CSE path (73/101)

emphysema/chronic bronchitis definition

weakening/enlargement of air spaces distal to bronchioles accompanied w/ hypertrophy of goblet cells + mucus glands.

emphysema/chronic bronchitis appearance

visual: barrel chested, clubbing, cyanosis

BS: diminished aeration and bilateral exp wheeze

percussion: tympanic, hyperresonant

cough: congested, productive, thick

emphysema/chronic bronchitis ABG, PFT

compensated resp acidosis w/ hypoxemia + hypercapnia

PFT: decreased flows

emphysema/chronic bronchitis treatment

SpO2 88-92%

bronchodilators, ICS, antibiotics (sputum culture), smoking cessation

NPPV, pulm rehab

asthma pt assessment

accessory muscle use + retractions (in children)

hyperresonant/tympanic note

pulses paradoxes during severe episodes

asthma CXR, ABG, PFT

depressed/flattened diaphragms

acute alveolar hyperventilation w/ hypoxemia, can develop hypercarbia in status asthmaticus

reduced flow, bronchodilator response, bronchial provocation test (FEV1 decreases w/ provocative agent)

asthma long term controllers

LABA, ICS, mast cell stabilizers, leukotriene inhibitors

asthma peak flow scoring

1. green PF >80% = stable, only steroids

2. yellow >50% = begin or increase steroids, start albuterol

3. red <50% or no improvement after increasing yellow treatment = ^ and call doctor
   
   danger signs = difficult walking + talking, peripheral cyanosis, call 911
   call doctor if meds aren’t working or PF drops following plan

bronchiectasis

chronic dilation/distortion of bronchi due to inflammation + destruction of bronchial walls, BV, elastic tissue and smooth muscle. can be unilateral or bilateral, but usually limited to lobe or segment. can have history of CF or pulm infections.

bronchiectasis pt assessment

cyanosis, clubbing, barrel chested

BBS dim. wheezes

percussion hyperresonant/tympanic

purulent, separating, FOUL SMELLING SPUTUM, hemoptysis

bronchiectasis CXR, ABG, PFT

hyperlucent lung fields, depressed/flattened diaphragm, enlarged or elongated heart

acute alveolar hyperventilation w/ hypoxemia → chronic ventilatory failure w/ hypoxemia

decreased flows, severe has decreased volumes

BRONCHOGRAM or CT scan = dilated bronchi, increased bronchial wall opacity

bronchiectasis treatments

antibiotics for acute infections, expectorants and SABA + anticholinergics. can also do via surgical resection.

CF definition

inherited, genetic disorder involving exocrine glands, causing thick, viscous mucus accumulation in lungs, blocking passageways of pancreas and prohibits enzymes from reaching intestine leading to inhibition of digestion of proteins + fats, and causing vitamin deficiencies

CF hx.

positive family hx., being a mec baby, recurrent resp infection, failure to thrive

CF appearance

barrel chest, cyanosis, clubbing, small for age, malnutrition, poor body development, peripheral edema

productive cough of hella sputum

dim. crackles + wheezes

hyperresonant/tympanic

CF CXR, ABG, PFT, CBC

translucent/dark, depressed/flattened diaphragm, RV enlargement, atx + fibrosis areas

acute alveolar hyperventilation w/ hypoxemia → chronic ventilatory failure w/ hypoxemia

PFT = decreased flow rates

CBC = elevated Hb + Hct

sputum = staph, flu H, pseudomonas

CF tests

1. newborn screening by IRT

2. sweat chloride test (>60)

3. genetic testing of CFTR mutation

CF treatment

dornase alfa (pulmozyme)

ICS = Advair, Flovent, pulmicort

antibiotics = TOBI, colistin, amikacin

digestive enzymes

AHI for sleep apnea

normal <5 episodes/hour
mild <15
mod <30
severe >30

pneumothorax

diaphoresis, bruising over affected area

pulsus paradoxus

pneumo treatment

<20% lung collapsed = rest and should absorb w/I 30 days

>20% = chest tube w/ hyperinflation therapy. needle asp. only if pt. is unstable

thermal lung injuries/smoke inhalation/CO poison CXR and PFT

CXR = normal early, p. edema/ARDS late stage

PFT = decreased DLCO

thermal lung injuries/smoke inhalation/CO poison treatment

1. hyperbaric

2. bronch to clear mucus plugs

3. monitor ABG, electrolytes, fluid levels

4. hyperinflation therapy

5. bronchodilators, mucolytics, ICS

6. monitor infection

CHF + pulmonary edema def

CHF reflects impaired cardiac pumping which can lead to p. edema due to excess fluid from pulm. vasc. system → extravasc. system (interstitial space) + alveoli

CHF/edema pt assessment

flat/dull percussion note

increased tactile + vocal fremitus

RR pattern = paroxysmal nocturnal dyspnea

CHF/edema diagnostic testing: CXR, ABG, PFT, hemodynamics

CXR = bilateral fluffy opacities, cardiomegaly, bat wing, kerley AB lines

ABG = resp alk w/ hypoxemia

PFT = normal ratio, reduced rest

hemodynamics = increased PCWP, PAP

elevated BNP

CHF/edema treatment

1. lasix

2. + inotropic agents (digitalis, dixogin, dobutamine, dopamine)

3. preload reduction agents (nitroglycerin, nitroprusside, morphine)

4. bradycardia = atropine, tachycardia = procainamide, metoprolol

how to treat PVC

lido + O2

pulm hypertension (PH) def

>25mmHg MAP at rest, complication typically from COPD + ILD

PH pt. assessment

JVD, peripheral edema, diaphoresis

BS wheeze, crackle, pleural friction rub

PH diagnostic testing: CXR, ABG, hemodynamics

CXR = enlarged pulm arteries

ABG = resp alkalosis w/ hypoxemia

hemodynamics = increased PAP

PH treatment

1. diuretics

2. blood thinners (eliquis, arixtra, lovenox, xarelto, coumadin)

3. inotropes (digitalis)

4. iNO for severe cases

MI

interruption of coronary BF

MI diagnostic testing

electrolytes = hyper/okalemia

ECG = inverted T waves, elevated ST

cardiac enzymes = elevated troponin

MI treatment

1. 100% FiO2

2. aspirin

3. moprhine

4. anti-arrhythmias (amiodarone, procainamide, atropine)

5. nitrates for chest pain

6. fluids/pressors (dopamine)

why do blood clots develop in peripheral BV (PEs)

1. venous stasis (inactivity, prolonged bed rest, CHF, varicose veins)

2. fat/air emboli

3. trauma, fractures, surgery

4. obesity, pregnancy, child birth

PE diagnositc testing: CXR, ABG, hemodynamics, capnography, Vd/Vt

CXR = increased density in infarcted area, dilation of pulm. arteries, wedge-shaped infiltrate

ABG = resp alkalosis

hemodynamics = increased PAP

capnography = decreased PeCO2 w/ normal PaCO2

Vd/VT = increased

PE special tests

1. spiral CT (most sensitive test)

2. VQ scan

3. Angiogram

PE prevention

1. anticoag (heparin)

2. anti-embolism stockings

3. pneumatic compression devices

4. early ambulation

PE treatment

1. analgesics for chest pain

2. digitalis, digoxin for circulation

3. thrombolytic agents = urokinase, streptokinase, tPA

peripheral vascular disease (PVD)

partial/complete obx. of BF to or from arteries outside chest

ex. arteriosclerosis, atherosclerosis, DVT, etc.

PVD primary assessment

1. kinds/degrees of PVD are characterized by numbness, pain, pallor, BP, impaired arterial pulsations

2. PVD w/ bacterial endocarditis can involve emboli in terminal arterioles + produce gangrenous infarctions of distal parts of body (tip of nose, pinna of ear, fingers, toes)

3. large emboli can occlude peripheral vessels + cause atherosclerotic disease

PVD secondary assessment

1. routinely perform basic lab. testing

2. venography

3. vascular ultrasound

PVD treatment

severe cases = amputation of gangrenous body parts

less severe = eliminating contributing factors (smoking), drugs (salicylates, anticoags)

cor pulmonale def + etiology

RV enlargement (hypertrophy and/or dilation) secondary to PHTN from disorders of CW or lungs

etiology = increased RV workload as result from PHTN causing hypertrophy of RV, often caused by COPD

cor pulmonale primary assessment

1. past hx of chronic lung disease

2. SoB/dyspnea

3. increased AP w/ obstx lung disease

4. distended neck veins, chest pain, peripheral edema

cor pulmonale secondary assessment: hemodynamics ,ECG

1. hemodynamics = increased CVP, decreased QT with exercise

2. ECG = RV hypertrophy

cor pulmonale treatment

1. treat underlying cause

2. decreased workload of RV by lowering PAP

3. digitalis, diuretics, pulm vasodilators (epo/iNO)

MG word vocab

ptosis = drooping eyelids

diplopia = double vision

dysphagia = difficulty swallowing

MG special testing

1. tensilon test

2. electromyography

3. blood test for Ach receptor antibodies

4. ice pack test (ice on eye lids, + test if ptosis improves

MG + GB spont vent parameters, ABG, PFT

decreasing VT, VC, MIP

ABG = acute ventilatory failure w/ hypoxemia, WATCH for vent. failure (>45mmHg CO2)

PFT = reduced volumes

MG tensilon test

1. VT, VC, MIP + weakness IMPROVE w/ tensilon:

   1. “myasthenia crisis” = maintain drug therapy (pro/neo/pyridostigmine)

2. if ^ WORSEN:

   1. “cholinergic crisis” = OD of anti cholinesterase drugs (administer atropine to reverse tensilon)

MG + GB treatment

1. monitor VT, VC, MIP

2. bedrest restriction + soft diet to reduce symptoms

3. hyperinflation therapy

4. GB ONLY = plasmapheresis + IVIG

GB def

rare autoimmune disorder of PNS causing inflammation + deterioration.

GB special tests

1. lumbar puncture (high protein level in CSF >500)

2. abnormal electromyograph

3. elevated immunoglobulin levels

drug OD reversal agents

1. naloxone/narcan

2. flumazenil/romazicon (benzo’s)

3. acetylcysteine (acetaminophen)

stroke/acute brain attack/cerebral infarction/cerebrovascular accident (CVA)

brain loses blood resulting from vascular occlusion or hemorrhage

past hx.: cerebral thrombi/emboli (MC), atherosclerosis, HTN, transient ischemic attacks (TIA)

stroke/acute brain attack/cerebral infarction/cerebrovascular accident (CVA) pt. assessment

motor + speech loss

bradypnea, cheyne-stokes

HTN, fever

stroke/acute brain attack/cerebral infarction/cerebrovascular accident (CVA) special test

brain CT/MRI, cerebral angiogram

ICP monitoring

stroke/acute brain attack/cerebral infarction/cerebrovascular accident (CVA) treatment

1. anticoagulant, vasodilators, thrombolytics/tPA (for acute ischemic stroke)

2. all treatments should be initiated w/I 6hours

poliomyelitis/tetanus/muscular dystrophy/amyotrophic lateral sclerosis (ALS) def + etiology

NMD involving loss of voluntary muscle action

etiology = viral infection (polio), genetic disorder (musc. dystrophy), puncture wound (Tetanus/botulism)

poliomyelitis/tetanus/muscular dystrophy/amyotrophic lateral sclerosis (ALS) primary assessment

1. past medical hx: hx of present illness, previous admission for disease

2. current meds: drug therapy for specific disease

poliomyelitis/tetanus/muscular dystrophy/amyotrophic lateral sclerosis (ALS) secondary assessmenet

1. ABG (watch for vent failure)

2. spont vent parameters: decreased Vt, VC, MIP

poliomyelitis/tetanus/muscular dystrophy/amyotrophic lateral sclerosis (ALS) treatment

1. monitor VT, VC, MIP

2. paralyzing agents (relax jaw for intubation in case of tetanus/botulism)

ARDS etiology

1. SEPSIS (MC)

2. aspiration, pneumonia

3. trauma, massive blood transfusion

4. drug abuse

ARDS pt assessment

cyanotic, retractions, tachypnea

bronchial crackles

flat/dull note percussion

tachycardia, HTN

ARDS CXR, ABG, PFT, special tests

CXR = increased opacity, diffuse alveolar infiltrates w/ honeycomb or ground glass appearance

ABG = refractory hypoxemia, acute alveolar hyperventilation w/ hypoxemia

PFT = decreased V and capacities

special test = elevated PAP w/ normal PCWP

ARDS alternative approaches to mech vent

1. IRV (inverse ratio ventilation)

2. aPRV

3. PRVC

4. HFV (high freq ventilation)

5. permissive hypercapnia

infectious disease/pneumonia def

infection causing capillary fluid/serum to spill into alveoli

infectious disease/pneumonia BS, drug therapy

crackles, bronchial, whispered pectoriloquy

antipyretics controls fever

immunocompromised medical conditions risk factors

1. LGBTQ (HIV risk)

2. IB drug abuse, blood transfusions

3. living in crowded conditions (prisons, shelters)

treatment boosting immune system

1. Igb therapy

2. interferon-gamma therapy

3. growth factors

4. stem cell transplantation

shocks

failure of CV system to perfuse tissues, impairing metabolism

1. neurogenic/vasogenic = alterations in vascular smooth muscle tone

2. anaphylactic = hypersensitivity/alergic reaction

3. traumatic = components of hypo + septic shock

shocks hemodynamics + treatment

hemodynamics = decreased everything

pressors for vasogenic shock (dopamine, dobutamine)
inotropic for ❤ failure (digitalis, digoxin)

bariatric def + risks

aka obesity!

aspiration risk, difficult to ventilate + intubate, hemodynamic instability, DVT + PE

bariatric diagnostic testing

1. OSA can lead to obesity hypoventilation syndrome/pickwickian syndrome, compensated resp acidosis, cor pulmonale

2. sleep study/polysomnograph

3. rhabdomyolysis (pressured-induced myoglobinuria) due to extra pressure on tissue (muscle deterioration)

bariatric treatment

1. surg procedures (risk for resp dysfxn + delayed recovery (increased stay)

2. LPV!

laryngectomy: perm vs temp stoma

1. permanent stoma: entire larynx, epiglottis, thyroid cartilage removed. NO oral or nasal intubation! tube removed 3-6wks and stoma is considered stable + permanent by then

2. temporary stoma: only cords removed, stoma repairs itself.

treat w/ cool aerosol for secretions + good sxn’ing technique

treatment for pre + post op

pre op. = hyperinflation (IS/SMI, IPPB)

post op = ^, prevent infection, watch out for hypovolemic shock

may require LPV for lung resections or lobectomies

normal ICPs. how to treat? how to treat seizures?

5-10mmHg, use LOW PEEP! treat w/ mannitol if ICP >20mmHg.

seizures = dilantin

diabetes/renal failure RR, BBS, ABG, urine output, blood glucose

RR = kussmaul’s breathing

BBS = rales if CHF present (watch out for CHF development!)

ABG = met. acidosis

Urine output = decreased <500mL/day

Blood glucose = >160mg

exposure/accidental hypothermia

MARKED cooling of core temp <35C

hypothermic pt and ABG

ABG should be measured AT PT’S BODY TEMP (normally measured @37). if body temp is lower than the ABG temperature, pH INCREASES, PCO2 and PO2 DECREASE.

ex.: pt is 35C, ABG analyzed @37 = 7.32, 53, 67, x
pt is 35C, ABG analyzed @35 = 7.40, 45, 59, x

hypothermic treatment

1. mild = passive rewarming

2. mod >30C= active rewarming may be required

3. severe <30C = active rewarming no faster than few degrees per hour

near drowning wet vs dry drowning

wet = glottis relaxes + water floods lungs

dry = glottis spasms + prevents water from entering lungs

near drowning treatment

1. FiO2 100%

2. intubate PaO2 <60 on <50% FiO2

3. inotropes

4. diuretics

5. neck injury = intubate w/ flexible bronch

PEDS: asthma signs + diagnostic tests

signs = complaining of stomachache, lethargy + decreased play activity

tests = PFT, FENO, bronchoprovocation challenge (methacholine)

PEDS: asthma control meds

1. ICS: beclomethasone, budesonide, fluticasone

   1. systemic = prednisone, methylprednisone

2. leukotriene: montelukast, zileuton

3. immunomodulators: omalizumab, palivizumab

PEDS: asthma ER care

1. O2 therapy

2. 3 SABA treatments/hour or continuous

3. inhaled anticholinergics

4. system corticosteroids

PEDS: status asthmaticus

failure to respond to normal treatments. may use:

1. cont. bronchodilator

2. subcutaneous epi

3. IV steroids

4. Mg sulfate

5. Helios therapy

6. inhaled anesthetics (isoflurane, sevoflurane, halothane)

coryza

runny nose

PEDS: croup (laryngotracheobronchitis) def + treatment

SUBGLOTTIC swelling primarily caused by VIRAL infection (no fever!)

“steeple sign”, “pencil point”, “picket fence”, “hour glass narrowing of UA”

1. mild = cool mist, racemic epi, steroids if dont respond to those

2. severe = intubation if tiring/worsening, T-piece or CPAP

PEDS: epiglottitis def

SUPRAGLOTTIC swelling just above cords caused by bacterial infection/flu.

appearance: muffled cough, lifeless, drooling, tongue + jaw thrust forward

“thumb sign”

IMMEDIATELY INTUBATE!

PEDS: bronchiolitis/RSV PFT and special test

decreased flows

RSV-enzyme immunoassay (EIA) or resp infectious disease panel (RIDP) by polymerase chain reaction (PCR)

PEDS: bronchiolitis/RSV treatment

1. RSV immune globin (RespiGam)

2. Palivizumab (Synagis)

3. humidification + oral decongestants

PEDS: BPD def + how to treat

results from treatment of RDS w/ vent + high FiO2 for >28days

can treat w/ diuretics to reduce edema

PEDS: CHF

R→L shunts: TOF, TGV

heart murmur, “egg shaped ❤” w/ TGV, “boot-shaped ❤” w/ TOF

TEST WITH ECG!!

treat: PaO2 50-80, prostaglandin for PDA

PEDS: pre + post ductal

pre ductal >15torr HIGHER = R→L shunt

2 transq monitors: 1 upper right thorax (pre), 1 lower left thigh or abdominal region (post)

NEO: infant respiratory distress syndrome (IRDS)/hyaline membrane disease (HMD) def, hx. and appearance

low surfactant

hx. low APGAR, RDS @birth, L:S <2:1, fine crackles/rales

ground glass appearance + air bronchograms

NEO: infant respiratory distress syndrome (IRDS)/hyaline membrane disease (HMD) treatment

1. CPAP (4-6cmH2O)

2. low PaO2/SpO2

3. surf (delivered 5Fr, administered in 4 portions on PPV)