10mmHg
PEDS, (age/4)+4
PaO2/FiO2 ratio
measurement of oxygenation in ventilated patients. Normal 300-500mmHg, abnormal < 300mmHg, Severe < 200mmHg
how much dead space is there with most mechanical ventilation? Why is this important?
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)
what can a FiO2 > .6
Hyperoxemia causes the release of reactive oxygen intermediates (ROIs) =
- absorbtive atelectasis
- accentuation of hypercapnia
- airway injury
- bronchopulmonary dysplasia
- parenchymal injury
- extrapulmonary toxicity
absorptive atelectasis
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)
how is absorptive atelectasis corrected
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
accentuation of hypercapnia
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.
mechanisms that cause hyperoxic hypercapnia
● 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
Permissive hypercapnia
PCO2 is maintained at a higher than normal level (>45 mm Hg)
Decreased Vt (protect agains baro/volutrauma)
Indicated for ARDS, status asthmaticus
risks of permissive hypercapnia
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
effects of mech vent on the body dystems
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
