Exam 3 Flashcards
What is ventilation?
ventilation is the process of exchanging gas (O2 and Co2) between the atmosphere and the lungs
Ventilation 2 critical functions:
- O2 delivered to Hgb too support aerobic metabolism
- CO2 (primary end product of aerobic metabolism) eliminated from the blood.
_____& _______contract during inspiration (tidal breathing)
diaphragm and external intercostals
Is exhalation passive or active?
passiveW
What is exhalation driven by?
recoil of the chest wall
Accessory muscles for inspiration?
sternocleidomastoid and scalene muscles
Accessory muscles for active expiration
internal intercostals (secondary)
TIRE
Transverse abdominis
Internal Oblique
Rectus abdominis
External oblique
When does exhalation become an active process?
when minute ventilation increases or in patients with lung disease, such as COPD
What vital capacity is required for an effective cough?
15ml/kg
A forced exhalation is required to cough and clear the airway of secretions
Function of the conducting zone
bulk gas movement
-does not participate in gas exchange
it is anatomic dead space
Where is the conducting zone?
begins at the nares and mouth and ends with terminal bronchioles
What are the last structures perfused by the bronchial circulation?
terminal bronchioles
What does the transitional zone contain?
respiratory bronchioles
function of the transitional zone?
bulk gas movement
-respiratory bronchioles serve dual function of air conduit and gas exchange
function of the respiratory zone?
gas exchange
Where does the respiratory zone begin?
at the alveolar ducts and extends to the alveolar sacs
gas exchange occurs across flat epithelium (type 1 pneumocytes) by _________.
diffusion
What is transpulmonary pressure?
the difference between the pressure inside the airway and pressure outside the airway
TPP=alveolar pressure-intrapleural pressure
What determines the rate of removal of carbon dioxide from the body?
alveolar ventilation
When is TPP negative?
during forced expiration.
If it is negative the airway collapses.
What is the amount of gas that is inhaled and exhaled during a breath?
tidal volume Vt
normal TV
6-8ml/kg
normal dead space
2ml/kg or 150ml
When you exhale, which zone’s gas is removed first?
conducting zone gas removed first.
Any condition that increases the volume of the conducting zone (Vd) makes itmore difficult to eliminate expiratory gases from the lungs
Minute ventilation (Ve)
amount of air in a single breath multiplied by number of breaths per minute
What only measures the fraction of VE that is available for gas exchange and removes dead space from MV equation?
alveolar ventilation
Definition of anatomic dead space
air confined to conduction airways
ex. nose and mouth–>terminal bronchioles
definition alveolar dead space
alveoli that are ventilated but not perfused
ex. decreased pulmonary blood flow
physiologic dead space
anatomic Vd + alveolar Vd
variable
increased Vd–>airway
-facemask
-heat and moisture exchanger
-positive pressure ventilation
Which drugs increase Vd
-atropine because its bronchodilator action increases the volume of the conduction airway
anticholinergics
does old age increase or decrease Vd?
increase dead space
Which neck position increases dead space?
neck extension because it opens the hypopharynx and increases its volume
What neck position decreases dead space?
flexion
what pathophysiology increases dead space?
-decreased cardiac output
-COPD
-PE (thrombus, air, amniotic fluid)
Which position increases Vd?
sitting
Which position decreases Vd?
supine and trendelenberg (head down)
What can physiologic dead space be calculated with?
bohr equation
Vd/Vt= (paCO2-PeCO2)/PaCO2
compares partial pressure of CO2 in blood vs the partial pressure of CO2 in exhaled gas. The greater the difference between these values the greater amount of dead space
in the circle system, where does dead space begin?
at the y-piece
anything proximal to the y-piece does not influence dead space nor does increasing the length of the circuit.
Only exception to the rule is an incompetent valve in the circle system. In this situation the entire limb with the faulty valve becomes apparatus dead space.
What is the most common cause of increased Vd/Vt under general anesthesia?
reduction in cardiac output. If ETCO2 acutely decreases you should first rule out hypotension before considering other causes of increased dead space
Ventilation is ___L/min and perfusion is _____L/min
ventilation=4L/min
Perfusion=5L/min
What is the V/Q ratio assuming patient is standing
0.8
What is alveolar compliance?
change in alveolar volume for a given change in pressure
Where is ventilation poorest?
in the alveoli in the apex due to poorest compliance.
The slope of the curve is less steep in this region so there’s a smaller volumetric change throughout the respiratory cycleW
Where is the ventilation the greatest?
the alveoli in the base due greatest compliance.
The slope of the curve is steeper in this region so there’s a greater volumetric change throughout the respiratory cycle
What is the most common cause of hypoxemia in the PACU?
V/Q mismatch specifically atelectasis
The tendency of the alveolus to collapse is directly proportional to:
surface tension (more tension==more likely to collapse)
The tendency of the alveolus to collapse is inversely proportional to
-alveolar radius (smaller radius=more likely to collapse)
What does surfactant do?
equalizes the effet of surface tension by type 2 pneumocytes. This prevents alveolar collapse
When do type 2 pneumocytes begin producing surfactant?
22-26 weeks
When is peak production occur for surfactant?
35-36 weeks
zone 1
dead space
PA>Pa>Pv
zone 2
waterfall
Pa>PA>Pv
zone 3
shunt
Pa>Pv>PA
zone 4
pulmonary edema
Pa>Pis>Pv>PA
Normal A-a gradient
<15mmHg
Normal IRV
3,000 mL
IRV
volume of gas that can be forcibly inhaled after tidal inhalation
ERV normal
1,100 mL
ERV
Volume of gas that can be forcibly exhaled after tidal exhalation
Normal RV
1,200 ml
RV
volume of gas that remains in the lungs after complete exhalation
-the volume cannot be exhaled from the lungs
-this provides a “windbag” of alveolar gas that provides an oxygen reservoir during apnea
Total Lung capacity
IRV+TV + ERV +RV
Normal TLC
5,800mL
normal VC
4,500 ml
normal IC
3,500 ml
normal FRC
2,300ml
normal CC
variable
VC
IRV + TV + ERV
IC
IRV + TV
FRC
RV + ERV
What is Functional residual capacity?
The volume of air in the lungs at end-expiration
-the reservoir of oxygen that prevents hypoxemia during apnea
What is static equilibrium?
At FRC, the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall
What effects do GA have on FRC?
decrease FRC
-diaphragm shifts cephalad 4cm due to decreased inspiratory muscle tone and increased expiratory muscle tone
What effects does obesity have on FRC?
decrease FRC
-decreased chest wall compliance
increased airway collapsibility
What effects does pregnancy have on FRC?
decreased FRC
-diaphragm shifts cephalad as a result of gravid uterus
-decreased chest wall complaince
What effects does a neonate have on FRC?
decreased FRC
less aveoli
decreased lung compliance
cartilaginous ribcage that is prone to collapse during inspiration
What effects does advanced age have on FRC?
increased FRC
decreased lung elasticity–> increased air trapping–> increased residual volume–>increased FRC
Which positions decrease FRC?
supine
lithotomy
t-burg
which positions increase FRC?
prone
sitting
lateral none or increased
What effects do NMB have on FRC?
decreased FRC
diaphragm shifts cephalad–>decreased lung volumes
What effects does light anesthesia have on FRC?
decreased FRC
straining–>forcefu expiration–>decreased lung volumes
What effects does excessive IVF have on FRC?
decreased FRC
fluid accumilation in dependent lung regions favor zone 3 development
What effects does high FiO2 have on FRC?
decreased FRC
-absorption atelectasis –>conversion of low v/q unit–?shunt unit
-newer evidence suggests FiO2< 80% at emergence PEEP or CPAP reduces atelectasis
What effects does COPD have on FRC?
increase FRC
airtrapping–>increased RV–>increased FRC
What effects does PEEP have on FRC?
increase FRC
recruits collapsed alveoli
partially overcomes effects of GA
What effects do sigh breaths have on FRC?
increased FRC
recruits collapsed alveoli
Factors that increased closing volume
CLOSE-P
COPD
LV failure
Obesity
Surgery
Extremes of Age
Pregnancy
At age 30, CC~FRC when
under general anesthesia
by age 44, CC ~FRC when
supine
by age 66, CC ~ FRC when
standing
a right shifted curve means what?
Hgb has a decreased affinity for oxygen. During normal physiology, this occurs at the metabolically active tissue
a left shifted curve means what?
hgb has increased affinity for oxygen. During normal physiology, this occurs in the lungs
What is the Bohr effect?
CO2 & hydrogen ions cause a conformational change in the hgb molecule; this facilitates the release of oxygen
-An increase in the partial pressure of CO2 and a decrease in pH cause Hgb to release oxygen
What is 2,3 DPG
produced during RBC glycolysis (Rapoport-Leubering Pathway)
-it maintains the curve in a slightly right shifted position at all times
What effect does hypoxia have on 2,3 DPG?
increased 2,3 DPG production. This facilitates O2 offloading
-2,3 DPG is an important compensation mechanism during chronic anemia
-
what happens to 2,3 DPG in banked blood
concentration fo 2,3 DPG falls. This shifts the curve to the left and reduces the amount of O2 available to the tissue load
Does Hgb F respond to 2,3 DPG?
no, which explains why Hgb F has a left shift (P50 =19 mmHg)
What is the primary substrate used for ATP synthesis?
Glucose
Glycolysis =net gain of how many ATP?
2
Kreb’s cycle =net gain of how many ATP?
2
Oxidative phosphorylation =net gain of how many ATP?
34
In the absence of oxygen, pyruvic acid is converted to what?
ATP
What is the primary bi-product of aerobic metabolism?
carbon dioxide
3 primary ways CO2 is transported (buffered) in the blood?
- as bicarbonate (70%)
- bound to hemoglobin as carbamino compounds
- Dissolved in plasma (7%)
What enzyme facilitates the formation of carbonic acid from H20 and CO2?
carbonic anyhydrase
Haldane effect
describes CO2 carriage.
It says that oxygen causes the erythrocyte to release CO2.
Hypercapnia is defined as
PaCO2 greater than 45mmHg
causes of Hypercapnia-increased CO2 production
-sepsis
-overfeeding
-MH
-intense shivering
-prolonged seizure activity
-thyroid storm
-burns
cause of hypercapnia-decreased CO2 elimination
-airway obstruction
-increased dead space
-increased Vd/Vt
-ARDS
-COPD
-repiratory center depression
-drug overdose
-inadequate NMB reversal
causes of hypercapnia-rebreathing
-exhausted soda lime
-incompetent unidirectional valve in the circle system
-inadequate fresh gas flow with mapleson circuit
pathophysiology of hypoxemia
increased alveolar CO2 displaces alveolar O2–>arterial hypoxemia
pathophysiology increased P50
oxyglobin curve shifts to the right releases more O@ to the to the tissues
-partially compensates for hypoxemia
increased PVR-patho of CO2
CO2 is a smooth muscle dilator except in the pulmonary vasculator
-CO2 increased PVR-increases workload in the right heart
How does hypercarbia affect blood pH
during respiratory acidosis, the kidneys excrete hydrogen and conserve bicarb to return pH to normal. This process begins within hours but may require several days for full compensation to occur
The carbon dioxide ventilatory response curve describes the relationship between pa CO2 and minute ventilation
What is the primary monitor of PaCO2?
central chemoreceptor in the medulla
What play a secondary role in monitoring PaCO2?
peripheral chemoreceptors in the carotid bodies and transverse and aortic arch
What is the apneic threshold?
highest PaCO2 at which a person will not breathe. Once the PaCO2 exceeds the apneic threshold the patient will begin to breathe.
Left shift in CO2 curve implies that apneic threshold has_______.
decreased
right shift in CO2 curve implies that apneic threshold has_______.
increased
causes of a left shift of the CO2 curve
-hypoxemia
-metabolic acidosis
-surgical stimulation
-CNS etiologies: increased ICP, fear, anxiety
Drugs:
-salicylates
-aminophylline
-doxapram
-norepinephrine
causes of right shift of CO2 curve
-metabolic Alkalosis
-carotid endarterectomy
-natural sleep
-drugs:
-volatile anesthetics
-opioids
-NMBs
Where is the respiratory center located in?
The reticular activating system in the medulla and pons
What is the primary job of the respiratory center?
Determine how fast and deep you breathe
What modifies the responses of the respiratory center?
cerebral cortex
location of the DRG?
medulla
nucleus tractus solitarus
function of the DRG
pacemaker for inspiration
primarily active during inspiration
location of the VRG?
medulla
-nucleus ambiguous
-nucleus retroambigus
function of the VRG
inspiration and expiration functions (primarily active during expiration
what contains the pre-Botzinger complex?
VRG
What group inhibits the DRG?
pneumotaxic center
function of the pneumotaxic center (upper pons)
triggers end inspiration by inhibiting DRG
-strong stimulus–>rapid shallow breathing
weak stimulus–>slow and deep breathing
pontine respiratory centers
pneumotaxuic and apneustic center
apneustic center -lower pons funciton
antagonized the pneumotaxic center which causes inspiration
-action is inhibited by pulmonary stretch receptors (J receptors)
Classic teaching says the DRG is considered the primary respiratory pacemaker. Newer evidence says that this function is performed by the :
-central pattern generator which includes the DRG, pre-Botzinger complex ( in the VRG) and other medullary structures
What do central chemoreceptors respond indirectly to
PaCO2 and this region sends stimulatory impulses to the dorsal respiratory center
What ions doesnt pass through the BBB
H+ & HCO3
Chief responsibility of the carotid monitor
for hypoxemia (PaO2< 60mmHg) they do not respond to SaO2 or CaO2
Why do we not do bilateral CEA simultaneously?
carotid endarterectomy severs the afferent limb of the hypoxic ventilatory response.
takes time for the body to recalibrate
sub-anesthetic doses of inhalation and intravenous anesthetics ____MAC depress the hypoxic ventilatory drive.
0.1
Hering breuer deflation reflex
when lung volume is too small, this reflex helps prevent atelectasis by stimulating the patient to take a deep breath
paradoxical reflex of the head
causes a newborn baby to take her first breath
What does J receptor stimulation cause?
tachypnea
The J receptors are activated by things that JAM traffic in the pulmonary vasculatture such as pulmonary embolism or CHF
Pulmonary C fiber receptors also called
J receptoras
What is a local reaction that occurs in response to a reduction in alveolar oxygen tension (not arterial PO2)
hypoxic pulmonary vasoconstriction
What does HPV minimize?
shunt flow during atelectasis or one0lung ventilation
What is the only region in the body that responds to hypoxia with vasoconstriction?
pumonary vascular bed
What factors inhibit HPV?
-volatile anesthetics >1.5 MAC reduce effectiveness of HPV
-vasodilators, PDEI, dobutamine, some CCB increase shunt flow by inhibiting HPV
What has the most significant contribution to airflow resistance?
radius of the airway
Which physiologic systems determine airway diameter?
PNS (vagus nerve)–>bronchoconstriction
mast cells and non-cholinergic PNS–>bronchoconstriction
non-cholinergic PNS (nitric oxide)–>bronchodilation
SNS (circulating catecholamines)–>bronchodilation
Are there SNS nerve endings in the airway smooth muscle?
no. Instead B2 receptors embedded in airway smooth muscle are activated by catecholamines in the systemic circulation
Beta 2 agonists MOA
B2 stimulation–>increased cAMP–>decreases iCa+2
-stabilizes mast cell membranes –>decreased mediator release
Side effects of B2 agonists
-tachycardia
-dysrhthmias
-hypokalemia
-hyperglycemia
-tremors
Beta-2 agonist drugs
-albuterol
-metaproterenol
-salmeterol
Anticholinergics MOA
M3 antagonist–>decreased IP3–>decreased iCa2+
anticholinergics used for bronchodilation
-atropine
-glycopyrrolate
-ipatropium
side effects of anticholinergics
-inhibits secretions
-dry mouth
-urinary retention
-blurred vision
-cough
-increased intraocular pressure with narrow angle glaucoma
corticosteroids moa
-stimulates intracellular steroid receptors
-regulates inflammatory protein synthesis
-decrease airway inflammation
-decreases airway hyperresponsiveness
side effects of corticosteroids
-dysphonia
-mypathy of larygneal muscles
-oropharyngeal candidiasis
-possible adrenal suppression
corticosteroid drugs
-beclomethasone
-budesonide
-flunisolide
-fluticasone
-tramcinolone
cromolyn moa
stabilizes mast cell membranes
leukotriene modifiers moa
inhibits 5-lipooxygenase enzyme
decreases leukotriene synthesis
leukotriene modifier drugs
-zileuton
-monteleukast
-pranlukast
-zafirlukast
theophylline moa
inhibits phosphodiesterase–>increases cAMP
increases endogenous catecholamine release
inhibits adenosine receptors
theophylline se plasma concentration >20mcg/ml
-N/V/D
-headache
-disrupted sleep
theophylline se plasma concentration >30mcg/ml
-seizures
-dysrythmias
-CHF
normal FEV1
> 80% predicted value
FVC male normal
4.8 L
FVC female normal
3.7L
FEV1/FVC normal
75-80% predicted value
MMEF normal
100+/- predicted value
MMV normal male
140-180L
MMV normal value female
80-120L
DLCO normal
17-25ml/min/mmHg
What is the volume of air that can be exhaled after maximal inhalation in 1 second?
FEV1
-depends on patient’s effect
-declines with age, so predicted value takes age into account
Volume of air that can be exhales after a maximal inhalation
FVR
<___% of FEV1/FVC suggests obstructive disease
70
is FEV1/FVC normal or abnormal with restrictive disease?
normal
What value is useful in dx of obstructive vs. restrictive disease?
FEV1/FVC
What is the most sensitive indicator of small airway disease?
MMEF (mid maximal expiratory flow rate)
What is the best test of endurance?
MMV (maximal voluntary ventilation
What measures airflow in the middle of FEV ?
mmef
mid maximal expiratory flow
MMEF obstructive disease
reduced
MMEF in restrictive disease
normal
Maximum value of air that can be inhaled and exhaled over the course of 1 minute
MMV
-maximum voluntary ventilation
What is DLCO (diffusing capacity)
-volume of carbon monoxide that can transver the alveolocapillary membrane per a given alveolar partial pressure of carbon monoxide
-based on Fick’s law of diffusion
In a flow-volume loop flow is zero at _______
the line that transverses the loop
In a flow-volume loop , flow occurs during_____
inspiration (it moves away from zero)
In a flow-volume loop , flow becomes zero at ____.
end inspiration
In a flow-volume loop , what is the width of the loop?
Vital capacity
Patient examples of independent risk factors for pulmonary complications
-age >60 years
-ASA >2
-CHF
-COPD
-cigarette smoking
procedure examples of independent risk factors for pulmonary complications
aortic> thoracic
upper abdominal ~neuro~peripheral vascular>emergency
general anesthesia
duration of anesthesia >/=2 hours
diagnostic testing examples of independent risk factors for pulmonary complications
albumin <3.5g/dL
What are the short term benefits of smoking cessation?
-carbon monoxide t1/2 =4-6 hours
-P50 returns to near normal in 12 hours
-short term cessation does not reduce pulmonary complications
what are the intermediate term benefits of smoking cessation?
-return of pulmonary function takes atelast 6 weeks
this includes:
-airway functin
-mucociliary clearance
-sputum production
-pulmonary immune function
-hepatic enzyme induction also subsides after 6 weeks
How can you reduce PPC (postop pulmonary complications) in preop?
-tx expiratory outflow obstruction with bronchodilators and corticosteroids
-tx active infection with abx (no indication for prophylaxis from pulmonary infection)
-instruct patient on pulmonary recruitment maneuvers
-tx RV failure
How can you reduce PPC (postop pulmonary complications) intraop?
-consider regional instead of general
-minimally invasive surgical approaches instead of open
-avoid procedures lasting >3 hours
How can you reduce PPC (postop pulmonary complications) postop?
utilize effective analgesia
-use pulmonary recruitment manuevers (incentive spirometer, deep breathing, pulmonary toilet, CPAP)
obstructive disease is characterized by
-small airway obstruction and increased resistance to expiratory flow
-the problem is getting air out
restrictive disease is characterized by
a proportionate reduction in all lung volumes along with poor compliance
-the problem is small lung volumes
asthma is defined by an
acute, reversible airway obstruction that is accompanied by chronic airway inflammation and bronchial hyperreactivity
What is the greatest risk factor for developing asthma?
atopy
The condition of being “hyper-allergic”
s/s of asthma
wheezing
-dspnea
-chest discomfort or tightness
-production or non-productive cough
-prolonged expiratory phase
-eonsinophilia
most common ABG finding in asthma
respiratory alkalosis with hypocarbia
an elevated PACO2 on abg in asthma suggests:
-air trapping
-respiratory muscle fatigue and impending respiratory failure
in asthma, ekg may show
right ventricular strain and right axis deviation during a severe attack
-pulmonary vascular resistance increases the workload of the right heart
Are PFTs predictive of postop respiratory complications?
no, the exception is for lung reduction surgery
severe bronchospasm can cause
hypoxemia due to V/Q mismatch
what does CXR show with asthma
hyperinflated lungs with diaphragmatic flattening
Ventilator goals for asthmatic patients
-limit inspiratory time
-prolong expiratory time and tolerate moderate permissive hypercapnia
True/false: avoidance of tracheal intubation is a good idea if patient can safely receive regional or LMA
true
Which volatile anesthetics reduce airway resistance?
all VA dilate the airway and reduce airway resistance
sevo reduces risk of coughing and may reduce risk of bronchospasm
Which IV induction agent causes bronchodilation?
ketamine-only IV indiction drug that causes bronchodilation
What dose of lidocaine reduces airway reflexes at extubation?
1-1.5mg/kg before extubation suppresses airway reflexes
are anticholinesterases safe in a patient with asthma?
although they can precipitate bronchospasm coadministration of anticholinergics negates risk
How does intraop bronchospasm present?
-wheezing
-decreased breath sounds
-increased airway resistance
-increased PIP with normal plateau pressure
-increased alpha angle on capnogram (expiratory upsloping)
How is intraoperative bronchospasm treated?
-100% FiO2
-deepen anesthetic (volatile agent, propofol, lidocaine, ketamine)
-short-acting inhaled B2 agonist (albuterol)
-inhaled ipatropium
-epi 1mcg/kg IV
-hydrocortisone 2-4 mg/kg IV (does not tx acute symptoms but prevents problems later)
-aminophylline(theophylline doesn’t work well for acute bronchospasm)
-helium-oxygen (heliox) reduces airway resistance
is montelukast used in the tx of acute bronchospasm?
no
COPD is characterized by
a reduction in maximal expiratory flow and a slower forced emptying of the lungs. Unlike asthma, the airflow obstruction is not fully reversible
Etiologies of COPD
-cigarette smoking
-respiratory infection
-exposure to dust with higher risk in the coal mining, gold mining, and textile industries
-alpha 1 antitrypsin deficiency
In COPD, chronically elevated PACO2 causes what?
respiratory acidosis. The kidneys reabsorb bicarbonate which provides a metabolic alkalosis
What happens to a patient with COPD who is administered supplemental O2?
it can ause oxygen induced hypercapnia
-it does not inhibit the hypoxic drive
Goal SPo2 Sat in COPD patients to minimize risk of oxygen-induced hypercapnia in a patient with severe cOPD
88-92%
Do not consider neuraxial anesthesia if the patient requires sensory blockade higher than__________.
T6
This impairs expiratory muscle function and reduces ERV. This hinders the patient’s ability to cough and clear secretions
Which block causes paralysis of the ipsilateral hemidiaphragm so isn’t the best block for a patient with severe COPD.
interscalene
For COPD patients which type of volatile agent is best?
low blood: gas solubility to minimize post op respiratory depression.
All halogenated anesthetics are bronchodilators (sevo and iso> des)
Volatile agents impair hypoxic pulmonary vasoconstriction >____MAC and increase shunt.
1.5
nitrous oxide is associated with
rupture of pulmonary blebs–>pneumothorax
How should you set the ventilator in a patient with COPD?
-use TV 6-8ml/kg IBW
-slow inspiratory flow helps has redistribute from high compliance areas to those with longer time constants. This maximizes matching of ventilation and perfusion throughout the entire lung.
-peep maintains airway patency in the alveoli at the flat portion of alveolar compliance curve.
increased expiratory time to minimize air trapping and auto peep
What can cause dynamic hyperinflation? (AUTO peep)
-if patient is unable to fully exhale with each breathe the portion of the previous breath remains in the lungs. If this occurs with subsequent breaths the effect is additive and airway pressure continues to rise.
-this is most evident by watching the waveforms baseline increase with each breath
Tx for dynamic hyperinflation
-risk can be reduced by emplying manuevers that prolong expiratory time (this allows patient to get the air out)
-options include decreasing the I:E ratio (such as 1:2 to 1:3)) reducing respiratory rate and reducing flow resistance
-for immediate tx you can disconnect the circuit you will hear whooshing sound as volume of air exits the lungs
Acute intrinsic restrictive lung disease examples
pulmonary edema
-upper airway obstruction
-aspiration
-reversal of opioid overdose
-cocaine overdose
-reexpansion of collapsed lung
-neurogenic
Chronic intrinsic restrictive lung disease examples.
-sarcoidosis
-drug induced pulmonary fibrosis
-amiodarone
How should you set the ventilator in restrictive lung disease?
-best ventilator strategy is to minimized risk of barotrauma
-best accomplished with smaller TV (6ml/kg IBW) and faster RR (14-18 breaths/min)
-keep peak inspiratory pressure below 30cmH20
-prolonged inspiratory time I:E 1:1
When does aspiration most commonly occur?
during anesthetic induction and intubation or within 5 minutes of extubation
What complications arise from aspiration?
- gastric contents enter the airway–>risk of airway obstruction
- gastric contents cause chemical burn to the airway and lung parenchyma–>risk of bronchospasm and impaired gas exchange
- Infectious material enters the airway (bacterial infection)
Risk factors for aspiration
-trauma
-emergency sx
-pregnancy
-GI obstruction
-GERD
-peptic ulcer dz
-hiatal hernia
-ascites
-difficult airway management
-cricoid pressure
-impaired airway reflexes
-head injury
-seizures
-residual nBNM
s/s of aspiration
-most asymptomatic
-hypoxemia=hallmark
additional findings
-dyspnea
-tachypnea
-cyanosis
-tachycardia
-HTN
Initial tx for aspiration
1st head tilt down or to side
-upper airway suction to remove particulate matter
-lower airway suction is only useful for removing particulate matter. does not help chemical burn from gastric acid
-secure airway to support oxygenation
-peep to reduce shunt
-bronchodilators to reduce wheezing
-IV lidocaine to help reduce neutrophil response
-steroid probably wont help
-abx only indicated if patients develop a fever or increased WBC count >48 hours
How can you determine readiness for discharge if patient has aspirated
if they have not experienced any of the following within 2 hours of aspiration event:
-new cough or wheeze
-radiographic evidence of pulmonary injury
-SPO2 decrease >10% of preeop values on room air
-A-a gradient > 300mmHg
The best method to prevent ventilator associated pneumonia is _______
to avoid intubation altogether
if intubation unavoidable, the next best preventative measure is to minimize duration of mechanical ventilation
in pneumothorax POCUS will reveal
lack of lung sliding or absence of comet tails
emergency tx of tension pneumothorax includes____
insertion of a 14g angiocath into:
-2nd intercostal space at the mid-clavicular line or
-4th or 5th intercostal space at the axillary line
risk factors for pneumo
-central line insertion
-supraclavicular, interscalene and intercostal nerve blocks
-surgical procedures including radical neck dissection, shoulder arthroscopy, mastectomy, axillary lymph node dissection, mediastinoscopy, laparoscopy, nephrectomy
-chest trauma increased peak inspiratory pressure following chest trauma should raise suspicion
-barotrauma, higher or high inspiratory pressures
-lung cysts or bullae can explain and rupture when nitrous used
tx of flail chest
reducing pain with epidural catheter or intercostal nerve block
patient position risk of VAE highest to lowest
sitting>supine>prone>lateral
consequences of air trapped in pulmonary circulation from vneous air embolism include:
- increased pulmonary artery pressure
- increased RV stroke work index
- RV failure
- decreased pulmonary venous return
- decreased LV preload
- decreased CO
- aasystole/CV collapse
S/s of VAE
-air observed on TEE
-mill wheel murmur on precordial doppler
-decreased ETCO2
-increased ETN2
-increased pumonary artery pressures
-hypotension
-dysrhthmias
-pulmonary edema
-hypoxia
-cyanosis
how to treat VAE
administer 100% FiO2
-flood surgical field with NS
-if surgical insufflation used, d/c gas insufflation and release pneumoperitoneum
-place patient left lateral decubitus position (durant’s maneuver)
-Aspirate air from CVC
pulmonary ertery HTN is defined as mean PAP>
> 25mmHg
pulmonary vascular resistance increases as a function of:
-increased vascular smooth muscle tone
-vascular cell proliferation
and/or pulmonary thrombi
normal PVR
150-250 dynesxsec x cm-5
things that increase PVR
-hypoxemia
-hypercarbia
-acidosis
-SNS stimulation
-pain
-hypothermia
-increased intrathoracic pressure
-mechanical ventilation
-PEEP
atelectasis
Drugs:
-nitrous oxide
-ketamine
-desflurane
things that decrease PVR
-increased PaO2
-hypocarbia
-alkalosis
-decreased intrathoracic pressure
-spontaneous ventilation
-preventing coughing/straining
drugs:
inhaled nitric oxide
-nitroglycerin
-phosphodiesterase inhibitors (sildenafil)
-prostaglandins PGE1 and PGI2
-calcium channel blockers
-ACE inhibitors
Carbon monoxide binds to the oxygen binding site on hgb with an affinity ___x that of oxygen. This displaces O2 from Hgb which reduces ____
200x
CaCO2
Does CO shift the curve?
left
T1/2 of carboxyhemoglobin
4-6 hours breathing room air
Does pulse ox measure COhgb?
no and may give falsely elevated result.
What is required to diagnose carboxyhemoglobinemia?
co-oximeter
What is the treatment for carboxyhemoglobinemia?
100% supplemental O2. Hyperbaric Oxygen therapy may be required
Hyperbaric o2 is indicated if COHgb exceeds _____.
25% or if patient is symptomatic
What drugs can you give down the ETT?
NAVEL
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine
Strong indications for mechanical ventilation-Vital Capacity
<15ml/kg
Strong indications for mechanical ventilation-inspiratory force
<25cm H20
Strong indications for mechanical ventilation-PaO2 at 21% FiO2
<55mmHg
Strong indications for mechanical ventilation-PaO2 at 100% FiO2
<200mmHg
Strong indications for mechanical ventilation-A-a gradient at 21% FIO2
> 55mmHg
Strong indications for mechanical ventilation-A-a gradient at 100% FiO2>
> 450mmHg
Strong indications for mechanical ventilation-PaCO2
> 60
Strong indications for mechanical ventilation-respiratory rate
> 40 or <6
What testing is indicated when preop assessment suggested an increased risk of postop pulmonary complications?
split lung V/Q function testing
normal VO2 max male
35-40 ml/kg/min
normal VO2 max female
27-31 ml/kg/min
best predictors of postoperative pulmonary complications for patients undergoing pulmonary surgery:
FEV1: <40% predicted
DLCO: <40% predicted
VO2 max < 15ml/kg/min
FRC can be measured indirectly by:
- nitrogen washout
- helium wash-in
- body plethysmography
Vo2
3.5ml/kg/min
250ml/min (assuming 70 kg male)
Respiratory rate and pattern are determined by:
- neural control in the respiratory center-medulla
- chemical control in the central chemoreceptors-medulla
- chemical control in the peripheral chemoreceptors carotid body and aortic arch
- baroreceptors-lungs
Which surface of the medulla is the central chemoreceptor located?
ventral
What are the type 1 Glomus cells
sensors that transduce PaO2 into an action potential and mediate the hypoxic ventilatory drive