Respiratory Emergencies Flashcards
For a pt with dyspnea, what three questions do we need to ask ourselves?
Does this pt need to be intubated immediately?
Is this rapidly reversible?
Can he/she run?
How do we know when to intubate immediately?
Failure to protect the airway?
Failure to oxygenate?
Failure to ventilate?
If yes to any of the above, intubate immediately
There are two types of respiratory failure. What are they?
Hypoxemic pO2 less than 60
Hypercapneic
pCO2 >50 (if not a chronic retainer)
There are five reasons for a type 1 respiratory failure (due to hypoxemia). What are they?
- Low PiO2
- Hypoventilation ( not enough room for oxygen to get in)
- Diffusion (DLCO)
- Shunt (CV defect, atelectasis)
- V/Q mismatch (give oxygen and it wont help a shunt pt. it will help a VQ mismatch)
There are two reasons for a type 2 respiratory failure (due to hypercapnia). What are they?
Increased CO2 production
Alveolar hypoventilation
What are examples of increased CO2 production that may cause respiratory failure? 3
What are examples of alveolar hypoventilation that may cause respiratory failure? 2
- (sepsis, fever, burns, etc)
- Reduced minute ventilation
(absolute hypoventilation)
Increased dead space
(relative hypoventilation)
Signs of hypoxemia
10
- Cyanosis
- Restlessness
- Confusion
- Anxiety
- Delirium
- Tachypnea
- Bradycardia or tachycardia
- HTN
- Cardiac dysrhythmias
- Tremor
Signs of hypercapnia (CO2)
8
- Dyspnea
- Headache
- Hypertension
- Peripheral and conjunctival hyperemia
- Tachycardia
- Tachypnea
- Impaired consciousness
- Papilledema
How should we evaluate a pt that may be approaching respiratory failure?
5
- O2 sats
- ABG’s
- Chemistry
- CXR
- EKG
Severe respiratory dysfunction that threatens the function of vital organs. This will show us poor oxygenation and ventilation. What values do we need to look for and what should they be?
Consider if PO2 is less than 60 mmHg or PCO2 is > 50 mmHg
Which pts respond best to NIPPV/Bipap?
2
Why does this help?
COPD exacerbations
CHF
Helps relieve the stress on the respiratory muscles from fatigue
(would seem counterintuitive for COPD pts)
What do we need to be aware of when assessing a pt for acute asthma attack?
7
What would clue us in that this is impending respiratory failure?
4
- use of accessory muscles of respiration;
- fragmented speech;
- orthopnea;
- diaphoresis;
- agitation;
- low blood pressure (consider anaphylaxis);
- severe symptoms that fail to improve with initial treatment
- inability to maintain respiratory effort and rate;
- cyanosis;
- depressed mental status;
- severe hypoxemia (SpO2 ≤ 95% despite high flow O2 by nonrebreather)
How would we evaluate a pt who is having an acute asthma attack?
6
- Measure peak flow if able
- Supplemental O2
- ABGs are generally not useful initially
- CXR generally not useful initially
- Establish IV access
- Frequent reassessment to determine if intubation and mechanical ventilation is needed
Acute asthma: peak flow. What does it measure?
3
- Helps give an objective measurement as to the severity of airflow obstruction
- Peak flow less then 40 % of predicted = severe
- Measure before and after each nebulizer or MDI treatment
Danger signs that signify impending ventilatory failure include:
7
- Deteriorating mental status
- Silent chest
- Pulsus paradoxus (>15 to 20 mmHg)
- CO2 retention/ elevated pCO2
- Acidosis
- Cyanosis
- Hypoxemia
Asthma medical therapy. Which medications would we give?
5
- Bronchodilators
- Glucocorticoid
- Mag sulfate
- Epi
- Terbutaline
What kind of the following would we give acute asthma pts:
- Bronchodilators
- Glucocorticoid
- Albuterol (inhaled beta 2 agonist)
- Ipratropium bromide (atrovent) (anticholinergic)
Give with the albuterol - Methylprednisolone (Solu Medrol)
Why would you give mag sulfate?
Why would you give epi?
Why would you give terbutaline?
For life threatening exacerbations that remain severe after 1 h of intense bronchodilator therapy - benefits unclear
For suspected anaphylactic rxn or unable to use inhaled bronchodilators
For severe asthma unresponsive to standard therapies
Emphysema pts will often present with what as their primary complaint? (what will you notice right away?)
Chronic bronchitis pts will present with what as their primary complaint? (How will they appear when they come into your office? 2)
Emphysema predominant pts will often present with dyspnea as their primary complaint
Often uncomfortable appearing; frequently with accessory muscle use
Bronchitis predominant pts will present primarily with chronic productive cough
On exam, frequently
1. overweight and
2. cyanotic but can appear comfortable
COPD exacerbation meds?
5
- Ipratropium-
- Albuterol-
- Corticosteroids- Consider: Prednisone 30-40 mg/day x 10-14 days;
Methylprednisolone 125 mg IV for more severe exacerbations - Antibiotics- Reasonable; often recommended
- Oxygenation-
Watch for CO2 retention!
What should the FiO2 be?
FiO2 to achieve pO2 > 55-60 or SaO2 to 90-93%
Other interventions for COPD exacerbations?
What are the benefits of this intervention?
3
NIPPV
- 58% reduction in need for intubation
- Decreased LOS by 3.2 days
- Decreased mortality
When should we intiate NIPPV early?
4
Initiate early if
- mod/severe dyspnea,
- acidemia,
- hypercapnea, or
- RR >25
What are the three kinds of high altitude sickness?
3
- Acute mountain sickness (AMS)
- High-altitude pulmonary edema (HAPE)
- High-altitude cerebral edema (HACE)
What is moderate altitude defined as?
What is high altitude defined as?
Moderate altitude: 8000-10,000 feet
High altitude: 10,000-18,000 feet
O2 sat falls below 90%
Serial adaptation steps for acclimitization
2
- Allows tissues to restore oxygen pressures toward sea level values
- Requires gradual ascents above 8000 feet
Hypobaric hypoxic condition pathophysiology?
5
- Fluid retention
- Vasoconstriction
- Pulmonary artery hypertension
- Increased endothelial permeability
- Edema
AMS Presentation:
- Onset? (when is it the worst?)
- Headache plus at least one of following: 4
- Gradual resolution by _______?
- Requires several hours at new altitude
Maximum severity 24-48 hours - GI upset (anorexia and/or nausea)
- Generalized weakness or fatigue
- Dizziness or lightheaded
- Difficulty sleeping
- 3-4 days
Management of AMS?
6
- Further ascent contraindicated until symptoms resolve
- Descent if severe symptoms or if worsening
- Supplemental oxygen
- Acetazolamide (250 mg at onset and BID-TID)- diuretic
- Non-narcotic analgesic
- Antiemetics
Why would we want to give acetazolamide? 2
Alternative to acetazolamide?
- Speeds acclimatization
- More rapid resolution of symptoms
Alternative: dexamethasone (8 mg loading dose, 4 mg q6h)
What is the most common FATAL manifestation of high-altitude illness?
Describe its onset?
(usually at what altitudes?)
What is it exacerbated by?
High altitude pulmonary edema (HAPE)
Onset:
Usually occurs 2-4 days after arrival
Rare below 8000 feet
Exacerbated by heavy physical activity
Presentation of HAPE? 9
whats the major symptoms?
- Dyspnea at rest!
- Cough
- Fatigue
- Headache
- Anorexia
- Cyanosis
- Rales
- Tachypnea
- Tachycardia
Managament of HAPE?
5
- Hyperbaric therapy
- Descent of at least 2000 ft
- Oxygen and CPAP if available
- Rest/warmth
- Pharmacotherapy
What kinds of meds would we use with HAPE?
5
- Acetazolamide,
- dexamethasone,
- sildenafil,
- nifedipine,
- salmeterol
Prevention of HAPE?
4
- Slow ascent
- Mild-moderate exercise
- High-carbohydrate diet/hydration
- Pharmacologic prophylaxis
For a slow ascent to prevent HAPE, what should our timeline be?
3
What meds could we take prophylactically for HAPE? 2
- First night altitude – 7000-8000 feet
- Ascend no more than 2000 feet per night
- Extra night added for every 3000 to 4000 feet of altitude gain above 10,000
Acetazolamide
Dexamethasone
3 consequences of smoke inhalation
- Impaired oxygenation
- Thermal injury to the upper airway
- Injury to the lower airway and lung parenchyma
We get Impaired oxygenation from inhalation of what things? 3
What does this cause?
- Hypoxemic gas mixture
- Carbon monoxide
- Cyanide
and V/Q mismatching
Thermal injury of the upper airway:
Usually the gases are cooled enough not to burn the tissues below the level of the vocal cords except in cases of ______inhalation
Causes? 3
Swelling is most evident when?
Most people need what kind of intervention?
- steam
- mucosal edema,
- upper airway obstruction,
- inability to clear oral secretions
Swelling most evident by 18-24 hours
Most people need prophylactic intubation
Inhalation of toxic gases results in injury to the ______ ______ and ____ _________.
lower airways
lung parenchyma
What does the inhalation of toxic gases usually cause?
9
- 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
Treatment of smoke inhalation?
5
- Supplemental oxygen
- -Humidified - Bronchodilators
- Suctioning of debris from airway
- Maintaining a patent airway (likely will need intubation)
- PEEP if bronchiolar edema
How much stronger does CO bind with Hgb compared to O2?
High O2 extracting organs quickly become dysfunctional from CO intoxication. What are these? 2
CO binds with Hgb 230-270 times stronger than with O2
heart/brain
What are the CNS symtpoms of CO poisoning?
Cardio symptoms?
CNS: HA, Fatigue, malaise, flulike, 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 capillary refill, hypotension, cardiac arrest
Why cant pulse oximetry be used to access oxygenation?
What PE finding will you see on CO poisoning?
because the device confuses COHgb for O2Hgb and gives falsely high values!
“cherry red” coloring of the skin with CO poisoning
What would you treat CO poisoning with?
- Treatment is administration of 100% O2 for 4 hours
- What is the half life of COHgb on room air?
- On 100% FiO2?
- On 100% FiO2 at 2.5 atmospheres?
- Half-life of COHgb is 4h on room air,
- 60 minutes when breathing 100% FiO2, and
- 15 minutes with 100% FiO2 at 2.5 atmospheres (HBO)
Hyperbaric oxygen therapy may be used to treat severe cases of CO poisoning if:
10
- Altered mental status or abnormal neuro exam
- History of LOC or near-syncope
- History of seizure
- Coma
- History of hypotension during or shortly after exposure
- Myocardial ischemia
- History of prolonged exposure
- Pregnant with COHgb levels > 15%
- Persistent acidosis
- Concurrent thermal or chemical burns
- Common sources of cyanide posioning?
2 - Mode of attack?
- Onset of symptoms is based upon what two things?
- How much do you have to inhale to have symtpoms?
Ingest?
- Fruit pits (Peaches, plums, cherries, apricots)
- Product of burning wool, nylon, cotton, silk, acrylic, polyurethane, plastics
- May be inhaled as hydrogen cyanide (HC) gas or ingested
- route of exposure and amount
- LD 50 by inhalation is 200 ppm
- LD by ingestion is as low as 100mg (4 peach pits)
Who do we need to consider CN toxicity in?
all patients with smoke inhalation who have CNS or CV findings(red flags)
Difficult to confirm but frequently concomitant with CO toxicity
How much more toxic is CN gas than CO?
What can it cause immediately?
Its directly stimulates which receptors (2) leading to what?
CN gas: 20x more toxic than CO
Can cause immediate respiratory arrest
Directly stimulates chemoreceptors of carotid and aortic bodies, leading to brief periods of hyperpnea
What is the pathopohysiology behind cyanide poisoning?
Prevents cellular oxygen utilization
Symptoms of CN poisoning?
HA, dizziness, nausea, abd pain, anxiety, confusion, syncope, shock, seizures, coma, death
What lab values will be affected in CN poisoning?
4
- Increased lactate production
- Anion gap metabolic acidosis
- Elevated venous oxygen saturation
- Lactate levels don’t elevate right away
Cyanide poisoning treatment (antidote)
Three pronged approach?
Inhaled nitrites (amyl nitrites) Injected nitrites (sodium nitrite) Injected Sodium Thiosulfate
Describe what each of the following works to do in CN poisoning: Inhaled nitrites (amyl nitrites) 2 Injected nitrites (sodium nitrite) 2 Injected Sodium Thiosulfate 1
Who is this contraindicated in?
- Scavenges free cyanide
- Encourages formation of methemoglobin with binds with cyanide to form cyanomethemoglobin
- Same as above
- Enhances rhodanese which catalyzes the transfer of sulfate from thiosulfate cyanide which yields thiocyanate (which can be excreted by kidneys)
Contraindicated with concomitant carbon monoxide poisoning
Overall what does the three pronged antidote kit do for CN pts?
Induces methemoglobinemia to speed conversion to less toxic thiocyanate
What is the newer kit for CN poisoning called and how does it work?
Cyanokit
Hydroxocobalamin converts cyanide to vitamin B12
(cyanocobalamin)
Cyanide poisoning - Pearls
- Oxygen helps to do what?
- No evidence of improvement with _______ oxygen
- When cyanide exposure is suspected - (A comatose, bradycardic, hypotensive) patient MUST be given __ ______ even though it may lower ___ further
- DON’T BE FOOLED BY ______ __________ or even ____ regarding oxygenation status!!!!!
- decrease the binding of cyanide to cytochrome oxidase)
- hyperbaric
- the antidote
BP - PULSE OXIMETRY
ABGs
What is a pneumothorax and what can it be caused by (2)?
Accumulation of air in the pleural space
Can be spontaneous or trauma induced
Pneumothorax: Physical exam findings?
5
- Decreased chest excursion
- Decreased breath sounds on the affected side
- Hyperresonant to percussion
- Possible subcutaneous emphysema
- Hypoxemia
We would suspect tension pneumothorax if we observed what with the pt?
5
- Labored breathing
- Tachycardia
- Hypotension
- Tracheal shift
- JVD
If there is a serious pneumothorax it can be rapidly fatal. How should we treat? 2
- Thorocentesis. 16 gauge. Over the second rib midclaviclular line
- Chest tube
What is shock?
Shock- inability to perfuse at the cellular level
