NTG for APE and Broncoconstriction

Question 1

Patho of ape

Answer 1

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.

Question 2

What causes ape?

Answer 2

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

Question 3

Patho of CHF

Answer 3

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

Question 4

what causes CHF

Answer 4

Chronic HTN, diabetes, old MI, inflammation etc.

Question 5

Presentation of APE

Answer 5

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

Question 6

Asthma patho

Answer 6

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

Question 7

what causes asthma exacerbations?

Answer 7

allergies, exercise, cold air, etc.

Question 8

patho of asthma exacerbation

Answer 8

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.

Question 9

types of meds for asthma?

Answer 9

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

Question 10

Emphysema patho

Answer 10

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

Question 11

Chronic bronchitis patho

Answer 11

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

Question 12

how to asses if a pt is SOB

Answer 12

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

Question 13

acute cariogenic pulm edema indications

Answer 13

Moderate to severe resp distress & suspected acute cardiogenic pulm edema

Question 14

Acute cardiogenic pulm edema Conditions

Answer 14

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

Question 15

Contraindications NTG for acep

Answer 15

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

Question 16

TX for ACEP NTG

Answer 16

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

Question 17

bronchoconstriction medical directive indications

Answer 17

resp distress ad Suspected bronchoconstriction

Question 18

bronchoconstriction conditions

Answer 18

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

Question 19

bronchoconstriciton tx

Answer 19

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

Question 20

Salbutamol toxicity s/s:

Answer 20

tremors, tachycardia, hypokalemia, cardiac arrhythmias etc.

Question 21

what is the pro of using dex

Answer 21

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

Question 22

Dex should not be given with…

Answer 22

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