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Pulmonology 2 > Respiratory emergencies > Flashcards

Respiratory emergencies Flashcards

1
Q

The decision to intubate is determined upon what 3 things?

A
  1. ) Failure to Protect the airway?
  2. ) Failure to Oxygenation?
  3. ) Failure to Ventilation?

*if yes to any of these, intubate!

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2
Q

In a critical care situation, what are 3 questions you should be thinking when assessing dyspnea?

A
  • Does this patient need to be intubated immediately?
  • is this rapidly reversible?
  • Can he/she run?
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3
Q

Failure to oxygenate/ventilate = ?

A

respiratory failure

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4
Q

What are the two types of respiratory failure and their subtypes?

A 
Type1: Hypoxemic
-p02 less than 60
Subtypes: 
-Low Pi02
-hypoventilation 
-Diffusion 
-Shunt
-V/Q mismatch
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5
Q

How do you tell the difference between shunt and V/Q mismatch?

A

if you give the patient O2 and nothing happens you know its a shunting problem. If you give O2 and the underlying problem is a V/Q mismatch you will see their O2 increase.
**most cases are a V/Q mismatch.

Type 2: Hypercapneic

  • PCO2 greater than 50 (if not a chronic retainer)
  • increased CO2 production (sepsis, fever, burns)
  • alveolar hypoventilation
  • -Reduced minute ventilation
  • -increased dead space.
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6
Q

Signs of hypoxemia

A
  • cyanosis
  • restlessness
  • confusion
  • anxiety
  • delerium
  • tachypnea
  • brady or tachypnea
  • HTN
  • cardiac dysrhythmias
  • tremor
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7
Q

Signs of hypercapnia

A
  • dyspnea
  • HA
  • HTN
  • peripheral and conjuntival hyperemia
  • tachycardia
  • tachypnea
  • impaired conciousness
  • papilledema
  • lethargy
  • AMS
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8
Q

Evaluation of emergent dyspnea

A 
O2 sats
ABGs
Chemistry
CXR 
EKG
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9
Q

Which two diseases have good outcomes with the use of BIPAP?

A

COPD, CHF

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10
Q

“Can the patient run for his/her life?” Why do we assess this?

A
  • were assessing their reserve *how much work are they doing?
  • how long have they been doing it?
  • what effect is it having?
  • *How long can they continue doing it?
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11
Q

Acute Asthma

  • sx of impending respiratory failure
  • whats happening to their tidal volume?
  • Residual volume?
  • co2?
A
  • inability to maintain respiratory effort and rate
  • cyanosis
  • depressed mental status
  • severe hypoxemia

Tidal volume: decreases
Residual volume: decreases
CO2: increases

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12
Q

Acute Asthma: assessment

A
  • measure peak flow
  • supplemental O2
  • ABGs are generally not useful initially
  • Establish IV
  • CXR generally not useful initially
  • Frequent reassessment to determine if intubation and mechanical ventilation is needed**
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13
Q

What does peak flow measurement tell us?

What is peak flow less than 40% of predicted categorized as?

A
  • the severity of airway obstruction

- less than 40% predicted is SEVERE

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14
Q

Danger signs that signify impending ventilatory failure?

A
  • deteriorating mental status
  • silent chest
  • pulsus paradoxus
  • CO2 retention/elevated PCO2
  • Acidosis
  • Cyanosis
  • Hypoxemia
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15
Q

What is pulsus paradoxus? what diseases might you find this?

A

-increased lung volumes lead to very high negative pressures in the chest causing more venous return to get “sucked in.” This increased venous return can be dramatic enough to distend the right ventricle to the point of compressing the left ventricle, thus affecting left ventricular outflow. Once can feel decreased peripheral pulses during inspiration.

May occur with asthma, cardiac tampanode, pericarditis.

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16
Q

Acute Ashtma Medical Therapy

A
  • albeuterol
  • ipatropium bromide
  • methylprednisolone
  • magnesium sulfate (relaxes smooth muscle)
  • Epinephrine (for suspected anaphylactic rxn or unable to use inhaled bronchodilator)
  • Terbutaline (only when severe and unresponsive to standard therapy)
17
Q

COPD Exacerbation Tx

A
  • Ipratropium (bronchodilator)
  • Albeuterol (bronchodilator)
  • Corticosteroids
  • Abx
  • Oxygenation Fi02 to achieve pO2 greater than 55-60 or SaO2 90-93%.
  • watch for CO2 retention!
18
Q

High Altitude Illness

-what are the types?

A
  • acute mountain sickness (AMS)
  • high altitude pulmonary edema (HAPE)
  • High altitude cerebral edema (HACE)
19
Q

what is hypobaric hypoxia?

A

Hypobaric hypoxia is a condition where the body is deprived of a sufficient supply of oxygen from the air to supply for body tissues whether in quantity or molecular concentration. Hypoxic hypoxia affects the body’s ability to transfer oxygen from the lungs to the bloodstream.

20
Q

What happens physiologically to the body when it is exposed to hypobaric hypoxic conditions?

A

fluid retention

vasoconstriction

pulmonary artery HTN

increased endothelial permeability

edema

21
Q

Acute Mountain sickness presentation:

  • onset
  • sx
  • tx
A

onset: several hours at new altitude, maximum severity 24-48hrs

Sx:

  • HA plus 1 or more of the following:
  • -GI ubset
  • -generalized weakness/fatigue
  • -dizziness or lightheaded
  • -difficulty sleeping

Tx:

  • oxygen
  • gradual descent and acetazolamide (carbonic anhydrase inhibitor),
  • others for sx relief:
  • -non-narcotic analgesic
  • -antiemetics
22
Q

High Altitude Pulmonary Edema (HAPE)

  • onset
  • sx
  • tx
A

onset: 2-4 days after arrival of 8000feet, exacerbated by heavy physical activity

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

Tx:

  • Hyperbaric therapy
  • descent of at least 2000ft
  • oxygen and CPAP
  • rest/warmth
  • Acetazolamide, dexamethasone, sildenafil, nifedipine, salmeterol (LABA)
23
Q

Smoke Inhalation;

-3 main consequences

A
  1. impaired oxygenation
  2. thermal injury to upper airway
  3. injury to the lower airway and lung parenchyma
24
Q

What are three things that may be inhaled cause impaired oxygenation?

A
  • Hypoemic gas mixture
  • carbon monoxide
  • cyanide
25
Q

Thermal injury of the upper airway:

  • why was the lower airway not injured?
  • effects of thermal injury
  • prophylaxis
A
  • usually the gases are cooled enough to not burn the tissues below the level of the vocal cords, except in case of steam inhalation.
  • effects: mucosal edema, upper airway obstruction, inability to clear oral secretions.
  • prophylactic intubation may be required.
26
Q

Inhalation of toxic gases results in injury to the lower airways and lung parenchyma, what are some of the effects of injury?

A
  • sputum production
  • bronchospasm
  • dyspnea
  • tachypnea
  • tachycardia
  • diffuse wheezing and rhonchi
  • ARDS 1-2 days after exposure
  • Sloughing of bronchiolar mucoas in 1-2 days
  • pna common by day 5-7
27
Q

Tx of smoke inhalation

A
  • supplemental O2 (humidified)
  • Bronchodilators
  • Suctioning of Debris from airway
  • maintain a patent airway (likely will need intubation)
  • PEEP if bronchoiolar edema

PEEP= is the pressure in the lungs (alveolar pressure) above atmospheric pressure (the pressure outside of the body) that exists at the end of expiration.

28
Q

Sx of CO poisoning?

A

-HA, fatigue, malaise, flulike, nausea, confusion, paresthesias, stroke, coma, sz, resp arreest.

chest pain, myocardial ischemia, palpitations, dysrhythmias, poor capillary refil, hypotension, cardiac arrest.

29
Q

with CO poisoning can pulse oximetry be used to access oxygenation? Why or why not?

what is a common sx?

A
  • cannot! because the device confuses COHgb for O2HGB and gives falsely high values.
  • cherry red coloring of the skin with CO poisoning.
30
Q

Tx of CO poisoning?

A

100% O2 for 4hrs!

-May use hyperbaric oxygen therapy when treating severe cases of CO poisoning (AMS, hx of LOC, Coma, Myocardial ischemia, pregnant with COhgb greater than 15%)

31
Q

Cyanide Poisoning

  • what are some common sources?
  • onset
  • who do we consider this in always?
A

Sources: fruit pits (peaches, plums, cherries)
-product of burning wool, nylon, cotton, silk

Onset:
-based upon route of exposure and amount.

ALways consider this in patients with smoke inhalation who have CNS or CV findings.
*CN gas 20x more toxic than CO.

32
Q

Cyanide Poisoning;

-sx

A

sx:
- HA
- dizziness
- nausea
- abd pain
- anxiety
- confusion
- syncope
- shock,
- coma
- death

33
Q

how does cyanide poisoning affect each of the following:

  • lactate
  • anion gap
  • venous oxygen sats
A

increased lactate production

anion gap metabolic acidosis

elevated venous oxygen sats.

34
Q

Cyanide poisoning tx

A 
inhaled nitrites (amyl nitrites) 
-scavenges free cyanide 
injected nitrites (sodium nitrite) 
-scavenges free cyanide

injected sodium thiosulfate
-enhances the conversion of cyanide to thiocyanate to be excreted by the kidneys)

this is CI with concomitant CO poisioning!!!!***

35
Q

Cyanide poisoning pearls

A
  • no evidence of improvement with hyperbaric oxygen
  • when cyanide is suspected (bradycaridc, hypotensive, comatose) patient MUST be given the antidote even though it may lower BP further.
  • pt exposed to HC gas from a fire may have both cyanide and CO exposure!
36
Q

Pneumothorax

-PE findings

A

PE:

  • decreased breath sounds on affected side
  • hyperresonant to percussion
  • hypoxemia
37
Q

what is a tension pneumothorax?

A

Tension pneumothorax is the progressive build-up of air within the pleural space, usually due to a lung laceration which allows air to escape into the pleural space but not to return. Positive pressure ventilation may exacerbate this ‘one-way-valve’ effect.

38
Q

Suspect pneumothorax if:….

A 
labored breathing
tachycardia
hypotension 
tracheal shift
JVD
39
Q

Treatment of pneumothorax?

A
  • needle decompression

- chest tube

Pulmonology 2 (8 decks)

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