DISEASE PHARMACOLOGICAL THERAPY / MANAGEMENT

Acute Respiratory Failure- sudden and life A. Physical

threatening deterioration of the gas exchange ● Elevate head of the bed at least 45 degrees in order
function of the lung and indicates failure of the to help expand the lungs
lungs to provide adequate oxygenation or ● If px has secretions, position them laterally for
ventilation for the blood. postural drainage and preventing aspiration
● If px needed to be suctioned, hyperventilate in
OXYGENATION FAILURE MECHANISM between. Suctions for only 10 seconds with a total of
- Decrease hemoglobin 15 seconds including the insertion of the catheter
- Low oxygen in atmosphere (mountain, (watch for increased ICP)
airplane) ● Anticipate a Chest Tube Placement if the patient has
- Too much fluid in the lungs, blocking the ○ Pneumothorax: place CT superior
oxygen to go from alveoli to blood (wet and anterior
lungs/ edema) ○ Pleural Effusion: inferiorly and
- Pneumonia posteriorly
- ARDS B. Chemical: Oxygen
- Heart failure ● V/Q mismatch
- COPD - Nasal Cannula can only be given 1-4L
- Pulmonary embolism - Simple face mask/ venturi mask: 32-34%
- Restrictive lung disease ● Intrapulmonary shunt
- CPAP/ BiPAP (Continuous positive airway
VENTILATORY FAILURE MECHANISM pressure therapy/ bi-level positive airway
● Imapired function of the CNS pressure)
○ Drug overdose, head trauma, - ET Tube
infection, hemorrhage, and sleep ● Tracheostomy (1-2 weeks post ET)
apnea ● Mechanical Ventilation
● Neuromuscular dysfunction C. Chemical
○ Myasthenia gravis, Guillain-barre ● Bronchodilator: dilate the airway of lungs
syndrome, amyotrophic lateral - Example: albuterol HHN (hand held
sclerosis and spinal cord trauma nebulizer)
● Musculoskeletal dysfunction - Call RT
○ Chest trauma, kyphoscoliosis and ● Mucolytics: liquefy secretions
malnutrition - Example: acetylcysteine
● Pulmonary dysfunction - Given with HHN
○ Asthma and cystic fibrosis ● Others:
- Corticosteroids
- Diuretics
- Antibiotics
- Pain management
- Anxiolytics
D. Supportive
● Hydration
- 2-3L/day PO or IV
- Thins mucus
- Monitor BP
- Contraindicated with HF or pulmonary
edema
- SIgn of fluid overload: crackles, dyspnea,
 increase CVP
● Nutrition
- Risk for aspiration: tube feeding, PN
- Consult dietician
- Balance between:
- Low carbohydrate due to
hypercapnia
- High caloric requirements due to
hyper metabolism
● Hemoglobin
- Monitor for bleeding
- Draw CBC for H/H (hemoglobin and
hematocrit)
● Coughing
- Quad Coughing
- Place palm below the xiphoid
process of the patient and move
downward
- Staged Coughing
- Breathe 3-4x through mouth, cough
with pillow
- Huff Coughing
- Inhale, hold breath, open mouth and
exhale rapidly until mucus at bronchi,
cough
● Chest Physiotherapy
- Indicated if sputum is >30mL/day

Acute Respiratory Distress Syndrome GOAL: Maintain airway/ functions (Improve gas
- Type of respiratory failure → capillary exchange, Inc 02, keep sacs free of fluid)
membrane that surrounds the alveoli sac
starts to leak fluid in this sac
- Fast onset; happens suddenly 1. Mechanical vent with PEEP (Positive end-expiratory
- Px gets this when they are sick of something pressure)
else (BURNS, SEPSIS) - Pa02 >60mmHg, 02 sat >90%
- Develops due to systemic inflammation - PEEP: High 10-20 cm H20 why? Because of dec. lung
- High mortality rate compliance, edema in sacs, dec surfactant-collapsed
sac
Indirectly (not lungs) Direct (lungs)
- PEEP open alveoli sacs that are collapsed especially
Sepsis, burns, blood Pneumonia, during exhalation
transfusion (multiple), aspiration, inhalation
pancreatitis, drug injury, drowning-near, COMPLICATIONS OF PEEP:
overdose embolisms - Inc Intrathoracic pressure (can compress heart)
- Decreased cardiac output (watch hypotension) -
1. Exudative: 24 hrs after injury sophisticated hemodynamic monitoring - colloid,
- Damaged cap membrane, leak fluid that’s crystalloid, IV solutions, inotropic cardiac drugs e.g.,
protein rich (enters interstitium & then sac) dobutamine
→ pulmonary edema - Hyperinflate lungs (pneumothorax- whole lungs can
- Damaged surfactant cells (helps sac’s collapse, subq emphysema- air is escaping the
 stability, so it won’t collapse) → atelectasis lungs (whole in the lungs) goes in to the tissues;
→ hypoxemia rice crispy, crunchy weird feeling
- Hyaline membrane; stiff lung can’t stretch →
dec. lung compliance → V/Q mismatch
HALLMARK SIGN: REFRACTORY 2. PRONE POSITIONING
HYPOXEMIA - given high amounts of 02 but still - Inc 02 without increasing 02 concentration
won’t increase 02 levels - Helps improve V/Q, airflow
- Inc RR, Dec, 02, dec C02 (respi alkalosis) as - Doesn’t compress the posterior part of the lungs
it progresses, hyaline membrane develops - Move the secretions to other areas; helps the
more and it gets harder for c02 to cross over atelectasis
then there will be increased CO2 levels
which leads to respi acidosis Pulmonary artery wedge pressure:
2. Proliferative: 14 days after injury - Measures left arterial pressure, inserted balloon
- Grow & reproduce cells quickly, repair - Rules out if cardiac related
structure, reabsorption fluid, lung tissue very - Less than 18 mmhG → ARDS
dense and fibrous, dec. lung compliance, - If greater than 18 mmHg → cardiac issue
worse hypoxemia
3. Fibrotic: 3 weeks after injury (worst case) Monitor:
- Dead space in the lungs, no gas - UOP, Mental status, BP and HR
exchange, prognosis very poor, major - Prevent: pressure injury, vent infections, nutritions
lung damage (lose weight)
Atelectasis
Refractory Hypoxemia Medications:
Decreased lung compliance a. Dobutamine (for dec cardiac output)
Surfactant cell damage b. Corticosteroids (dec inflammation)
c. Antibiotics (Sepsis, treat infection)
S/SX OF ARDS d. GI drugs (prevent stress ulcers)
- EARLY: barely noticeable normal to random
crackles
- Different breathing “air-hunger”
- Inc RR, Low 02, resp. Alkalosis in the
beginning
- Full respi failure, refractory hypoxemia,
cyanosis, mental status changes, Inc HR,
retractions, crackles throughout (pulmonary
edema)
- X-RAY: White out appearance; bilateral
infiltrates throughout the lungs

Chronic Obstructive Pulmonary Disease NURSING INTERVENTIONS:

-Pulmonary disease that causes chronic 1. Monitor respiratory system:
obstruction of airflow from the lungs, involving - Lung sound (may need nasotracheal suction)
the airways, pulmonary parenchyma or both. - Sputum production (for development of pneumonia) @
-Limited airflow (inflamed bronchioles, deformed risk for pus
and narrow with excessive mucus) - Keep 02 Sat 88.93% why?? COPD px are stimulated
-Inability to fully exhale (elasticity loss in alveoli to breathe due to low o2 levels rather than high C02
sac and air pocket develop. levels.. Give them too much 02 they stop breathing →
- Deficient antitrypsin protein: puts the patient at hyperventilation + increased c02 and will become toxic
risk for lung disease. - Administer 02 as prescribed 2L
- Monitor effort of breathing: Teach about pursed-lip &
CAUSES: most common ‘environmental’ from diaphragmatic breathing
harmful irritants that are inhaled into lungs. Ex. Pursed lip: inhale through nose, blow exhalation (breathe
SMOKING and SECONDHAND SMOKE longer) force air out, slow breathing, increase oxygen
Diaphragmatic: uses abdominal muscle rather than
-Happens gradually.. most ppl start to notice accessory muscle for breathing; helps strengthen
S&S in middle aged: dyspnea w/ activity, chronic diaphragm, slow down breathing and makes it easier, and
cough, recurrent lung infection etc. dec energy used to breathe: LAY DOWN, pillow underneath
the knees, put one hand in chest one hand in abdomen,
SIGNS AND SYMPTOMS: LUNG DAMAGE with abdominal muscles inhale without moving chest
Lack of energy muscles then force air in they will pursed lip breathe out
Unable to tolerate activity (SOB) using abdominal muscles
Nutrition poor (weight loss esp. emphysema - Administer breathing treatment: (RT helps)
Gases abnormal ( PCO2 > 45 & PO2 < 90 ;
respiratory acidosis 2. Education:
- Nutrition needs: pink puffers hyperventilate as a
Dry or productive cough (esp. chronic bronchitis) compensation mechanism, uses a lot of energy doing
Accessory muscle usage for breathing this: high calorie and protein meals: small and frequent
(emphysema) Abnormal lung sounds: - hyperinflated lungs and full stomach will only lead to
diminished, coarse crackles or wheezing further DOB, stay hydrated 2-3L (not contraindicated),
Modification of skin color pink to cyanosis to remove secretions and not block the airway
Anteroposterior diameter increase (Barrel chest) - Avoid sick people, irritants hot humid (smothering
Gets in tripod position to breathe (stands leaning days) extreme cold and hot tempt
forward while supporting hands on knee or - Stop smoking and avoid people who smoke (2nd hand
object) smoking)
Extreme dyspnea - Vaccine up to date: annual flu shot and pneumonia
vaccine every 5 years
COMPLICATIONS
- Heart disease: heart failure 3. Medications:
- Pneumothorax: spontaneous from air a. Corticosteroids: dec inflammation, dec mucous
sacs of alveoli in emphysema production, oral Iv, nhaled, used many time with
- Lung infections: PNA bronchodilators
- Increase risk of Lung CA - “Prednisone, Solumedrol, Pulmicort, Symbicort -
(steroid and long acting bronchodilator)”
- Side effects: easy bruising, easy skin tearing,
DIAGNOSED hyperglycemia, inc risk infection (long term use -
● Spirometry: test where a pt breathes bone loss, osteoporosis)
into a tube which measures: USE BRONCHODILATOR 1ST AND THEN
○ How much volume the lungs can CORTICOSTEROIDS INHALER AFTER 5 MINS - RINSE
hold during inhalation mouth after cortico due to THRUSH
○ How much & how fast air volume b. Phosphodiesterase-4 inhibitor: used for people with
is exhaled chronic bronchitis and helps dec COPD exacerbation..
● Measuring FVC (Forced Vital Not a bronchodilator
Capacity) : low reading → restrict - “Roflumilast”
breathing → largest amount of air - Side effects: cause suicide ideation and weight loss
exhaled after breathing in deeply in one c. Methylxanthines:
second - “Theophylline”
● Measures Forced Expiratory Volume: - Given orally many times, type of bronchodilator,
how much air a person can exhale within used long-term with px with severe COPD
1 second (low reading shows severity) - Narrow therapeutic range: 10-20 mcg/mL
- Increases digoxin toxicity and decreases effects of
 lithium and dilantin
Chronic bronchitis- BLUE BLOATERS: due
d. Short-acting Bronchodilators: relaxes smooth muscles
to cyanosis and edema. Retaining carbon
of bronchial tubes… emergency situations and quick
dioxide and not much oxygen is entering.
relief
● Bronchioles damaged- limit ability to
- Beta 2 agonist: Albuterol
exhale fully → increase volume
- Anticholinergic: Atrovent
because there is residual air →
e. Long-acting Bronchodilator: same action as short but
hyperinflation → low amount O2
effects lasts longer.. Used over a period of time..
entering and keeping
Scheduled
● Respiratory Acidosis → cyanosis →
- Beta 2 agonist: Salmeterol
compensate RBC by increasing (blood
- Anticholinergic: Spiriva
becoming too thick) → increase
- Use before inhaled corticosteroid
pressure in arteries (Pulmonary Artery)
- Beta 2 side effects: increased HR, urinary retention
from the shift of blood due to decrease
- Anticholinergic side effects: dry mouth, blurred
O2 → Pulmonary Hypertension →
vision
Right sided HF → bloating

Emphysema- PINK PUFFERS :

hyperventilate for compensation to decrease
O2 and maintain ‘pink’ complexion, with barrel
chest from usage of accessory muscle.
● Alveoli sac lose elasticity due to
inflammation response in body → air
gets trapped in sacs
● Hyperinflation (diaphragm to flatten)
due to retaining air volume
● Diaphragm is not working well →
compensatory: use of accessory
muscles/ hyperventilate the air out of
the lungs → leads to barrel chest
“anteroposterior diameter increase”
● Hyperventilation causing increase RR
→ have less hypoxemia than chronic
bronchitis