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Flashcards in Respiratory Emergencies Deck (58):

Most common causes of ARDS?

- direct lung injury: pneumonia, inhalation injury, aspiration
- indirect lung injury: sepsis, pancreatitis. trauma, blood transfusion
- shock


Tx of ARDS?

- 1: lung protective strategy: mechanical ventilation
- 2: fluid conservative strategy
- 3. treat underlying cause


2 types of positive pressure ventilation?

- non invasive (CPAP and Bipap)
- invasive


Indications for intubation?

- failure to protect airway
- failure of Oxygenation
- failure of ventilation


NIPPV considerations?

- before beginning: eval pt and potential for relieving underlying condition
- acute COPD exacerbations and cardiogenic pulm edema - good indications for NPPV
- best utilized in alert, cooperative pts whose resp condition is expected to improve in 48-72 hours


Disadvantages of NIPPV?

- claustrophobia
- increased workload for RRT
- unprotected airway
- inability to suction deep airway
- gastric distention
- delay in intubation



- hemodynamic instability
- facial trauma
- decreased LOC/inability to cooperate
- required sedation
- unable to clear secretions
- aspiration risk
- active upper GI bleed
- recent oral, esophageal or gastric surgery





5 things you need to remember with mechanical ventilation?

- mode
- rate: works as back up(most impt setting in obstruction pts)
- Vt = protection (small amt, think baby lungs)
- FiO2


Indications for mechanical ventilation?

- lung injury: ALI/ARDS, O2 failure
- obstructive: Severe asthmatic/COPD exac


What should you have at hand if there are complications with vent?

a Bag vlave mask


3 questions you need to think about when pt presents with dyspnea?

- does pt need to be intubated immediately?
- is this rapidly reversible?
- can he/she run?


When should you intubate?

- if you answer yes to any one of these:
- failure to protect the airway?
- failure to Oxygenate? (worried about pefusion to brain)
- failure to ventilate?


What does failure to oxygenate mean?

- means that respiratory failure will occur


What are the 2 types of respiratory failure?

- type 1: hypoxemic: PO2 less than 60
- type 2: hypercapnic: pCO2 greater than 50


Causes of Hypoxia?

- low PiO2 (high altitude)
- hypoventilation: LOC
- diffusion: fibrosis, pneumonia
- shunt: CV cause, or alveoli filled with fluid or collapsed (won't respond to supp O2)
- V/Q mismatch


Causes of type 2 (hypercapnia)

- incrased CO2 production: sepsis, fever, burns
- alveolar hypoventilation: reduced minute ventilation (absolute hypoventilation) or increased dead space (relative hypoventilation): COPD, PE


What are signs of hypoxemia?

- cyanosis
- restlessness
- confusion
- anxiety
- delirium
- tachypnea
- bradycardia or tachycardia
- cardiac dysrhythmias
- tremor


Signs of hypercapnia?

- dyspnea
- HA
- peripheral and conjuctival hyperemia
- tachycardia
- tachypnea
- impaired consciousness
- papilledema


eval of respiratory failure?

- O2 sats
- ABGs
- Chemistry


When should you worry about severe respiratory dysfunction?

- when PO2 less than 60 mmHg
- PCO2 greater than 50 mm Hg


What is a vital sign of the pulmonary pt?

- Pulse Ox


What should you watch for in acute asthma exacerbation?

- beware of accessory muscle use, fragmented speech, orthopnea, diaphoresis, agitation, low BP (consider anaphylaxis), severe sxs that fail to improve with initial tx
- impending respiratory failure: inable to maintain resp effort and rate, cyanosis, depressed mental status, severe hypoxemia
- is tidal volume getting smaller?


What should you assess in acute asthma pt?

- measure peak flow if able
- supp O2
- ABGs generally not used initially
- CXR generally not used initially
- establish IV access
- frequent reassessment to determine if intubation and mechanical ventilation is needed
- peak flow: gives objective measurement as to severity to airflow obstruction
- if peak flow less than 40% of predicted = severe
- measure before and afere each neb or MDI


What are danger signs that signify impending ventilatory failure?

- deteriorating mental status
- silent chest (not moving air)
- pulsus paradoxus (greater than 15-20 mm Hg change)
- CO2 retention/elev PCO2
- acidosis
- cyanosis
- hypoxemia


Main tx in acute asthma?

bronchodilators- albuterol or ipratropium
- glucorticoid: IV or PO (anti inflammatory)
- Magnesium sulfate: life threatening exacerbations that remain severe after 1 hr of intense bronchodilator therapy
- Epi: if you suspect anaphylaxis or unstable to use inhaled bronchodilators
- terbutaline: severe asthma, unresponsive to std therapies (don't give both terbutaline and epi)


What is emphysema?

- abnormal perm. enlargement of air spaces distal to terminal bronchioles with destruction of their walls and without obvious fibrosis


What is chronic bronchitis?

- excessive secretion of bronchial mucus and defined by daily productive cough for 3 months or more in at least 2 years


What will be an emphysema's pt primary complaint?

- dyspnea (will be uncomfortable appearing, will use accessory muscles)


Bronchitis pts primary complaint?

- chronic productive cough
- frequently overweight and cyanotic but can appear comfortable


Exacerbation of COPD tx?

- Ipratropium
- albuterol
- corticosteroids
- abx: infection most common reason for exacerbation
- O2: FiO2 to achieve greater than PO2 above 55-60 or SaO2 to 90-93% (watch for Co2 retention)
- NIPPV: initiate early if mod/severe dyspnea, academia, hypercapnia, or RR greater than 25
58% reduction in need for intubation
decreased LOS by 3.2 days
decreased mortality


3 types of high altitude illness?

- acute mountain sickness (AMS)
- High altitude pulm edema (HAPE)
- High altitude cerebral edema (HACE)


Moderate and high altitude levels?

- mod: 8000-10000 feet
- high: 10,000-18000 feet, O2 sats fall below 90%



- serial adaptation steps:
allows tissues to restore O2 pressures towards sea level values
- requires gradual ascents above 8000 ft


What is hypobaric hypoxic condition?

- fluid retention
- vasoconstriction
- pulmonary artery HTN
- increased endothelial permeability
- edema


Presentation of AMS?

- onset: requires several hours at new altitude
- max severity: 24-48 hrs
- HA + at least 1 of these:
GI upset
Generalized weakness or fatigue
dizziness or lightheaded
difficulty sleeping
- gradual resolution by 3-4 days


Management of AMS?

- further ascent is CI until sxs resolve
- descent if sxs worsen
- supp O2
- acetazolamide: speeds acclimatization, more rapid resolution of sxs, alt: dexamethasone
- other sx relief: non-narcotic analgesic, antiemetics


What is HAPE?

- most common fatal manifestation of high altitude illness
- onset is rare below 8000 feet, usually occurs 2-4 days after arrival, and is exacerbated by heavy physical activity


Presentation of HAPE?

- dyspnea at rest
- cough
- fatigue
- HA
- anorexia
- cyanosis
- rales
- tachypnea
- tachycardia


Management of HAPE?

- hyperbaric tx
- descent of at least 2000 ft
- O2 and CPAP if available
- Rest/warmth
- pharmacotherapy: acetazolamide, dexamethasone, salmeterol


Prevention of HAPE?

- slow ascent: 1st night - 7000-8000 ft, ascend no more than 2000 ft per night
- extra night added for every 3000-4000 ft of altitude gain above 10000
- mild-mod exercise
- high carb diet/hydration
- pharm proph: acetazolamide and dexamethasone


What are the 3 consequences of smoke inhalation?

- 1. impaired Oxygenation
- 2. thermal injury to upper airway
- 3. injury to lower airway and lung parenchyma


How is there impaired Oxygenation from inhalation?

- from hypoxemic gas mix
- CO
- cyanide
- V/Q mismatching


How does thermal injury of the upper airway occur?

- usually gases are cooled enough to not burn tissue below levels of vocal cords except for steam inhalation
- causes: mucosal edema, upper airway obstruction, inability to clear oral secretions
- swelling evident by 18-24 hrs
- most people need proph. intubation


How does the inhalation of toxic gases result in injury to lower airways and lung parenchyma present?

- sputum production
- bronchospasm
- dyspnea
- tachypnea
- tachycardia
- diffuse wheezing and rhonchi
- ARDS within 1-2 days after exposure
- sloughing of bronchiolar mucosa in 1-2 days
- pneumonia common by day 5-7


Tx of smoke inhalation?

- supp O2: humidified
- bronchodilators
- suctioning of debris from airway
- maintaining a pt airway (likely will need intubation)
- PEEP if bronchiolar edema


Why is CO posioning so deadly?

- CO binds with Hgb 230-270 tx stronger than with O2
- High O2 extracting organs (heart and brain) quickly become dysfunctional from CO intoxication


What are sxs of CO poisoning?

CNS: HA, fatigue, malaise, flu like, nausea, confusion, loss of memory, emotional lability, dizziness, paresthesias, weakness, vomiting, lethargy, somnolence, stroke, coma, seizures, respiratory arrest
Cardio: chest pain, myocardial ischemia, palpitations, dysrhythmias, poor cap refill, hypotension, cardiac arrest


What is a sign of CO poisoning?

- cherry red coloring of skin
- pulse ox cant be used to access O2 because the device confuses CO for O2 and gives falsely high values


Tx of CO poisoning?

- 100% O2 for 4 hours
- Hyperbaric O2 in severe cases if:
alt mental status or abnorm neuro exam
History of LOC or near syncope
hx of seizure
hx of hypotension during or shortly after exposure
hx of prolonged exposure
preg with COHgb levels greater than 15%
persistent acidosis
concurrent thermal or chemical burns


Common sources of cyanide?

- fruit pits
product of burning wool, nylon, cotton, silk, acrylic, polyurethane, plastics
- may be inhaled or ingested
- onset of sxs is based upon route of exposure and amt
(4 peach pits - LD by ingestion low as 100 mg)
- CN gas is 20x more toxic than CO
- can cause immed respiratory arrest
- directly stimulates chemoreceptors of carotid and aortic bodies, leading to brief periods of hyperpnea


Who should you consider CN toxicity in?

- in all pts with smoke inhalation who have CNS or CV findings
- diff to confirm but frequently concomitant with CO toxicity


Affects of cyanide? sxs?

- prevents cellular o2 utilization
- sxs: HA, dizziness, nausea, abd. pain, anxiety, confusion, syncope, shock, seizures, coma, and death
- increased lactate prod
- anion gap metabolic acidosis
- elevated venous O2 sat
- lactate levels dont elevate right away


CN poisoning tx (antidote)

- 3 way approach: (speed conversion to less toxic thiocyanate)
inhaled nitrites: amyl nitrites
scavenges free CN, encourages formation of methaglobin that binds with cyanide to form cyanomethoglobin
injected nitrites: sodium nitrite
injected Na thiosulfate: enhances rhodanese which catalyzes the transfer of sulfate from thiosulfate - CN which yields thiocyanate (can be excreted by kidneys)
newer: cyanokit - hydroxocobalamin converts cyanide to vit B12
- cyanocobalamin
- no evidence of improvement with hyperbaric O2


Sxs of suspected CN exposure?

- comatose, bradycardic, and hypotensive
- must be given antidote even though it may lower pressure
- have to think of CN and CO poisoning from fire


What is a pneumothorax?

- accum of air in pleural space
- can be spontaneous or trauma induced


How will a pneumothorax present on a PE?

- decreased chest exursion
- decreased breath sounds
- hyperresonant to percussion
- possible subq emphysema
- hypoxemia
- suspect tension pneumo if:
labored breathing, tachycardic, hypotensive, tracheal shift, JVD


Tx of pneumothorax?

- needle decompression
- chest tube