NTG for APE and Broncoconstriction Flashcards

1
Q

Patho of ape

A

acute pulmonary edema occurs when fluid shifts from the intravascular space to the interstitum and eventually into the alveolar space. hydorstatic p in the pulm vessels exceed the oncotic p pushing the fluid out of the extravascular.

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2
Q

What causes ape?

A

most commonly is a cardgiogenic cause such as CHF or LVF .
other causes: infection, inhaled toxins, radiation, pneumonia renal dysfunction

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3
Q

Patho of CHF

A

Loss of normal contactile ability which can cause congestions and fluids to leak into the lungs during exacerbations.

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4
Q

what causes CHF

A

Chronic HTN, diabetes, old MI, inflammation etc.

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5
Q

Presentation of APE

A

crackles, tachypnea, pale, cool , cyanosis, tachycardia frothy/pink sputum ( severe), accessory muscle use, dyspnea.

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6
Q

Asthma patho

A

chronic inflammation of the air passageways that cuses bronchile hyperactivity, inflammation, bronchoconstriction, wheeze and mucous production.

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7
Q

what causes asthma exacerbations?

A

allergies, exercise, cold air, etc.

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8
Q

patho of asthma exacerbation

A

release of inflammatory mediators ( histamine, prostaglandins leukotrienes), response causes damage to the epithelial layer of a/w’s causes wheeze, dyspnea, chest tightness , and cough. Air trapping occurs bc muscle surrounding the a/w tighten narrowing the a/w’s.

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9
Q

types of meds for asthma?

A

long-term meds (controllers)
- anti-inflammatory agents ( corticosteroids, budesonides)
- leukotriene inhibitors
quick relief/ rescue meds
- beta 2 agonists ( short/long acting)
short acting
- anticohlinergics ( Salbutamol,ipratropium/atrovent)
-systemic corticosteroids
- leukotriene receptor agonists

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10
Q

Emphysema patho

A

caused by life long smoking/2nd hand smoking that destroys alveolar septa and structures like the ge surface area. causes loss of recoil in bronchial walls, inflammation, mucous plugging, hyperinflation, Co2 retention

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11
Q

Chronic bronchitis patho

A

chronic a/w inflammation that causes an over production of thick mucous that blocks the a/w but the alveolar ge stays intact

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12
Q

how to asses if a pt is SOB

A

Distress, increased rr, accessory muscle use, <3 word dyspnea

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13
Q

acute cariogenic pulm edema indications

A

Moderate to severe resp distress & suspected acute cardiogenic pulm edema

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14
Q

Acute cardiogenic pulm edema Conditions

A

age: >/= 18 yrs, hr 60-159 bpm, normotension

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15
Q

Contraindications NTG for acep

A

a/s to nitrates, phophodiesterase inhibitor use in last 48 hours, ABP drops 1/3 or more of initial values after NTG given

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16
Q

TX for ACEP NTG

A

SBP: >/= 100mmHG-<140 mmhg, Iv/or HX ( yes), SL, 0.3or 0.4mg, max=0.4mg, 5 mins, 6 doses
SBP: >/140 mmhg, Iv or HX ( no), SL, 0.3-0.4mg, Max=0.4mg, 5 mins, 6 doses
SBP >/=140 mmhg, iv/hx ( yes), SL, 0.6-0.8 mg, 0.8mg ( max), 5 min, 6 doses

17
Q

bronchoconstriction medical directive indications

A

resp distress ad Suspected bronchoconstriction

18
Q

bronchoconstriction conditions

A

Sal=none epi; bvm resps, hx of asthma, Dex: hx of asthma, copd, or 20 pk yr smoking

19
Q

bronchoconstriciton tx

A

SAL: <25kg, mdi=600mcg, NEB=2.5mg, 5 mins, 3doses
>/=25kg, Mdi 800 mcg, NEB5mg, 5 mins, 3 doses

EPI= im, 1:100, 0.01mg/kg, 0.5mg ( dose), 1

Dex: Po,Im, IV, 0.5mg/kg, 8mg ( max), 1 dose

20
Q

Salbutamol toxicity s/s:

A

tremors, tachycardia, hypokalemia, cardiac arrhythmias etc.

21
Q

what is the pro of using dex

A

long acting corticosteroid that lowers hospital stays and advanced tx for pts

22
Q

Dex should not be given with…

A

other corticosteroids bc it will inhibits the function of dex and wont illicit any beneficial effects

23
Q
A