Pulm2 Flashcards
(234 cards)
1
Q
classications of pneumothorax
A
classified (primary, secondary)
traumatic (iatrogenic, tension)
2
Q
primary spontaneous pneumothorax
A
pneumo without an underlying lung disease
3
Q
Secondary Spontaneous Pneumothorax
A
pneumo resulting from a complication of a preexisting disease
4
Q
things that can result in iatrogenic pneumothorax
A
thoracentesis,
pleural biopsy,
subclavian or internal jugular vein catheter placement,
percutaneous lung biopsy,
bronchoscopy with transbronchial biopsy
positive-pressure mechanical ventilation
5
Q
what is the most serious type of pneumothorax
what is the typical cause
A
tension pneumo
penetrating trauma, lung infection, CPR, positive pressure ventilation
6
Q
what causes tension pneumothorax
A
air pressure in the pleural space exceed the pressure in the lungs allow air to enter the pleural space and not escaping on expriation
7
Q
life threatening complications of tension pneumo
A
compromised ventilation
compression on the heart due to positive pressure, resultiing in decreased venous return
8
Q
risk factors for primary pneumo
A
Tall, thin boys and men between 10 and 30 years old
Family history
Cigarette smoking
9
Q
risk factors for secondary pneumo
A
COPD
Aerosolized pentamidine and prior history of Pneumocystis pneumonia
10
Q
etiology of primary pneumo
A
rupture of subpleural apical blebs in response to high negative intrapleural pressures
11
Q
etiology of secondary pneumo
A
Most commonly as complication from COPD
Can also occur as complication of asthma, cystic fibrosis, TB, Pneumocystis pneumonia, menstruation (catamenial pneumothorax), and wide variety of interstitial lung diseases
12
Q
catamenial pneumo defined
etiology
A
a typically right side pneumo thorax cause by endometriosis or diaphragm perforation that needs surgical repair 1/3 of the time
13
Q
typical presentation of pneumothorax
A
chest pain, dyspnea
14
Q
T/F chest pain and dyspnea realted to pneumothorax often starts during exertion and doesn’t resolve
A
false, it usually occurs during rest and resolves in 24 hrs
15
Q
despite the fact that chest pain and dyspenia usually resolves, when can pneumothorax cause a respiratory failure
A
when there is underlying COPD or asthma
16
Q
signs and symptoms of pneumothorax
A
chest pain
dyspnea
occassionally mild tachycardia
17
Q
what additional signs of pneumothorax will be present if its large
A
diminished breath sounds
decreased fremitus
decreased movement of the chest
18
Q
signs and symptoms of tension pneumothorax
A
Marked Tachycardia
Hypotension
Mediastinal or Tracheal Shift to contralateral side
Enlarged hemithorax without breath sounds
Hyperresonance to percussion
19
Q
lab studies for pneumothorax
A
ABG - often not needed but will show hypoxia and respiratory alkalosis
ECG - a left sided pneumo may produce changes misinterpreted as an acute MI
20
Q
how will a right pneumothorax present on ECG
left
A
right will look like right bundle branch block
left will have axis deviation and low amplitude QRS
21
Q
imaging for pneumothorax
A
CXR
pleural line
may need expiratory film
poss air fluid level from secondary pleural effusion
deep sulcus sign
tension: blacked out lung and contralateral mediastinal shift
22
Q
DDx in pneumothoerax
A
Emphysematous bleb
Myocardial Infarction
Pulmonary embolization
Pneumonia
23
Q
complications with spontaneous pneumo
A
pneumomediastinum
subcutaneous emphysema
24
Q
if pneumomediastinum is found in conjunction with pneumothorax, what should be be considered
how can this be confirmed
A
esophageal or bronchial rupture
swallow study
25
treatment of a small stable spontaneous pneumo
oxygen to induce absorption
observation
26
treatment for a large or progressive spontaneous pneumo
Aspiration drainage of pleural air with a small-bore catheter (16 gauge angiocatheter or larger)
Small bore catheter or chest tube attached to a one-way Heimlich valve
Follow with serial chest radiographs every 24 hours
27
pneumothorax indication for chest tube placement
Secondary Pneumothorax, Large Pneumothorax, Tension Pneumothorax or severe symptoms or those who have a pneumothorax on mechanical ventilation should undergo
28
describe the process of a chest tube placement (tube thoracostomy)
The chest tube is placed under water-seal drainage
suction is applied until the lung expands and maintains.
the tube is water-seal trialed to ensure resolution of leak.
Removed after the leak subsides
29
emergency management of tension pneumo
does this confirm pneumo
how long does the needle stay in
insertion of a large bore needle into the second anterior intercostal pleural space
if there is gas escaping it is confirmation of pneumothorax
the needle stays in place until a chest tube is put in
30
what would indicate thorascopy or open thoracotomy treatment for pneumothorax
Recurrence of spontaneous pneumothorax
Bilateral pneumothorax
Failure of tube thoracostomy for the first episode (failure of lung to reexpand or persistent air leak)
31
what does surgical treatment of pneumothorax entail
resection of blebs responsible for the pneumothorax
pleurodesis by mechanical abrasion and application of talc or povidone-iodine
32
risk factors for pneumothorax
smoking increases risk by 50%
exposure to high altitudes, flying without cabin pressure, or scuba diving can cause recurrence
33
what percent of patients with spontaneous pneumowill have recurrence
what if there is a surgical repair
are there any sequela after treatment
30%
recurrance is less frequent after surgery
no long term sequela
34
A tall, thin 24yo male presents to the clinic with sudden onset of left-sided chest pain and dyspnea.
Examination shows:
Vitals: T 99.2, R 24, P 112, BP 146/76
Neck: supple
Pulmonary: appears dyspneic, decreased breath sounds to the left chest on auscultation
Cardiac: tachy, but regular rhythm
**what labs or studies are needed**
**what is the treatment**
CXR, supplemental oxygen
needle decompression
35
pleural effusion
abnormal accumulation of fluid in the pleural space
36
etiolgy of pneumothorax
normal fluid secretion into the pleural space outpaces normal fluid absorption
can come from too much fluid or too little absorption
37
five pathological processes that account for most of pleural effusion
Transudates
Exudates (increased fluid)
Exudates (decreased removal of fluid)
Empyema
Hemothorax
38
transudate causes of pleural effusion
Increased production of fluid in the setting of normal capillaries due to increased hydrostatic or decreased oncotic pressures
## Footnote
Increased hydrostatic pressure
CHF (accounts for greater than 90% of transudates)
Decreased oncotic pressures
Hypoalbuminemia, cirrhosis
Greater negative pleural pressure
Acute atelectasis
39
causes of transudate pleural effusion
CHF
cirrhosis with ascities
nephrotic syndrome
peritoneal dialysis
myxedema
acute atelectasis
constrictive pericarditis
pulmonary empbolism
40
what causes exudative pleural effusion
Local factors that influence the formation and absorption of pleural fluid are altered
41
what would differentiate effusion form heart failure and that from pneumonia
bilateral pneumonia is pretty rare, so if effusion is bilateral its probably not pneumonia
42
causes of exudative pleural effusion
pneumonia
cancer
pulmonary embolism
tuberculosis
CTD
infection
uremia
chylothorax
43
general considerations for empyema
infection in the pleural space confirmed with cultures
44
why is history important to idenify when working up pleural effusion
if left alone the fluid will start wall itself off and make pockets which can make thoracentesis more difficult
45
general presention of pleural effusion
Dyspnea
Cough
Respirophasic Chest Pain
46
T/F small pleural effusions generally have no physical findings
true
47
signs and symptoms associated with large pleural effusion
Dullness to percussion
Diminished or absent breath sounds over the effusion
Compressive atelectasis may cause bronchial breath sounds and egophony over the effusion
Contralateral shift of the trachea and bulging of intercostal spaces (massive effusion with increased intrapleural pressure)
Pleural friction rub (infarction or pleuritis)
48
imaging studies for pleural effusion
upright CXR
lateral decubitus
49
how much fluid need sto be present on lateral upright chest xray to be a visible sign of pleural effsion
AP
75-100 mL
175-200m\<
50
howmuch fluid on lateral decubitus is needed to attempt blind thorocentesis
1 cm of fluid
51
what is the advantage of CT imaging in pleural effusion
it can decet small amounts of fluid (10mL) and help with thoracentesis
52
what is the advantage in ultrasound imaging for pleural effusion
can help guide thoracentesis of small effusions
53
Dx pleural effusion
fluid on x ray
thoracentesis
serum protein, LDH, glucose levesl
54
when is a diagnostic thoracentesis reccomended for pleural effusion
New pleural effusion and no clinically apparent cause
Atypical presentation
Failure of an effusion to resolve as expected
55
what information can be gathered from a diagnostic thoracentesis of pleural effusion
Visualization of the fluid
Micobiologic and chemical analysis to identify pathophysiology
Presumptive diagnosis based on DDx
Definitive diagnosis with positive cytology and culture of infectioous agent
56
what should be pleural fluid be tested for
pH
Description of fluid
Protein
Glucose
LDH
Amylase
Total WBC count
Differential WBC count
RBC count
Gram stain
Culture
Cytology
57
gross appearance of pleural fluid
Normal= clear to straw-yellow
Grossly Purulent= empyema
Greenish= bilopleural effusion
Yellow-green= rheumatoid effusion
Milky White= chylous effusion
Bloody
58
when pleural effusion is bloody what should be obtained from the fluid
hematocrit
59
diffentiating between exudative and transudative pleural effusion based on lab tests of pleural effusion labs
if your protein ratio is is \>.5, its exudative
if the LD ratio is \>0.6, its exudative
if the pleural fluid LDH is in the upper 2/3 of the limits, its exudative
60
T/F only one part of light's criteria needs to be positive for exudate to assume exudative pleural effusion
true
61
distinguishing lab findings for transudative pleural effusion
glucose in the fluid equal to serum glucose
pH between 7.4 and 7.55
fewer than 1000 WBC/mcL with mostly mononuclear cells
62
labratory findings that would indicate a more agressive draiing proceudre than thoracenesis
loculated pleural fluid
pleural fluid pH\<7.3
positive gram stain or culture
presence of gross pus in the pleural space
63
decreased pH of pleural fluid indicates what
empyema
malignancy
esohpageal rupture
TB
rheum onditions
64
elevated amylase in pleural fluid would indicate what
pancreatic pleural effusion (pancreatitis or pseudocyst)
malignancy (lung or pancreas)
esophageal ruture
65
glucose \<60 in pleural fluild would indicate what
malignancy
infection
TB
esophageal rutpure if \<60 is less than serum
rheumatoid pleuritis
66
what would be indicative of TB pleural effusion
thoracentesis with pleural biopsy shows exudate with small lymphocytes and high levels of TB markers in the fluid
67
general characteristics of treating transudative pleural effusion
treat the underlying condition
theraputc thoracentesis offers only transient relief
pleurodesis and tube thoracostomy are rarely indicated
68
wha percent of terminal cancer patients have malignany pleural effusion
15%
69
90% of malignant pleural effusions are exudative
treu
70
treatment of malignant pleural effusion
Systemic or local (thoracentesis or chest tube)
Pleurodesis after chest tube
Indwelling pleural catheter
71
Parapneumonic Pleural Effusion definded
three categories
Exudates that accompany ~40% of bacterial pneumonias
simple, complicated, empyema
72
define simple Parapneumonic Pleural Effusion
Free-flowing sterile exudates of modest size that resolve quickly with antibiotic therapy
73
treatment for complicated Parapneumonic Pleural Effusion
Tube thoracostomy if pleural fluid glucose is \<60mg/dL or the pH is \<7.2
74
treatment for empyema
Gross infection in the pleural space via positive gram stain or cultureà drain by tube thoracostomy
often will need intrapleural lytic therapy or surgical decortication
75
how are small volume hemothorax managed
if stable or improving on chest x-ray may be managed with close observation
76
treatment large volume or hemodyanmically unstable hemothorax
Large-bore thoracostomy tube, Drain existing blood and clot, Quantify amount of bleeding
Permit apposition of the pleural surfaces in an attempt to reduce hemorrhage
Thoracotomy may be needed to control hemorrhage, remove clot and treat complications
77
DX and treatment of mesothelioma
Diagnosis- thoracoscopy or open pleural biopsy
Treatment- chest pain- opiates; oxygen for SOB
78
T/F people with viral infections causing pleural effusion rarely get better on their own
false, they often recover with no sequela
79
dx of pulmonary embolism
Diagnosis with CT or pulmonary arteriography
80
general chacteristics of community acquired pneumonia
Acquired in the home or nonhospital environment
In most cases of CAP, the causative agent is not identified. However, in those cases where an agent is identified, bacteria are more commonly found.
Common causative agents include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis,
81
typical presentation of community acquire pneumonia
1- to 10-day history of increasing cough, purulent sputum, shortness of breath, tachycardia, pleuritic chest pain, fever or hypothermia, sweats, and rigors.
82
PE findings indicative of community acquired pneumonia
altered breath sounds and crackles,
dullness to percussion if an effusion is present,
bronchial breath sounds over an area of consolidation.
83
diagnostic studes for community acquired pneumonia
Organisms may be detected with conventional sputum Gram stain or sputum culture
Chest radiography (CXR) shows lobar or segmental infiltrates, air bronchograms, and pleural effusions.
Procalcitonin levels rise in response to a proinflammatory stimulus, especially bacterial infection.
84
age/gender/race bias for sleep apnea
most common in men, age 50-70, more prevalent in african americans
85
T/F sleep apnea increses with increased weight and age
true
86
T/F asian populations have a lower risk of sleep apnea because of their cranofacial make up
false, their risk is higher even without obstity
87
spectrum of sleep apnea diease
normal
primary snoring
upper airway resistance syndrome
obstructive hypoventilation
obstructive sleep apnea syndrome
88
causes of respiratory effort related arousals
➢Crescendo snoring
➢Thoraco-abdominal paradoxing
➢Increased intercostal EMG
➢Terminated by arousal or jerk
➢Oxygenation does not have to be affected
89
cumuluative RERAs lead to what
upper air way resistance syndrome
90
hypopnea
shallow breath that least to SaO2 decrease in 3% over 10 seconds
91
pathophysiology of apnea
soft palate and tounge slide back to close off the airway
leads to hypoxia
increased ventillatory effort
arousal from sleep
pharyngeal muscle tone is restored
airway opens
hyperventilation to correct hypoxia
92
criteria of apnea on a sleep study
complete blockage of the airway despite attempts to breath, requires a 3% desat and have \>10second duration
93
risk factors for sleep apnea
➢Obesity (BMI\>30)
➢Habitual snoring
➢Excessive daytime sleepiness
➢Age
➢Gender (male:female = 2-3:1)
Race (African-Americans, Hispanics
94
pediatric risk factors for sleep apnea
* Adenotonsillar hypertrophy
* Neurologic/Genetic Conditions (CP, Low Birth Weight)
95
clinical presentation of sleep apnea
* Decreased memory
* Morning headache
* Fatigue
* Decreased motor coordination
* Nocturnal gasping/choking
* Loss of libido/secondary impotence
* Irritability/depressed mood
* Frequent Napping/Falling asleep while sedentary
96
co-morbid conditions with sleep apnea
oPulmonary HTN
oCVA/TIA
oDiabetes
oFibromyalgia
oCardiovascular Disease
97
what is the link between sleep apnea and depression
* 18% of individuals with a major depressive disorder diagnosis also have a breathing-related sleep disorders diagnosis
* 18% of subjects with a breathing-related sleep disorders diagnosis have a major depressive disorder diagnosis
98
mimicers of the nocturnal symptoms of apnea
* Nocturnal heartburn
* Chest pain, palpitations
* Coughing and choking
* Asthma attacks
* Night sweats
99
differential for obstructive sleep apnea syndrome
❖PLMD/RLS
❖Shift Work Syndrome/Circadian Rhythm Disorder
❖Narcolepsy
❖Chronic Fatigue Syndrome
❖Primary Snoring
❖Nocturnal GERD
100
STOPBANG questionairre for sleep apnea
* **S**noring
* **T**ired
* **O**bserved Apnea
* **P**ressure
* **B**MI \>35
* **A**ge \>50
* **N**eck Circumference
* **G**ender
101
PE findings indicative of sleep apnea
✴Neck circumference (\>17 inches in males,\>16 inches in females)
✴craniofacial anatomy
✴posterior oropharynx
○BMI\>30 with 8-12 fold increase in risk
102
retrognathia
back set jaw
103
mallampati score
a scoring system that indicates a class I mallampati has a naturally open airway, while a class IV has no airway
104
lab studies for management of apnea
* Nurse observation record - Hospital/Home Health - not diagnostic
* Overnight oximetry (Profox) - Screen Only
* Home sleep test (HST)
* Portable - Inpatient stay
* In lab polysomnogram (PSG) - Gold Standard
105
how is the severity of sleep apnea measured
polysomnograph or home sleep test
106
apnea hypopnea index scores indicative of astham
No evidence of apnea
•AHI of 0-5
▪Mild Sleep Apnea
•AHI of 5-15
▪Moderate Sleep Apnea
•AHI of 15-30
▪Severe Sleep Apnea
•AHI \>=30
▪Extremely Severe Sleep Apnea
•AHI \>100
107
clinical criteria for sleep apnea that requires treatment
AHI of \>15 without comorbidity
AHI between 5-15 with at least one comorbid factor (DM, HTN, CAD, BMI)
108
mortality conditions associated with sleep apnea
* Ischemic heart disease
* Congestive heart failure
* Cerebrovascular disease
* Pulmonary hypertension
* Atrial Fibrillation
109
what comorbity puts a patient at the highest risk for apnea
drug resistant HTN
110
T/F a higher AHI score will lead to a greater increase in in HTN
treu
111
apnea puts patient at risk for what types of CHD
fatal and non fatal CV events
arrhytmias
112
Men with AHI \>19 are 2.86 times likely to have a ischemic stroke
true
113
why can obstructive sleep apnea be more prone to weight gain
* OSA patients are more desensitized leptin
* Ghrelin hormone secreted by the intestinal tract when empty. Tells us we are hungry. OSA patients have more
* Neuropeptide Y - Released by sympathetic nervous system. It is a strong vasoconstrictor and also increases adipose cell production. It also acts to increase food intake and store energy as fat.
114
•Patients with untreated severe OSA have a 2-3 fold increase in all cause mortality
true
115
descrive the link beween MVA and sleep apnea
▪MVA’s are 2-3 times more likely in individuals with OSAS
▪Can be due to excessive daytime sleepiness, impaired cognition, inattention, etc due to fatigue of untreated sleep apnea.
116
treatments for sleep apnea
* Behavioral (lose weight, stop smoking)
* PAP Therapy (sleep on your back)
* Mandibular Advancement Devices
* Provent
* Surgical Interventions
117
how does a continuous positive airway pressure (CPAP) work
it forces air dow you nasopharynx and keeps your airway open with positive airway pressure
118
patient issues with CPAP
* Mask Discomfort
* Pressure intolerance
* Patient Acceptance
* Claustrophobia
* Aerophagia
* Chest Discomfort
* Nasal congestion
119
T/F treating apnea will decrease nighttime and daytime blood pressure
treu
120
describe the link between CPAP and CHF
CPAP will reduce LV afterload, increase stroke volume, reduce cardiac sympathetic tone, reduce atrial naturetic peptide, and increase LVEF
121
what is a mandibular advancement device used for
to pull the jaw forward during sleep so it won't close off the airway
122
non CPAP treatment of apnea
mandibular advancement devices
tongue retainer device
provent nasal system
123
surgical options for treatment of apnea
genioglossus stimulatir
snoreoplasty
Uvulopalatopharygoplasty
(UPPP)
```
Mandibular Osteotomy with
Genioglossus Advancement (GAHM)
```
Maxillomandibular Advancement Osteotomy
124
two conditions that can cause apnea and be treated by •Maxillomandibular Advancement Osteotomy
crouzons syndrome
mandibular hypoplasia and retrognathia
125
when would trachestomy be indicated for apnea treatment
❖Morbid obesity
❖Severe facial deformity
❖Significant cardiac arrhythmias
❖CPAP/BiPAP intolerance
❖Definitive Treatment for OSAS
126
describe asthma as an inflammatory disease
* Asthma is a chronic inflammatory process
* Results of inflammation (leads to Airway obstruction, Airway hyper-responsiveness, Limitation of airflow)
127
what happens due to remodeling found in asthma patients due to chronic inflammation
* Sub-basement fibrosis
* Mucous hypersecretion
* Injury to epithelial cells
* Smooth muscle hypertrophy
* Angiogenesis
128
three predictors of asthma development
genetics and environmental factors
atopy (genetic predispositon to getting allergies)
viral infection can trigger onset and exacerbation of asthma
129
signs and symptoms of asthmaq
* Wheezing
* Coughing
* Shortness of Breath
* Chest Tightness
* Difficulty with Exercise
* **Nighttime Cough**
* Throat Clearing
* Recurrent “bronchitis” or “pneumonia”
130
what is the gold standard for diagnosting asthma
spirometry with and without albuterol
improvement in FEV1 of 12% or 200L with albuterol is consistent with asthma
131
**Asthma is an obstructive pattern, not restrictive**
therefore, what will the values for FVC and FEV1 look like
FVC is usually normal
FEV1 is decpreased
132
FEV1/FVC ratio indicative of asthma
## Footnote
* \<20 years
* 20-39 years
* 40-59 years
* 60-80 years
* \<20 years =\>85%
* 20-39 years =\>80%
* 40-59 years =\>75%
* 60-80 years =\>70%
133
Which viral infection is most commonly associated with the development of asthma?
## Footnote
A.Metapneumovirus
B.RSV
C.Rhinovirus
D.Parainfluenza
C rhinovrius
134
why is it important to know FEV1 and FVC in diagnosing ashtma
people who have less than 100% of predicted FVC can have normal results
FEV1/FVC gives a true representation to obstructooon
135
if a pediatric patient has a history of multiple pneumonia and risk factors for asthma what might you suspect
inflammation from asthma can cause mucous that makes a good breeding ground for bacteria or could just mimick pneumonia
136
what lab tests might be ordered if asthma is suspected but spirometry is normal
(bronchoprovocation testing)
methacholine challenge
eucapnic voluntary hyperventiliation
exercise challenge
137
pediatric diagnostic factors for ashtma
* Symptom patterns
* Response to medications
* Ruling out other common causes
* Risk factors
* Modified Asthma Predictive Index
138
what is the Modified Asthma Predictive Index used for
Used to predict asthma in patients \<3 years with at least 4 episodes of wheezing in the past year
139
how many major predictive factors on the Modified Asthma Predictive Index indicate a positive result
what are they
one
* Parent with asthma
* Child with eczema
* Child with environmental allergies (skin test/Immunocap)
140
how many minor predictive factors on the Modified Asthma Predictive Index indicate a positive result
what are they
2 or more
* Food allergies
* Eosinophilia \>4%
* Wheezing outside of colds
141
what percent of children who are postiive on the Modified Asthma Predictive Index will be asthmatic in 5 years
75%
142
DDx when faced with asthma symptoms
1. Vocal cord dysfunction
2. Airway lesions or congenital malformations
3. Foreign body aspiration
4. Chronic aspiration
5. CHF
6. COPD/emphysema
7. Reflux
8. Allergies/chronic sinusitis
9. Cystic fibrosis
143
EPR-3 Asthma Guidelines
Four Components of Asthma Care
* Assessing Severity, Monitoring Control
* Education
* Control of Triggers
* Medications
144
what is the severity of asthma based on
what are the grades
impairment and risk
## Footnote
* Mild intermittent
* Mild persistent
* Moderate persistent
* Severe persistent
145
T/F methacholine challenge is useful for ruling out asthma but not for ruling in
treu
146
general rules of asthma treatment
step up when you need to, step down when you can
## Footnote
* Maintain the patient on the lowest dose of medication that effectively controls symptoms
* Treatment plan should be individualized based on the patient’s triggers and patterns
147
environmenta triggesr of asthma
* Viral infections
* Allergens
* Irritants, especially cigarette smoke!!!
* Exercise
* Emotions
* Cold air
148
what is the role of medication in asthma treatment
* Controller medications vs rescue medications
* Safety of inhaled steroids vs oral steroids
* Safety of LABA medications
149
LABA
long acting broncodilators
150
T/F taking a long acting bronchodilator with an inhaled steroid is fatal
false, LABA only therapy will increase risk of death
151
T/F everyone should use a spacer for meter dosed inhalers
treu
152
inhaler technique for infants, toddlers, or impaired people
1. Shake the inhaler several times (unless QVar)
2. Remove the plastic cap from the inhaler
3. Insert the inhaler into the rubber ring in the back of the chamber
4. Check the mask to make sure there is nothing in it
5. Place the mask over the nose and mouth with enough pressure to get a good seal
6. Spray one puff of medication into the chamber
7. Observe the child taking 5-6 breaths (may count also)
8. Remove the mask, allow the child to rest for at least a minute
9. Repeat steps 5 through 9 if a second puff is prescribed
153
Inhaler Technique—School Age & Up
1. Shake the inhaler several times (unless QVar)
2. Remove the plastic cap from the inhaler
3. Insert the inhaler into the rubber ring in the back of the chamber
4. Check the mouthpiece of the chamber to make sure there is nothing in it
5. Exhale fully
6. Place the mouthpiece of the chamber in your mouth
7. Spray one puff of medication into the chamber
8. Take a SLOW DEEP breath in, taking XX seconds to fill your lungs completely (determined by formula below from FEV1)
9. Hold your breath for 10 seconds
10. Exhale and relax for at least a minute
11. Repeat steps 5 through 10 if a second puff is prescribed
154
co-morbidities that can worsen asthma if left untreated
allergic rhinitis
chronic sinusitis
GERD
obestiy
155
simple methods to help manage allergic rhinitis
saline rinses
dust mite covers
proper technique for nasal steroids
avoid triggers
156
clinical pearls for the managment of chronic sinusitis
saline nasal rinses
treat empirically with broad spectrum ABx for 14-21 days
157
clinical pearls for management of reflux associated with asthma
* H2 blocker therapy to start with in a THERAPEUTIC DOSE
* Consider adding Atrovent for asthma symptom flares
* Non-pharmacologic interventions
üElevate head of bed
üNo food or drink 2 hours prior to bed
üSmall frequent meals, avoid overeating
üAvoid trigger foods
158
vocal cord dysfunction is a condition where vocal folds are “twitchy” or adduct during breathing that causes acute shortness of breath, especially with exercise that can be called asthma
what sets it apart
asthma medications is not effective
attacks with no trigger
not waking up at night
159
treatment for vocal cord dysfunction
* Treated with breathing exercises
* Sometimes complicated by reflux
* Referral to speech therapy may be indicated
160
Sources of clots that lead to PE
venous circulation (most from DVT)
right side of the heat
invasive tumors
air embolis
fat embolus
amniotic fluid
161
risk factors for a pulmonary embolism
virchow's triad
surgical procedures
cancer
oral contraceptive
pregnancy
IV drug use
162
Signs of PE
sudden pleuritic chest pain
dyspnea
apprehension
cough
hemoptysis
diaphoresis
163
What is the 3rd most common cause of death in hospitalized patients
why?
PE
because they are frequently misdiagnosed
164
Timing classification of PE
Acute
subacute
chronic
165
hemodynamic classification of PE
–Massive
–Hypotension (SBP \<90 mmHg or drop in SBP ≥40 mmHg from baseline for \>15 min)
–Frequently results in acute RV failure and death (often within 1-2 hours)
–Usually large clot, but could be due to small clots if underlying CV disease
166
location classification of PE
–Lobar
–Segmental
–Subsegmental
–Saddle
167
Symptomoligy classification of PE
T/F all patients be symtomatic
–Symptomatic
–Asymptomatic
No, but almost all will have SOME sign
168
Virchows triad
hypercoagulable state
venous stasis
vascular intimal inflammation of injurty
169
•Virchow’s Triad
–Hypercoaguable States
* **Meds**: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* Disease: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* Inherited genetic disorders: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
HRT, Oral contraceptives
170
•Virchow’s Triad
–Hypercoaguable States
* Meds: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* **Disease**: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* Inherited genetic disorders: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
malignancy, surgery
171
•Virchow’s Triad
–Hypercoaguable States
* Meds: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* Disease: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* **Inherited genetic disorders**: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Factor V Leiden
Protein S & C def
antithrombin III
prothrombin gene mutation,
antiphospholipid ab syndrome
172
Virchows triad: Venous stasis
immobility (post op, stroke)
hyperviscosity (PCV)
increased central venous pressure (low cardia output)
173
Virchows triad: vascular intimal infammation
prior thrombus
surgery
trauma
174
What is the pathophysiology of dysfunction related to PE
increased peripheral vasuclar resistance, vasoconstiction
175
what causes increased periperal vasuclar resistannce in a PE
increased PVR does what
* Physical obstruction of the vascular bed with thrombus and hypoxic vasoconstriction leads to increased PVR.
* Increased PVR impedes RV outflow and reduces LV preload
176
what might precipitate a more rapid deterioration in cardiac output during a PE
preexisting cardiopulmonary disease
177
what will increase the risk of respiratory failure with a PE
coexisting coronary artery disease
178
what is the value of D dimer in PE Dx
a positive D dimer cannot rule in PE, but a negative D-Dimer will rule out a PE
179
describe the process that impairs gas exchange related to PE
* Mechanical obstruction of the vascular bed alters the ventilation to perfusion ratio
* Release of inflammatory mediators causes surfactant dysfunction and atelectasis, resulting in intrapulmonary shunting
* Hypoxia
* Increased respiratory drive resulting in hypercapnia and respiratory alkalosis
180
what makes Dx of PE difficult
* Clinical findings depend on size of embolus and patient’s preexisting cardiopulmonary status
* Common symptoms and signs of PE are not specific to the disorder
181
symptomaic presentation of PE
**•Dyspnea/ Breathlessness**
**•Pleuritic CP/ Painful inspiration**
**•Cough**
* Orthopnea (\>2 pillow or more)
* Calf or thigh pain or swelling
* Wheezing
* Hemoptysis
* Diaphoresis
182
clinical signs of PE
**•Tachypnea (\> half of patients diagnosed)**
**•Tachycardia**
**•Erythema, edema, tenderness, or palpable cord in calf or thigh**
* Rales
* Diminished breath sounds
* Accentuation of the pulmonary component of the 2nd heart sound
* Elevated JVD
* Hypoxia
* Low grade fever
183
Signs of circulatory collapse related to PE
* Dyspnea
* Tachypnea
* Acute right heart failure (JVP, cyanosis, right sided S3)
184
signs of probable RV strain and impending shock in a PE
Transition from tachy to brady, or from a narrow complex to a broad complex tachycardia
185
hypotension with elevated CVP is _____ unless proven otherwise
PE
186
labratory studies for PE: routine labs
–Leukocytosis
–Elevated ESR
–Elevated serum LDH or AST with normal bili
187
lab studies for PE: ABGs
–Respiratory alkalosis secondary to hyperventilation
–Hypoxemia
–Hypocapnia
188
Labs used for PE Dx
non-specific labs
ABGs
D-Dimer
Troponin
BNP
189
EKG findings related to PE
* non specific ST-T wave changes and tachycardia
* Severe right ventricular dysfunction: T-wave inversion in the precordial leads
190
EKG findings related to massive acute PE or cor pulmonale (uncommon)
–Classic S1Q3T3 Pattern
–Right ventricular strain
–New incomplete RBBB
191
EKG signs of a PE that indicate a poor prognosis
* Atrial arrythmias
* RBBB (new)
* Inferior Q waves (II, III, Avf)
* T-wave inversion and ST-segment changes (anterior leads)
* Bradycardia
192
CXR signs of PE
* Atelectasis
* Pleural effusion
* Cardiomegaly
193
Imaging studies for PE
Pulmonary angiography
CT Pulmonary angiography
VQ Scan
Venous ultrasound
194
what is the intial test of choice for PE
why is it prefered over the gold standard
CT pulomnary angiography
its faster and can provide alternate explanation for symptoms
195
If a patient is postive for DVT and you suspect PE, but CTA is negative, what should you do
treat and do further testing
196
what is the primary utility of pulmonary angiography in treating a PE
it gives a definitive dx
if the patient can't take anticoags and you want to put in an IVC filter
197
when is echocardiogram useful in Dx of PE
what is the limitation
can be useful to Dx a massive PE if you ned to confirm a presumptive Dx
•Only 30-40% will have echocardiographic abnormalities suggestive of PE
198
echocardiogram signs of PE
* Increased RV size
* Decreased RV function
* Tricuspid regurgitation
* RV thrombus
* Regional wall motion abnormalities that spare the right ventricular apex “(McConnell’s sign”)
199
what is the best diagnostic approach to confirm a Dx of PE
•Combine clinical assessment/ suspicion with D-dimer testing and imaging (CT-PA)
200
wells criteria
what would indicate PE
a diagnostic test that indicates probability of a PE
\<4, PE unlikely
\>4, PE likley
201
immediate treatment of PE
STABILIZE
O2, IV access, consider empiric anticoagulation
202
Resuscitation of a critical patient with PE
Respiratory support
Hemodyanmic support
empiric coagulation if not contraindicated
203
Resuscitation of a critical patient with PE: respiratory spport
–Supplemental oxygen
–Mechanical ventilation
204
Resuscitation of a critical patient with PE: hemodyanmic support
–IVFs (500-1,000 mL NS during initial period)
–IV vasopressors: norepinephrine, dobutamine
205
Resuscitation of a critical patient with PE: empiric anticoagulation
when would you used this?
–If no excess risk for bleeding
–High clinical suspicion (Wells score \>6)
–Moderate clinical suspicion and diagnostic w/u \>4 hours
–Low clinical suspicion and diagnostic w/u \>24 hours
206
if empiric coagulation is contraindicated, what should you do
expedite diagnosis so alternate therapies can be initiated if PE is confirmed
207
adjunctive therapy for PE
General (O2, analgesics, IVFs)
* Encourage early ambulation/ mobility
* Compression garments
* SMI
208
when should anticoagulation be initiated for treatment of PE
when should it stop
once PE is confirmed
empirically if needed and low risk for bleeding
if the PE is excluded
209
parenteral anticoag therapy to treat PE
low molecular weight heparin
fondaparinux
IV UFH
SC UFH
210
caution with LMWH should be used if what condition is present
renal insufficiency CrCl\<30
211
risk factors for uncontrolled bleeding related to anticoagulation
**age \>65 yrs,**
**previous bleed,**
**thrombocytopenia,**
**antiplatelet therapy,**
**poor anticoagulant control,**
recent surgery,
frequent falls,
reduced functional capacity,
previous stroke,
DM,
anemia,
cancer,
renal failure,
liver failure,
alcohol use
212
how many risk factors for anticoagulation therapy are considered moderate risk
high risk
one
two or more
213
when is fonaperinux contraindicatied
when should caution be used
CrCl \<30
CrCL 30-50
214
when would IV or SC unfractionated heparin be used in treatment of PE
–Persistant hypotension due to massive PE
–Increased risk of bleeding
–Consideration for thrombolysis
–Concern for subcutaneous absorption (obesity)
215
when would warfarin treatment be used in treating PE
what testing must be used with this therapy
lag time?
what is the goal of therapy
the same day or after parentaeral therapy
requires daily INR
you need at least 5 days for the drug to become effective
INR of 2.5
216
what is the advantage of new novel agents for anticoagulation treatment of PE
–Fixed dose, oral agents
–No routine laboratory monitoring
–No antidotes
–Renal insufficiency parameters
217
two exampes of new, novel agents for PE treatment
•**Factor Xa Inhibitors**
–Rivaroxaban
–Apixaban
–Endoxaban
•**Direct Thrombin Inhibitors**
–Dabigatran
218
what determine the duration of anticoagulation therapy following PE
the clinical situation that precipitated the event
219
Duration of Anticoagulation Therapy: reversible risk factor
–3 months
220
Duration of Anticoagulation Therapy: unprovoked
–3 months and reassess
221
Duration of Anticoagulation Therapy: recurrent
–3 months and reassess
–Consider lifetime
222
Duration of Anticoagulation Therapy: special considerations
–Cancer
–Pregnancy
223
thrombolytic treatment agents used for PE
•tPA, Streptokinase, Urokinase
224
when is thrombolysis used in treating PE
•Patients with confirmed PE and persistent hemodynamic comprise (“Massive PE”) and no risk of bleeding
225
what is the action of thrombolytic treatment for PE
risks?
can it be used with anticoagulation
* Accelerates clot lysis and has short term hemodynamic benefits
* Increases risk of major bleeding
* Still follow with anticoagulation therapy
226
when is embolectomy warranted in treatment of PE
•Presentation severe enough to warrant thrombolysis, but thrombolysis fails or contraindicated.
227
when are IVC filters indicated for treating PE
* Contraindications to anticoagulation
* Failed anticoagulation
* Developed complication due to anticoagulation
* Hemodynamic or respiratory compromise severe enough that recurrent PE would be lethal
228
T/F May be prophylactic in selected populations if high risk DVT and contraindication to mechanical or pharmacological prophylaxis
true
229
indications that outpatient treatment is viable for a PE
•**Low risk of death**
**•No supplemental oxygen**
**•No need for narcotic pain control**
**•Normal pulse and BP**
**•No recent h/o bleeding**
* No serious comorbid conditions (ischemic heart disease, chronic lung disease, liver or renal failure, thrombocytopenia, or cancer)
* Normal mental status with good understanding of risks and benefits
* Good home support
* No concomitant DVT
230
T/F PE has a good prognosis
True, if Dx and Tx quickly and there is not an unerlying condition
231
what is the most cause of morbidity associated with PE
shock or recurrent PE
232
factors that will increase mortality risk associated with PE
* RV dysfunction
* Accompanying DVT
* RV thrombus
* BNP
* Troponin
* Hyponatremia
* Lactate levels
233
key prevention considerations for patients at high risk for PE
* Early ambulation
* Intermittent pneumatic compression stockings
* Low-dose heparin/ Low-dose LMW heparin
* Combination of mechanical and pharmacological measures
* Compression stockings
* STOP SMOKING!
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