Clin Med: Pulm (3)

asthma pathophysiology

• what is the cause?

• manifestation?

• acute? chronic?

• how is expiratory airflow changed? FEV1 and FEV1/FVC?

cause: AIRWAY INFLAMMATION

manifestation: wheezing

chronic, inflammatory lung disease

prolonged expiratory airflow (decrease I/E ratio) where FEV1 and FEV1/FVC <80% predicted

asthma signs and symptoms (4)

increased airway responsiveness (mechanism) due to triggering stimuli leading to:

1. cough

2. wheezing

3. dyspnea

4. chest tightness

triggering stimuli for asthma

Nonspecific stimuli includes stress, exercise, lack of sleep

Environmental triggers include viral URI’s, environmental pollutants, allergens, cold air

asthmatic events

• are they reversible?

• how?

partially OR completely reversible w/ use of bronchodilator (improves expiratory airflow by at least 12%)

hallmarks of asthma (things that result in airflow obstruction) (7)

1. smooth muscle hypertrophy (narrows airways)

   1. muscle thickening → encroaches on airway lumen

2. airway wall edema

   1. edema = fluid leaking to interstitial

3. intraluminal mucus hypersecretion and accumulation

   1. mucus cells hyper secrete → airway full of mucus

4. inflammatory cell infiltration

5. basement membrane thickening

   1. BM is b/w endothelial cells + capillary beds

   2. due to general ischemic of airway

6. neovascularization

   1. new blood vessels grow b/c of chronic hypoxic issues

   2. not good long-term b/c they rupture easily and cause blood accumulation in tissue

7. epithelial injury

nocturnal aggravation of asthma (5)

• what is a rare complication?

1. circadian production of histamine (inc at night, can cause bronchoconstriction)

2. dust mites in pillow

3. dust blowing from fans/furnace

4. GERD (recumbency)

   1. lying flat → acid regurg → coughing/bronchospasm

5. OSA

rarely, remodeling can happen over years

asthma epidemiology

• who is more likely to have asthma?

• most common chronic disease where?

• what regional differences?

• does city/rural/surburban living affect chances of having asthma?

more likely to have asthma: children, women, african and hispanics

most common chronic disease in childhood in developed country

residents of northeast and midwest more likely (Regional diffs)

chances of having asthma is unrelated to city vs. rural/suburban living

asthma associated condition in adults (10)

1. Atopy (A like Apple, Topy like Tby with P): atopic dermatitis, allergic conjunctivitis/rhinitis, asthma

   1. Most people with atopy have asthma to some degree

   2. Atopy also runs in families, fun facts

2. Obesity (associated with higher asthma rates)

3. Chronic sinusitis

4. GERD

5. OSA

6. Stress/Depression

7. Exercise

8. Food allergies

9. Vocal cord dysfunction

10. Allergic bronchopulmonary aspergillosis (rare)

asthma associated conditions in children (5)

1. RSV

2. Foreign body aspiration

3. Bronchopulmonary dysplasia (due to treatment given to children)

4. Cystic fibrosis

5. Obesity

risk factors for asthma (4)

1. Host factor

   1. Genetic predisposition

   2. Gender

   3. Race

2. Environmental

   1. Viral infections

   2. animal/airborne allergens

   3. Smoke

3. Aspirin or NSAIDs hypersensitivity

4. Use of B blockers

   1. Sympathetic NS helps bronchodilate through B2 receptors

   2. If you use BB→ inhibits bronchodilation → can worsen bronchospasm

Intermittent Asthma

• how often daytime asthma symptoms occur?

• awaken at night?

• use of rescue inhaler?

• filling of rescue inhaler prescription?

• requires oral glucocorticoids?

• interference with normal activities b/w exacerbations?

• FEV1 and FEV/FVC ratio?

1. Daytime asthma symptoms occurring =< 2 days/wk

2. Awakened by sometimes =< 2 nights/month

3. Use of rescue inhaler =<2x/wk

4. Filling of rescue inhaler prescription =< 2x/year

5. <2 exacerbations/yr requiring oral glucocorticoids

6. No interference with normal activities between exacerbations

7. Between exacerbations, FEV1 and FEV/FVC ratio that are consistently >= 80% of predicted normal

   1. During exacerbations, your PFTs might be off

   2. Most exercise induced asthma would fall under this category ^^

mild persistent asthma

• how often daytime asthma symptoms occur?

• awaken at night?

• use of rescue inhaler?

• filling of rescue inhaler prescription?

• requires oral glucocorticoids?

• interference with normal activities b/w exacerbations?

• FEV1 and FEV/FVC ratio?

1. Symptoms more than 2x/wk (but not daily)

2. 3-4 nocturnal awakenings/month due to asthma

3. Use of rescue inhaler to relieve symptoms more than 2x/wk but not daily

4. Filling of rescue inhaler prescription >2x/year

5. 2 or more exacerbations/yr requiring oral glucocorticoids

6. Minor interference with normal activities

7. FEV1 and FEV1/FVC ratio between exacerbations are >= 80% of predicted

moderate persistent asthma

• how often are symptoms?

• nocturnal awakening?

• rescue inhaler usage?

• requiring oral glucocorticoids?

• limitation?

• FEV1 and FEV1/FVC?

• Daily symptoms

• Nocturnal awakening more than once per week

• Daily relief for rescue inhaler for symptom relief

• 2=+ exacerbations/yr requiring oral glucocorticoids

• Moderate limitation in normal activity between exacerbations

• FEV1 and FEV1/FVC = 60-80% predicted

severe persistent asthma

• how long are symptoms?

• nocturnal awakening?

• glucocorticoids?

• limitations?

• FEV1 or FEV1/FVC ratio?

• important note?

Symptoms of asthma all day

Nocturnal awakening nightly

CAN EVENTUALLY CAUSE ARCHITECTURE CHANGE (asthma -> COPD)

2=+ exacerbations/yr requiring oral glucocorticoids

Extreme limitation in normal activity between exacerbations

FEV1 or FEV1/FVC ratio between exacerbations are <60% predicted

asthma symptoms chart

asthma history (4)

Wheezing, cough, dyspnea on exertion, chest pain/burning

asthma physical exam

• general (3)

• severe cases (4)

• cardio-respiratory failure (4)

• Wheezing, hyperresonance to percussion (hyperexpanded), tachypnea

• In more severe cases:

  • Wheezing decreases (they’re not moving air anymore = no turbulence)

  • Pt unable to lie flat, speak full sentences

  • Use of accessory muscles, intercostal retractions

    • Intercostal muscles, sternocleidomastoid, internal scalene muscles

    • Nostril flaring b/c of nasalis muscle

• Diaphoresis

• Impending cardio-respiratory failure (

  • Silent chest (not moving any air anymore)

  • Cyanosis (not oxygenated)

  • Mental status changes (brain is becoming hypoxic)

  • Patient appears in extremis (generally looks bad = extremis)

tests for asthma (5)

1. Blood: might find eosinophilia or elevated serum IgE levels (mediators in a Type I sensitivity reaction)

2. Spirometry: Normal test does not rule out asthma

   1. If reduced predicted ratio of FEV1/FVC reverses (12% increase) with bronchodilators = asthma (specific test)

3. Broncho-provocation: (methacholine, histamine, cold air, or exercise) to stimulate bronchoconstriction, useful in atypical presentation/normal baseline spirometry

   1. Abnormal test result not entirely specific for asthma, but a normal test result excludes asthma (sensitive test)

4. Peak expiratory flow rate: used for MONITORING of symptoms and for following efficacy of treatment. DO NOT use for diagnosis

5. Chest x-ray: (for excluding alternative/complicated diagnosis. during asthma attack, lungs are hyperinflated, diaphragm is flattened)

controlling triggers of asthma

Hard to avoid: URI, hormonal fluctuations, exercise, emotions, cold air

Inhaled allergens: pollen, dust mites, molds, animal dander, and cockroaches (use air purifier, change your pillow, vacuum)

Respiratory irritants: tobacco smoke, wood smoke (think molds) from stoves or fireplaces, strong perfumes and other chemical vapors, and air pollutants

meds that aggravate asthma (4)

• beta blockers

• Aspirin

• non-COX 2 selective non-steroidal anti-inflammatory

• sulfites (beer, wine, processed potatoes, sauerkraut, dried fruit, shrimp)

beta blockers aggravating asthma

• what do they do?

• why is this an issue if you are using a BB and pt has asthma/COPD exacerbation?

• can trigger a asthma attack (esp non-selective BB like propranolol)

• blocks B2 receptors in lungs (B2: bronchodilation)

  • if pt is on BB and has asthma/COPD exacerbation, beta-agonist bronchodilators may not work well because the receptors they target are already blocked

  • → use selective B2 agonists and avoid non-selective BB

  • you can use beta 1 blockers but be careful if they have heart disease/asthma

atopy triad

1. atopic dermatitis (eczema)

2. asthma

3. allergic rhinitis (hay fever)

cardioselective beta blockers

Metoprolol (Toprol)

Atenolol (Tenormin)

Bisoprolol (Zebeta)

Betaxolol (Betopic, for glaucoma eye drops)

Acebutolol (Sectral)

aspirin and non-cox2 selective non-steroidal anti-inflammatory drugs aggravating asthma

• what population can this trigger asthma symptoms?

• what condition can lead to higher risk of aspirin-exacerbated respiratory disease?

• what asthma is uncommon in children?

• what asthma is common with children?

• can trigger asthma symptoms in 3-5% ADULT pts

• asthma pts with nasal polyps have higher chance of getting aspirin-exacerbated respiratory disease (known as “Triad Asthma” or Samter’s Triad)

• aspirin-sensitive asthma (and Samter’s Triad) UNCOMMON in children

• asthma associated with atopy is COMMON in children

Samter’s Triad

asthma, aspirin, and nasal polyps

immunizations for asthmatics

• can asthmatics get flu shots?

• flu mist spray vs. flu vaccine?

• when should you not get a shot?

all asthmatics can get flu shots

• flu mist spray: used for healthy ages 2-49 not pregnant and no asthma (b/c they have a live, intenuated virus)

• flu vaccine: NOT live virus

• children 6-24 months should be vaccinated IM

  • no shots if under 6 months

  • >8 y/o = 2 doses (second “half dose” = booster)

• Pneumovax as indicated

pharmacotherapy for asthma

• how should pt with mild and infrequent symptoms be treated?

• intensity of tx should match severity of asthma symptoms (if they have qualities of different categories, treat as the one they’re more severe in)

• pt with mild and infrequent symptoms = treated intermittently with rescue inhaler (non-sched fashion)

rescue inhalers

consist of formoterol/budenoside (symbicort) or formoterol/beclomethasone (Fostair)

A second choice is use of a pure SABA such as albuterol. The goal is quick relief of symptoms (I.e. rescue treatment)

escalating use of rescue inhaler

• how much?

• what is this a warning sign of?

>6-8 puffs/day from MDI (multi-dose inhaler) or use exceeding one canister per month

warning sign that patient’s underlying disease activity is not adequately controlled

patient with mild-severe persistent asthma

• what tx should they get?

scheduled meds AND rescue treatment

asthma pharmacotherapy Rule of 2’s

If answer is yes to any of these, asthma is not in optimal control = persistent-type asthmatic category

Do you:

Have symptoms >2 days a week

Use a rescue inhaler >2 times a week

Have nighttime symptoms > 2 times a month

Refill rescue inhaler > 2 times a year

Have a peak flow during exacerbation that is less than 2 times 10% (20%) from baseline (Shows severity of exacerbations)

short acting beta agonists (SABAs)

• examples

• what happens with repeated exposure?

• good?

• bad?

• what is something you can add to SABA to offset some of the effects?

albuterol, levalbuterol, pirbuterol delivered by a HFA MDI (hydrofluoroalkane metered dose inhaler) or nebulizer, for bronchodilation

associated with increased airway hyper-responsiveness, increased allergic response, and increased eosinophilic infiltration of bronchial tissues

Good: the time of onset is very short/fast-acting drug

Bad: the more you use rescue inhaler beta agonist, the more the beta receptors decrease in number on the cell membrane and decrease in sensitivity to agonist = downregulating regulator. Risk of not working anymore (uh oh!)

Repeated exposure to SABAs → drug less effective over time → risk of failure at crucial time of needed

If you add steroid to short-acting beta agonist, you offset some of the loss in receptor number and sensitivity, allergic reaction responses, and eosinophilic infiltration of the bronchial tissues

inhaled glucocorticoids (steroids) - 2nd tier

• what is this good for? what should you add to this for that?

• ____ agent of choice for pt with persistent asthma

• good? (3)

• bad (3)

good maintenance drug/therapy

scheduled inhaled glucocorticoids are the primary treatment used to reduce airway inflammation and prevent symptoms

second agents of choice for pts w/ persistent asthma (after rescue inhalers)

reduces frequency of symptoms (and need for inhaled bronchodilators), improves overall quality of life, and decreases risk of exacerbations (can use nebulized form)

NOT for rescue, onset is slow, do NOT use alone for COPD

inhaled glucocorticoid examples (4)

Budesonide (Pulmicort) - available for nebulization or MDI

Mometasone (Asmanex)

Fluticasone (Flovent)

Beclomethasone (QVar)

long-acting beta agonists (LABAs) - 3rd tier

• can you use alone?

• what should this be combined with?

• examples of LABA

• what are combination inhalers? when are they preferred?

• warning with LABA?

Bronchodilators, but do NOT use alone as long-term controllers

MUST BE USED COMBINED with inhaled gluco-corticoids (steroids) for asthmatics

Examples include salmetrol (Serevent) and formoterol (Foradil)

Combination inhalers have LABA and a ICS, used when ICS alone is not enough to control asthma symptoms

Preferred in all forms of persistent disease (Advair, Symbicort, Dulera)

Repeated exposure to LABAs → drug less effective over time → risk of failure at crucial time of needed

muscarinic antagonists (SAMAs and LAMAs) - 4th tier

• cholinergic effects

  • what is a result of anticholinergic agents?

AKA anticholinergic agents

cholinergic mediates effects of parasympathetic system, which induces bronchial smooth muscle contraction (nono!)

using anticholinergic agents blocks cholinergic receptors = no bronchospasm

short acting muscarinic agents (SAMA) - 4th tier

• example

• when are they useful?

• better for acute or maintenance tx w/ SABA?

• what other drug can SAMA be combined with?

• speed of effectiveness

Ipratopium bromide (Atrovent): short acting and useful in nebulized form

SAMA + SABA combo for acute treatment (rather than maintenance)

SAMA + albuterol: dunoeb (beta 2 agonist + muscarinic antagonist) and in MDI as combivent

Takes a while to work/slow

long acting muscarinic agents (LAMAs)

• examples

• when are they useful?

• why are they not good for rescue/monotherapy?

• add-on treatment for what patients?

• warning

Tiotropium, aclidinium, umeclidinium, and glycopyrrolate

long acting and useful in control of moderate and severe persistent asthma

NOT good for rescue/monotherapy b/c they work slower (30 mins) and causes less bronchodilation compared to beta 2 agonist

add-on treatment for pts who are on medium dose ICS-LABA

high risk of severe exacerbations

should be used first before muscarinic/anticholinergic agents

beta agonist

leukotriene inhibitors - 4th tier (others)

• what do leukotrienes do?

• are they as effective as inhaled glucocorticoids?

• when is this the drug of choice?

• drug examples w/ dose

• rare case reports what? what do you do as a result?

Block leukotrienes = less inflammation, allergic response, and bronchoconstriction

In general, not as effective as inhaled glucocorticoids

Drugs of choice in aspirin-sensitive asthmatics

Zafirleukast (Accolate) 20 mg po bid and monteleukast (Singulair) 10 mg po qd

Rare case reports of depression and SI (screen before and during treatment)

Lipoxygenase pathway inhibitor - 4th tier (others)

• drug example

• when would you consider using this?

Zileuton (Zyflo); adjunctive (additional therapy) treatment in patients >= 12 years

arachidonic acid pathway

prostaglandins and leukotrienes are the two formed in this pathway

in cell membrane, a membrane lipid → makes leukotrienes and PGE

if cell has phospholipase-A2, then the membrane lipid → arachidonic acid

prostaglandin part of arachidonic acid pathway

arachidonic acid using COX-1 and COX-2 → converted to endoperoxides (PGG2, PGH2)  → prostaglandins, prostacyclin, and thromboxane

endoperoxides

progenitor (parent/”before”) for prostaglandins

prostacyclin effects (2)

decreases plt aggregation and uterine tone, vasodilates

prostaglandins effects (4)

1. mediator of pain

2. increases uterine tone

3. increases temp (fever)

4. decreases vascular tone

thromboxane

increases plt aggregation = vasoconstriction

leukotrienes part of arachidonic acid pathway

arachidonic acid with lipoxygenase → HPETES → leukotrienes

lipoxygenase

converted to hydroperoxides (HPETEs) → makes leukotrienes

hydroperoxides

progenitor (before) for leukotrienes

leukotrienes

chemo-taxic agents, makes neutrophils move around. lots of these = bronchoconstriction. in an asthmatic, making too much leukotriene will trigger asthma

corticosteroids

inhibits phospholipase A2 and certain protein synthesis needed to make COX-1 and COX-2

High up on the list. If you can block the pathway up there, you’ll get less stuff coming out of it

NSAIDS, ASA, and COX-2 inhibitors

• what do they do?

• effects (4)

block COX-1 and COX-2’s ability to convert arachidonic acid -> endoperoxides

effects:

1. less pain (they block prostaglandins, which is a mediator of pain)

2. good for fever

3. anti-inflammatory (they block prostacyclin and thromboxane)

4. INCREASE formation of leukotrienes (b/c the PGE path is blocked) → bronchoconstriction

Nonsteroidal Anti-inflammatory Drug-exacerbated Respiratory Disease (N-ERD)

Taking NSAIDs (which block COX-1 enzyme) → shift toward the leukotriene pathway → triggers bronchoconstriction

Zileuton

block the formation of leukotriene side of the cascade because you block lipoxygenase

steroid + fast acting medicine

the preferred combo for inhalers

ie: formoterol + ICS (like Symbicort) = daily control and rescue

albuterol + steroid is good too

LABA

should NEVER be used by itself - use with a steroid

Theophylline - 4th tier (other)

• good

• bad

Good: inexpensive, may have anti-inflammatory and immunomodulary effects in low doses (lower than amt needed for bronchodilation effects), bronchodilator

Bad: low therapeutic index -> theotoxicity and many drug interactions

immunosuppressive agents - 5th tier

• systemic corticosteroids

• immunomodulators

systemic corticosteroids (5th tier)

• when do you give to patients?

• how long for mod-severe asthma?

• acute vs. maintenance?

given to all pts with acute asthma exacerbations to reduce inflammation

mod-severe asthma: short-term as add on for 7 days in adults and children 3 days = no tapering due to no adrenal gland suppression

NOT FOR MAINTENANCE OR LONG-TERM

immunomodulators (5th tier)

• name the two drugs and what they do

• name important SE in one drug

• what is something both drugs do?

1. Omalizumab (Xolair): Anti IgE antibody (mediates type I hypersensitivity reactions, if you block the IgE, you reduce the bronchospasm); adjunctive therapy for patients >= 12 years with allergies and severe persistent asthma. Administered subcutaneously, significant side effects such as anaphylaxis

   1. Expensive

   2. Inactivates IgE

2. Benralizumab (Fasenra): Anti eosinophil antibody for patients with asthma and big eosinophil counts

   1. Inactivates eosinophils

BOTH = anti-inflammatory → prevents bronchospasm

cromoglycate agent (historical interest)

• what does it do?

• when it is used?

• treatment choice for asthma?

• fast or slow acting?

Prevent mast cell degranulation -> anti-inflammatory, but have no bronchodilator effect.

Used for prophylaxis before exercise. Not a treatment choice for asthma

Type I hypersensitivity drug

Quick acting

general order for asthma meds

• first general thing every one gets

• asthma vs. COPD tx

1. rescue inhaler (Everybody)

2. ASTHMA: next is ICS or ICS/LABA

3. COPD: next is LAMA → LABA → LABA/ICS

4. start adding stuff: LABA, LAMA, etc

intermittent asthma preferred tx

formoterol/ICS or albuterol/ICS* (*pick this one unless insurance doesn’t cover)

mild persistent asthma preferred tx

formoterol/ICS on a scheduled basis and PRN for rescue. If you use albuterol for rescue, add an ICS or a long-acting LABA. basically add a steroid in there for mild

moderate persistent asthma preferred tx

play around with dose of LABA/ICS, add a third drug (either leukotriene inhibitor or a LAMA). If pt has been using SABA PRN/ICS alone, change ICS to LABA/ICS (aka prescribe combined things so the patient doesn’t have a ton of inhalers)

severe persistent asthma preferred tx

add leukotriene inhibitor or LAMA to the regimen (Whichever of the two were not added previously)

Continue to add or substitute other agents until the right combo is found

if still using SABA, add LAMA or leukotriene inhibitor next. Then add the other if needed. Continue to add or substitute other agents until right combination is found

managing acute asthma exacerbations (10)

1. Assess severity of attack (HR, RR, O2 sat, peak flow)

2. Check adherence, environmental control, comorbidities

3. Give inhaled SABA early and frequency

4. Consider concomitant use of ipratropium (Atrovent) for severe exacerbations

5. Start systemic glucocorticoids if no immediate response to the inhaled SABA

   1. You want systemic steroids on board (Even though they take a while to work)

6. In more severe cases, subcutaneous epinephrine or terbutaline (Breathine)

   1. Terbutaline: pure beta 2 agonist, given subcutaneously

7. Frequently (q1-2h) objective assessment of the response ot therapy until definite, sustained improvement is documented

8. Admit patients who do not respond well after 4-6 h to a setting of high surveillance and care

9. Educate patients about the principles of self-management for early recognition and treatment of a recurrent attack and develop an “asthma action plane” for recurrent symptoms

10. Step up maintenance meds, if needed. May try stepping back down once symptoms are well controlled for 3 months (to see if it’s a seasonal issue)

severe asthma attack findings (8)

• Marked breathlessness

• Tripoding

  • “Sniffing Position”: “jutting” out head (smelling roses)

    • You are making the airway as straight as possible from the mouth -> trachea (less turbulent airflow/more laminar flow)

    • In nose, you have more turbulent flow to help warm air and remove the viruses and bacteria

• Inability to speak more than short phrases

• Use of accessory muscles, retractions

• Drowsiness

  • Not ventilation = carbon dioxide rises, in high levels CO2 will suppress your neurological function (CO2 narcosis)

  • Drowsy because you’re hypoxic and you have CO2 narcosis

• Inability to lie supine

• Peak flow <50% predicted/personal best

• Pulse oximetry <90%

Risk factors for Fatal Asthma

1. Use of LABAs for too long and without ICS

   1. Never take away rescue inhaler or the steroid** you can remove LABAs though, or replace with a leukotriene for 6 months to increase number and sensitivity of B receptor again “Drug Holidays” for LABAs

2. Use of >2 canisters of short-acting beta agonist/mo

3. Previous SEVERE exacerbation (intubation/ICU admission)

4. 2 =+ hospitalizations for asthma in the past year

5. 3 =+ ED visits for asthma in the past year

6. Hospitalization or ED visit for asthma in past month

7. Difficulty perceiving asthma symptoms or severity

8. Low economic status, inner city residence, illicit drug use, major psychosocial problems

9. Comorbidities (CVD, chronic lung, psych disease)

pO2 = 60 mmHg

O2 stat of 90%

(2N1S)

Criteria for intubating a patient with an asthma exacerbation

1. Pts with Hypoxemia pO2 < 60 mmHg (90% O2)

2. Pts with hypercapnia (excess CO2/elevated partial pressure of CO2) or even normal pCO2

   1. pCO2 should be LOW. if you see normal pCO2, that means pCO2 is getting higher → hypercapnia (think pseudonormal)

3. Pt exhaustion leading to respiratory arrest

hypoxemia

paO2 =< 60 mmHg

hypercarbia

paCO2 >= 50 mmHg

acidosis

pH =< 7.30

pH is a logarithmic curve

Small changes in pH will change the hydrogen ion concentration/acid

benefits of bipap and cpap (8)

1. Increased FRC (functional residual capacity)

2. Decreases work of breathing

3. Dec closing capacity = means airway closure happens at a lower lung volume compared to before you put them on the machine = good

4. Recruits alveoli

   1. Pops them back open/engage them -> decrease shunt

   2. Shunt = has blood but not air

5. Improves gas exchange

6. Reverses hypoventilation

7. Maintain upper airway patency

   1. Helps open airway if you have big tongue, tonsils, etc., that tends to collapse

8. Might decrease cardiac output (nonbeneficial result)

   1. b/c we normally breathe by negative pressure, whereas this machine is positive pressure = pushing air in you

   2. It increases mean intra-thoracic pressure over time = venous return decrease -> decrease preload -> decrease cardiac output

types of NIV (non-invasive ventilation)

• CPAP

• BiPAP

CPAP

• what does it normally start with?

• is pressure constant?

• why do neonates and infants get nasal cannulas?

• Constant pressure (Will not go below 5 cm of H2O even at the end of exhalation)

• Usually starts at 5 cm H2O

• Older kids-oro-nasal mask

• Binasal prongs for neonates and infants

• Works well in neonates and infants

  • I need a closed system. If there’s a leak, it’ll drop the pressure, which is why for older-adults it’s the whole mask

  • Infants are obligate nasal breathers

biPAP

• what is the inspiratory and expiratory pressure?

• who is this a better option for?

Inspiratory pressure (10-15 cm) (assists in inhalation = positive pressure peaks)

Expiratory pressure (5-10 cm)

Might be helpful for ventilatory problems

Better for older kids

CPAP airway affects

reduces closing capacity, slows down airway pressure, slows down exhalation, ensures minimum pressure in lungs → resistance in the lungs → prevents airway closure and slows emptying

good candidates for NIV (3)

Alert

Cooperative

Readily reversible cause

poor candidates for NIV (5)

Hemodynamic instability

UGI bleed (aspiration of blood a possibility)

Uncooperative

Large secretions or vomiting

Post upper abdominal or thoracic surgery (painful to expand chest)

Likely to fail for NIV (3)

Large acid-base derangements

ARDS

Persistent tachypnea (breathing rapidly -> dec time in exhalation -> airtrapping)

conditions good for NIV (4)

Pneumonia

Asthma

Bronchiolitis

OSA

pitfalls of NIV (5)

Hypotension

Aspiration

Must watch closer

Always be ready to intubate

Patient tolerance

Contraindications for NIV (10)

Cardiac or respiratory arrest

Non-respiratory organ failure

Severe encephalopathy (GCS < 10)

Severe upper GI bleeding

Hemodynamic instability or unstable cardiac arrhythmia

Facial or neurological surgery, trauma, deformity

Upper airway obstruction

Inability to cooperate/protect airway

Inability to clear secretions

High risk for vomiting/aspirations

ICU management of asthma (5)

1. intubation and mechanical ventilation

2. Magnesium: good smooth muscle relaxant

   1. Lowers BP in pregnancy and relaxes uterus

   2. Can turn off and on

   3. Good for relaxing broncho smooth muscle/bronchodilator

   4. Caffeine (part of the Methylxanthines class) and theophylline (is a chemical cousin of caffeine) = relieves bronchospasm (bronchodilator)

3. Ketamine: dissociative agent, unhooks brain from peripheral nervous system. Makes you indifferent to pain impulses. A great bronchodilator! But don’t give them ketamine without giving them a sedative, otherwise hallucinations

4. Heliox (helium/oxygen mixtures has a low viscosity)

   1. Less resistance to airflow compared to nitrogen/oxygen mixtures

5. ECMO (extracorporeal membrane oxygenation): bypasses lungs

Intubation

• what does it control?

• what does it require?

• what is the goal?

• what should you make sure?

Allows control of fiO2, RR, ventilatory pressures

Usually requires sedation

Goal is to support ventilation until bronchospasm can be reversed

Make sure bottom of tube is above carina, double check with CXR, otherwise only one lung will be ventilated

proactiveness in asthma (3)

Good primary care of asthma -> prevent severe exacerbations

Important to assess and re-assess severity and meds

Attention to environmental, socioeconomic factors, triggers