test 1 Flashcards
what does a one liner contain
Name
Age and occupation
Problem and diagnoses (or symptoms and differentials)
how is the patient in relation to their problem/diagnosis”
Impression statement
what is your assessment?
impression not your physical exam
what age is the airway anatomy and physiology similar to an adult
8 years old
in infants and young children what part is anatomically much larger in proportion to the rest of the skull and more protuberant than that in an adult
occiput
When the child is in a supine position, there is more neck ______ and potential for _______
flexion
airway obstruction
sinusitis can lead to _____ of the overlying dermal layers or ____ formation
cellulitis
abscess formation
where is the landmark for the tip into which the tip of a curved McIntosh laryngoscope blade is inserted during an intubation attempt
The vallecular space which is the area between the glossoepiglottic folds
resistance in a tube is inversely proportional to the radius to the fourth power
what is this
example?
Poiseuille’s law of resistance
demonstrated clinically when edema or secretions reduce the airway size in children and resp distress occurs
the amount of air that can occupy space in the lung
lung capacity
the amount of air that does occupy space in the lung
lung volume
the maximum amount of air the lung can hold after a maximal inspiration
Total lung capacity (TLC)
the maximal amount of air forcefully expired after a maximum inspiration
Vital capacity (VC)
the air present in the lung after completion of a forced expiration
Residual volume (RV)
the sum of vital capacity (VC) and residual volume (RV)
Total lung capacity (TLC)
___ decreases with increases in RV
examples
VC
as in the case of obstructive airway diseases such as asthma and emphysema
describes the lungs remaining volume at the end of normal expiration
functional residual capacity (FRC)
films useful in the evaluation of nasopharyngeal, oropharyngeal, and laryngeal pathology
lateral and AP films of neck
what x rays are useful in foreign body aspiration in cooperative patients and younger pt who may not be cooperative
inspiratory and expiratory AP CXR
decubitus CXR
if a tracheal compression is suspected, what test can you order
Barium esophagrams
further imaging such as MRI or angiography is warranted prior to surgical correction
imaging for soft tissue and pathology of face and neck
ultrasound
examples retropharyngeal or peritonsillar abscess
useful for difficulties involving nasal and paranasal structures
CT
ABG values that support the diagnosis of resp failure
PaO2 less than 60
PaCO2 of greater than 50
fluid resuscitation
isotonic crystalloids (NS or LR) 10-20ml/kg
if hemorrhage is known or highly suspected in rescusitation
administration of PRBCs
Fluid resuscitation increases
preload
signs of deteriorating cardiac function after fluid bolus
increase HR
decrease BP
crackles
tachypnea
choice of vasopressor for hypovolemic or distributive
drugs with A agonist such as epinephrine or norepinephrine (increase systemic vascular resistance)
choice of vasopressor for cardiogenic shock
positive chronotropy
epi
norepi
dopamine
drugs for afterload reduction
dobutamine
nitroprusside
milrinone
Higher MAP =
improved oxygenation
average pressure that distends the alveolus and chest wall
Mean airway pressure
PaO2
80 to 100 mm Hg
SaO2
95% to 100%
pH
7.35 to 7.45
PaCO2
35 to 45 mm Hg
HCO3-
22 to 26 mEq/L
compliance formula
change in volume over the
change in pressure
mean airway pressure is reflected by
the mean alveolar pressure
the volume of gas actually exchanged across the alveolar membrane
Alveolar ventilation
a practical metric representing the resting volume of air in the lungs after a spontaneous breath
FRC
At FRC the tendency of the lungs to collapse is exactly balanced by the
tendency of the chest wall to expand
restrictive lung disease results in
an abnormally low FRC
mechanical ventilation that delivers a set total volume to the patient during a preset inspiratory time
Volume regulated ventilation
what kind of ventilation has a decelerating flow
pressure control ventilation
advantages to volume regulated ventilation
disadvantages
reduce risk for volutrauma due to to preset TV or minute ventilation
disadvantages
delivering higher peak pressures to achieve the goal TV or minute ventilation
risk of not meeting pt demands due to continuous flow pattern gas delivery
volume ventilation is clinically useful when
lung compliance is relatively static bc this reduces likelihood of excessive pressure generated during mandatory volume delivery should compliance abruptly decrease
Cold shock give (cold extremities, think vasoconstriction)
epi
warm shock give (warm extremities, thing vasodilation)
norepi
the amount of pressure to put the breath in
PIP
sick lungs respond better to ____
healthy lungs respond better to ____
pressure (pt with stiff lungs due to decelerating flow)
volume
higher rate on vent will ____ CO2
lower
a form of assist-control ventilation which the vent breath is delivered as a set TV
PRVC (pressure regulated volume control)
time triggered pressure limited time cycled mode of ventilation that also allows unrestricted spontaneous breathing throughout the entire breath cycle
APRV (Airway pressure release ventilation) last ditch before oscillator to promote gas exchange for pt with poor lung compliance long inspiration, short expiration
last ditch before oscillator
to promote gas exchange
for pt with poor lung compliance
APRV (Airway pressure release ventilation)
if you are maxed out at vent settings, high risk for barotrauma so switch to
High frequency oscillatory ventilation
APRV is more for
oxygenation than ventilation
not for asthmatic
you would increase your PEEP for
high inspiratory pressures
peep is the lowest pressure that your lung should see
PIP is the
highest pressure that your lungs will see
if pressure controlled what if variable
volume
if volume controlled then what is variable
PIP
what setting is constant not variable
PEEP
CPAP is just a
PEEP
BiPap has what
PIP and a PEEP
the improvement of mucociliary transport system, the recruitment of atelectatic areas and the improvement of oxygenation while maintaining very low low TVs to avoid lung barotrauma
High frequency jet ventilation
used to treat hypoxemic lung diseases such as ARDS and persistent pulmonary hypertension in infants
Inhaled nitric oxide - vasodilates- more blood flow to lungs. Its continuous and if suddenly stopped they clamp down.
HFOV is characterized by high resp rates up to
15 HZ
using an oscillator, how to lower CO2 on ABG
increase amplitude
increase oxygenation on oscillator
increase mean airway pressure
higher frequency means
higher CO2
what is flow volume or pressure volume loops used for
the effectiveness of the breaths they are receiving.
aid in the evaluation of lung compliance and resistance
failure criteria for extubating trials
diaphoresis nasal flaring increased resp effort apnea hypotension cardiac arrhythmias increased CO2 decreased pH
predict risk for extubation failure due to swelling
airway leak test
absence of a leak around the endotracheal tube at a pressure > or equal to 30 increases risk of post extubation stridor and extubating failure
drain out air out of cuff -
if air leaks - no need for steroids
if air leaks - steroids are given prior to extubating
Sepsis Thermal injury Pancreatitis Trauma transfusion
indirect lung injury
ARDS
Pneumonia
Aspiration of stomach contents
Submersion injury
Inhalation injury
direct lung injury
ARDS
will determine severity of ARDS
Calculate PaO2/FiO2 ratio
OI (oxygenation index)
diagnostic tests for ARDS
BMP CBC with diff CXR echocardiography bronchoalveolar-lavage (BAL)
3 phases of ARDS
Phase 1: Acute/Exudative
Initial injury disrupts epithelial fluid transport & removal of fluid from the alveolar space → pulmonary edema
Impaired gas exchange d/t pulmonary edema, V/Q mismatch, increase in the A/a gradient
Inflammatory stage begins with neutrophil activation and cytokine release
Phase 2: Proliferative phase
Resolution can begin with improvement of alveolar surfactant release, promote fluid transport, and proliferate injured cells
If resolution doesn’t occur → persistent respiratory failure, hypoxemia, decreased lung compliance, fibrosis
Phase 3: Chronic/Fibrotic phase
Can be as early as 5-7 days after onset of ARDS
rapid onset of dyspnea leading to hypoxia and respiratory failure, SpO2 < 90% on room air, crackles, increased WOB
presentation of ARDS
management of ARDS
lung protective strategies, supplemental oxygen, non-invasive ventilation → mechanical ventilation → ECMO
Adjunct: nitric oxide, prone, surfactant administration
Conservative fluid management
Enteral nutrition
the differential diagnosis of airway obstruction subdivided to
supraglottic
glottic
subglottic
what upper airway noise is suggestive of vocal cord involvement
hoarseness or phonia
low pitched sound like a snore and suggests implosion of pharyngeal soft tissue structures
stertor
harsh sound caused by vibration of the airway structures, suggests vocal cord involvement, decreases during sleep, increases during agitation
stridor
risk factors BPD
prematurity, low birth weight, white males, genetic heritability
what is BPD
Disruption of lung development, alveolar hypoplasia (fewer & larger alveoli) which leads to less surface area for gas exchange
Stages of BPD for <32 weeks gestation mild
room air by 36 weeks (gest) or discharge (whatever is first)
Stages of BPD for <32 weeks gestation moderate
need for oxygen <30% at 36 wks/discharge
Stages of BPD for <32 weeks gestation: severe
need for oxygen > 30% and/or positive pressure at 36wks/discharge
BPD for >32 wks gestation
*for >32 wks gestation: same criteria but by day 56 of life
Treatment goals for BPD
supportive care with minimum additional injury, prevent hyperinflation or distention of airways
Treatment BPD
CPAP if possible (better outcomes than mechanical ventilation)
Fluid restriction to avoid pulmonary edema
Maximized calories to promote good nutrition and growth
Diuretics to improve lung compliance and decrease airway resistance
Watch for electrolyte imbalances
Bronchodilators (only for rescue, acute bronchoconstriction)
Corticosteroids (reserved for mechanically ventilated BPD with substantial support)
Prevention BPD
antenatal steroids - all pregnant women from 23-34weeks gestation with intact membranes at risk for preterm delivery within the next 7 days
fluid restriction - Positive fluid balance : a lack of postnatal weight loss during immediate postnatal period thought to be a predisposing risk factor for BPD
Protective ventilation strategies
Minimal ventilation with protective hypercapnia
High frequency oscillatory ventilation
Early continuous positive pressure ventilation
Noninvasive mechanical ventilation (NIPPV)
caffeine therapy
Used in same doses used to treat apnea of prematurity
Recommended for all infants < 1250 grams at birth
Usually continue until PMA of 35-36 weeks (until the infant is no longer at significant risk for apnea of prematurity)
Vitamin A: deficiency may promote development of BPD
Appears to reduce risk of BPD in susceptible
infants
5000 units IM 3 times a week X 4 weeks
Late surfactant therapy: between 3-10 days of age
Superoxidase dismutase: antioxidant, remains an investigational drug
clinical manifestations BPD
High CO2 (hypercapnia) ABG compensated - Bicarb elevated to compensate for the hypercapnia
R sided heart failure
poor growth
most require bronchodilators
Diuretics BPD
Thiazide diuretics: Chlorothiazide and/or
spironolactone produce short-term improvement in
lung mechanics
Loop diuretics: Furosemide (Lasix) in infants > 3 weeks of age results in improved pulmonary mechanics and oxygenation
what is primary problem with BPD
impaired gas exchange leads to impaired growth neurocognitive problems R heart failure pulmonary HTN cor pulmonale systemic HTN prone to asthma and resp infections prone to rehospitalizations in the first year
leading causes of hospitalization in children under 1 yr
Bronchiolitis
Bronchiolitis typically occurs in children less than
Peak incidence between
highest risk for death at
2 yrs
3-6 mths
infants less than 2-3 months of age, premature birth history, infants with an underlying cardiopulmonary, immunodeficiency or neuromuscular disorder
In bronchiolitis, the obstructed airways increase airway resistance during expiration and inspiration, which leads to
retained gas, air trapping and hyperinflation
As bronchiolitis progresses, what happens
cellular debris and mucous can form into plugs within the bronchiole lumens leading to obstruction, air trapping and lobar collapse
what virus causes more hospitalizations with bronchiolitis
RSV
risk factors for complications from bronchiolitis
male sex, chronic co-existing medical conditions, prematurity, low birth weight, immunodeficiency, exposure to cigarette smoke, lower socioeconomic status, lack of breastfeeding, exposure to crowded environments
Bronchiolitis presentation
Presents with rhinorrhea, leads to coughing, 2-4 days of low grade fever, congestion, mild conjunctivitis, pharyngitis, otitis media, dehydration if feeding poorly
and progresses to airway obstruction Bronchiolar obstruction: prolonged exhalation, nasal flaring, intercostal retractions, suprasternal retractions, and air trapping with hyperinflation Obstructed airways (air trapping, hyperinflation), mucus plugs (obstruction, air trapping, lobar collapse), increased airflow resistance (increased RR, respiratory failure) Can also manifest with apnea (especially in infants with history of prematurity)
Treatment Bronchiolitis
Treatment: CXR (hyperinflation + atelectasis), PCR (viral detection), HFNC/CPAP, Heliox (via face mask, improves airway resistance)
Self-limiting disease, generally self-resolves with supportive therapy, excellent prognosis overall
a complex constellation of inflammation, hyperresponsiveness, and airway obstruction, usually following a trigger or stimulus.
Asthma
Blood gas will reveal what during an asthma exacerbation
Blood gases reveal respiratory acidosis during acute exacerbations
Pt on continuous albuterol with have a transient low ______
Patients on continuous albuterol will have a transient low Potassium level (however it is not necessary to bolus potassium chloride unless the patient is on continuous Albuterol for periods longer than 24h or drops to less than 2.0 or the patient is otherwise hemodynamically unstable
At risk population for asthma
is more common in males than females, in African Americans and Hispanics, and in children from lower socio-economic households
asthma triggers
Allergens: dust mites, animal dander, cockroaches, mold pollen
Irritants: cigarette smoke, air pollution, chemicals/dust, aerosol sprays
Viral URIs
Medications: aspirin, NSAIDS, Non-Selective Beta Blockers
Sulfites in food and drugs
Acute weather changes
Physical Activity (the only trigger that should not be avoided)
rescue med for asthma
Short acting Bronchodilator
(a.k.a “rescue” or “quick relief”)
Treatment of bronchospasm
provide rapid relief but no long term effects on inflammation
Short acting (i.e. albuterol, levalbuterol, pirbuterol acetate, terbutaline and ipratropium)
Side Effects: palpitation, tremor
If asthma is well controlled, rescue medications should not be necessary more than two times per week
In asthma when should a spirometry be taken
Spirometry before and after administration of a short-acting bronchodilator
Reduced FEV1 and FEV1/FVC ratio
Reduced PEF
daily control for asthma pt
long acting Bronchodilator
Non-steroidal medications that are meant to be used in conjunction with an anti-inflammatory medication on a daily basis (not as a rescue for acute asthma symptoms)
Ex: Arformoterol, Salmeterol and Formoterol (are commercially available in combination with a corticosteroid within one inhaler)
Asthma med used in addition to a short acting B2 Agonist
anticholinergic
Block the action of acetylcholine at parasympathetic sites in bronchial smooth muscle resulting in bronchodilation
Not indicated as initial rescue therapy for acute bronchospasms when rapid treatment is required
Used only in addition to a short acting Beta 2-agonist
SE: dry mouth
Ex: Ipratropium Bromide
Non steroidal medication used in Asthma
intended as maintenance treatment for mild to moderate asthma
Mast Cell Stabilizers-reduce inflammation by preventing mast cell release of leukotrienes, and slow down the anaphylactic response to a trigger by inhibiting degranulation after contact with antigens. Thereby, preventing asthma symptoms
Relatively safe
Less effective than inhaled corticosteroids, intended as maintenance treatment for mild to moderate asthma
Ex: Cromolyn and Nedocromil
inhaled corticosteroids for asthma
Most effective control (maintenance and prevention of asthma)
Use for any severity and age
Once daily to twice daily use offers symptom reduction and improvement in lung function (Adjustable dose approach can result in effective cumulative dose decrease over time without decreasing asthma control)
Decrease exacerbations
Common Side Effects: oral candida, hoarseness
Examples: Beclomethasone Dipropionate, Budesonide, Ciclesonide, Flunisolide, Fluticasone, Mometasome
systemic corticosteroids for asthma
Used in severe acute exacerbation recovery
Effective secondary to anti-inflammatory or immunosuppressant properties
Once transitioned from intravenous to oral administration, may be continued for 5-10 days post exacerbation
SE: hyperglycemia, adrenal suppression, depression of growth velocity
Examples: Methylprednisolone, Prednisone, Prednisolone
Leukotriene-Receptor Antagonist
asthma treatment
Selectively inhibits the cysteinil leukotriene receptor (thereby blocking the symptoms of asthma)
Less effective than inhaled corticosteroids
Thought to help prevent exercise-induced bronchospasm
Example: Singulair
difference in a dry metered inhaler vs MDI
Delivers medication without using chemical propellants BUT requires that the user learn to produce a strong and fast inhalation.
Mild intermittent asthma:
< = 2 days per week
night wakenings 0 for 4 and younger
<=2x/mth in 5 and older
oral steroid use 0-1x/year
controlled with as needed B2 agonist (SABA)
Mild persistent asthma
> 2 days per week night wake - 1-2/mth 4 and younger 3-4x/mth 5 and older oral steroid use >=2x in 6 mths or >= 4x/year 4rs and younger >2x/yr in 5 and older
Low dose ICS
SABA PRN
Moderate persistent asthma
symptoms daily night wake - 3-4x/mth 4yr and younger >1x/week for 5 and older oral steroid use >=2x in 6 mths or >= 4x/year 4rs and younger >2x/yr in 5 and older
Med dose ICS or
Low dose ICS + LTRS or
Low dose ICS + LABA
SABA PRN
Severe persistent asthma
symptoms throughout the day night wake >1x/week for 4 and younger 7x/week for 5 and older oral steroid use >=2x in 6 mths or >= 4x/year 4rs and younger >2x/yr in 5 and older
Med dose ICS or Low dose ICS + LTRS or Low dose ICS + LABA SABA PRN referral to subspecialist
Treatment of moderate to severe asthma exacerbation
Identified by non-responsiveness to intermittent or nebulized Beta 2-agonist treatments
Require continuous Beta 2-agonist infusion, oxygen and Steroids (prednisolone, prednisone or dexamethasone) and may receive:
1. Ipratropium bromide x3 doses
4. IV Magnesium sulfate bolus
5. IV Terbutaline bolus and may require continuous infusion
6. Non-invasive ventilation or if not improving, lead to intubation
Pertussis caused by
mode of transmission
Bordetella pertussis, aerosol transmission
gram neg coccobacillus
Individuals with pertussis are most contagious during the
Catarrhal stage - first 2 weeks
increased secretions and low-grade fever
characteristic cough of pertussis develops during the
Paroxysmal phase:
Phases of pertussis
Catarrhal stage: most contagious stage, URI symptoms, begins insidiously (first 2 weeks), increased secretions and low-grade fever
Paroxysmal phase: increase in severity & frequency of cough, rapidly consecutive forceful coughs in a single exhalation followed by a “whoop”, post-tussive emesis and copious mucus
Cough occurs in paroxysms (pattern during expiration needed to dislodge plugs of necrotic bronchial epithelial tissues and thick mucus)
Convalescent phase: symptoms slowly diminish, but cough recurs easily with triggers
the problem when an infant gets pertussis
infants can easily become fatigued with the incessant coughing and post-tussive emesis leading to inadequate oral intake, dehydration, or resp failure. Intermittent apnea can also occur in infants associated with paroxysmal coughing - may be related to vagal stimulation
incubation period that precedes the 3 phases of pertussis lasts
7-14 days
secondary sequelae to forceful coughing
chest/abd pain
rib fractures
air leak syndromes
facial petechiae
Pertussis treatment
Treated with macrolide antibiotics
erythromycin most commonly - 14 days -
Bactrim-14 days >2 mos of age
Clarithromycin - also likely to be effective
Azithromycin- for infants
hospitalization for young infants
what type of isolation for pertussis
standard and droplet precautions
after diagnosis of pertussis, children must be excluded from school or daycare for how many days?
Must complete 5 days of effective therapy
if not treated, min of 21 days after onset of cough
Bronchiolitis Risk factors
Premature infants, children with chronic lung disease, congenital heart disease, neuromuscular weakness, and immunodeficiency.
Bronchiolitis s/s
Cough Rhinorrhea Noisy, raspy breathing and wheezing. Low grade fever Irritability Apnea
Bronchiolitis Evaluation
Nasal flaring, intercostal retractions, subcostal retractions.
Airway trapping with hyperexpansion of lungs.
Wheezing and hyperresonance on percussion.
Crackles throughout
Severe—grunting, cyanosis.
No routine testing required.
Rapid viral PCR: RSV, parainfluenza, influenza, and adenovirus to confirm diagnosis.
Optional x ray not routine
Bronchiolitis Treatment
control fever
Hydration
Upper airway suctioning
Oxygen if needed.
Hospitalization with ventilator support if severe
Croup or LTB (laryngotracheobronchitis) signs/symptoms
Parainfluenza viruses or RSV 6 months to 3 years of age 12-48 hours after URI Barking cough Low grade fever Inspiratory stridor Hoarseness Increased work of breathing or apnea
Croup or LTB (laryngotracheobronchitis) evaluation
Edema of the upper airway
Steeple sign on AP Chest X-ray
Suprasternal and/or intercostal retractions
Westley Croup Score
Routine labs not useful in establishing diagnosis
Croup or LTB (laryngotracheobronchitis) treatment
Antipyretics Oxygen if needed Dexamethasone Nebulized epinephrine Endotracheal intubation with tube 0.5 to 1 size smaller
Pertussis risk factors
less than 6 months of age, waning immunity from previous vaccine, under-immunized
Pertussis signs by stages
Catarrhal stage- Increased nasal secretions and fever
Paroxysmal stage- cough during expiration
Convalescent stage- gradual resolution of symptoms
Pertussis evaluation
shortness of breath, whooping cough due to forceful inhalation against narrow glottis
Posttussive emesis
Copious, viscid mucus
Whooping cough
The neonate may show signs of apnea and choking spells
Young infants have CNS damage due to hypoxia
Adolescents have a persistent, nonproductive cough
Pertussis treatment
Hospitalization, and elimination of Bordetella pertussis
Macrolide antibiotics- erythromycin is the treatment of choice
Azithromycin for neonates
Treatment during catarrhal stage eradicates organism within 3-4 days
Treatment in paroxysmal stage only reduces the risk of spreading infection
Trimethoprim-sulfamethoxazole in children older than 2 months old
Vaccination
Pneumothorax risk factors
trauma (open, communicating or “sucking” chest wound), acute changes in lung compliance, rupture of blebs in patients with CLD, potentially spontaneous
Pneumothorax signs/symptoms
chest pain
dyspnea
tachycardia
acute change in lung compliance in the mechanically ventilated patient
Pneumothorax evaluation
ipsilateral hyperresonance to percussion ipsilateral decreased air entry ipsilateral decreased vocal fremitus decreased oxygen saturations increased peak inspiratory pressure changes in expired tidal volumes on vent CXR will show line displaced from the chest wall (see air without vascular markings on one side of line) ABG will show impaired oxygenation ABG will show larger A-a gradient
Pneumothorax treatment
provide supplemental oxygen to ensure adequate oxygenation
some small pneumos can be treated with close observation
remove pathological air from cavity with placement of thoracostomy tube
if recurrent pneumos or CLD, consider thoracoscopy or pleurodesis
if cardiopulmonary compromise, emergent needle thoracentesis warranted
consider surgical consultations if emergent airway/ventilatory support needed
Pulmonary edema risk factors
Risk Factors
Changes in pulmonary capillary permeability
Abnormalities in lymphatic drainage and surfactant
Congenital pulmonary disease
Cardiogenic:
Left sided heart failure
CHD, HTN, cardiomyopathy
Pulmonary (intrinsic):
Infectious processes (pneumonia, ARDS, & Pulmonary Embolism) Neurogenic:
Surgery, trauma, seizures
Noncardiogenic:
Blood product transfusion
High altitude
Pulmonary edema symptoms
SOB Tachypnea Tachycardic Hypoxia Weakness Cough w/ frothy sputum Diaphoresis Orthopnea Paroxysmal Nocturnal dyspnea
Pediatrics:
Cyanosis
Subcostal retractions
Crackles on auscultation
S3 in those with cardiogenic Pulmonary edema
Pulmonary edema evaluation
CXR: haziness
- ABG: Lower PaO2 & increase A-a Gradient
- BNP: Elevated
- Pulmonary Capillary Wedge Pressure: Elevated
Pulmonary edema treatment
Airway management: ABC
Supplemental Oxygen: Noninvasive + Invasive with higher PEEP levels
Diuretics: Restore euvolemic body fluid balance to improve oxygenation and relieve dyspnea. (Loop, Potassium Sparing, Thiazide diuretics)
Inotropes/ ACE inhibitors in HF cases
ULTIMATE GOAL: Reverse the cause of airway obstruction, fix the failing heart and/or reverse the lung damage/disease.
