Lecture 6 - Pulm Emergencies Flashcards
What are signs of respiratory distress?
RR >30
retractions/use of accessory muscles
paradoxical abdominal wall movement with inspiration (diaphragmatic fatigue)
pulse ox <90%
cyanosis
unable to speak more than single word or short phrase
agitation or lethargy
Virchow’s triad
endothelial damage
venous stasis
hypercoagulability
PE
pulmonary embolism
clot in the pulmonary artery/arteries impairs perfusion of the lungs and can lead to lung infarction and death
Pts with pulmonary embolism may present how during the physical exam?
tachycardia tachypnea hypoxia rales wheezes fever LE erythema, swelling, redness variable BP
*pt may only have a few of these
most common sxs is CP (?) then SOB, then axiety
most common sign is tachypnea, then rales, then fever
What is the classic symptom triad of pulmonary embolism?
hemoptosis
dyspnea
chest pain (only found in <20% of PE cases)
97% of PE pts will have one of the following:
- dyspnea
- tachpnea
- pleuritic pain
Which labs do you NEED to order asap for a pt you suspect of PE?
ABG
-A-a gradient is normal in 50% of PE pts
-PaO2 is sensitive but not specific
-degree of hypoxemia does not accurately predict size of PE
Creatinine
-needed to determine kidney function prior to giving IV contrast
PT/PTT
Wells Criteria
Used in assessing PE
Clinically suspected DVT
Alternative dx less likely than PT
HR >100 BPM
Immobilization/surgery in the previous 4 weeks
History of DVT or PE
Malignancy (or treatment within the last 6 mo)
If >6 – high likelihood of PE
if 4.5-6 –moderate likelihood of PE
if = 4 - low likelihood of PE
PERC Score
pulmonary embolism rule out criteria
useful to determine who is at such a low risk of PE that no further diagnostic testing is required, and the pt can safely be discharged or worked up for other pathology
this decision making rule only works when you have a low pre-test probability to start with
criteria: SaO2 <95%? Unilateral leg swelling? HR >100 BPM? Recent surgery or trauma? History of DVT or PE? Hemoptysis? Age >50 yo? Current hormone use?
if the answer to ANY of these questions is “yes” you may NOT rule out PE
if the answer to ALL questions is “no” then there is a 1.8% chance you will miss a PE
D-Dimer
d-dimer is a breakdown product of cross linked fibrin by the fibrinolytic system
d-dimer levels become elevated when there is lysis of cross-linked fibrin within the thrombus
When is D-Dimer helpful?
if D-dimer levels are low in pts who seem to have low probability of having a PE, we can be re-assured that the likelihood of the pt having a PE is very low
extraordinarily high D-dimer levels should create increased suspicion of PE, but not diagnostic
When is D-Dimer useless?
recent surgery or trauma pt has other auto-immune or inflammatory process going on in the body liver/renal/heart failure pregnancy sepsis sickle cell disease acute MI or Stroke
What imaging modality is useful for pulmonary embolism?
CT
What imaging modality is useful for pulmonary embolism in pregnant pt?
VQ scan
What is CXR role in PE?
the greatest utility of the CXR in dx of PE is exclusion of alternate disorders
Might see weestermarks, hamptom hump effusion, elevated hemidiaphragm
What can you see on EKG with a pt having a PE?
Deep S in 1, Q in 3, inverted T in 3
tachycardia is the most common finding
the greatest utility of the EKG in dx of PE is exclusion of alternate disorders
How do you manage a pt with PE?
manage airway
anti-coagulation: stable pt
–Lovenox 1mg/kg SQ, no coag studies required
Anti-coagulation: unstable pt
-Heparin 80u/kg bolus, then 18u/kg per hour IV
-monitor aPTT every 6 hours until level 50-90 achieved
-lovenox 1mg/kg SQ, no coag studies required
Treat shock with IV fluids if no evidence of pulmonary edema
use dopamine if vasopressor indicated
thrombolysis (tPA, streptokinase)
Non-cardiogenic vs cardiogenic pulmonary edema?
non-cardiogenic: change in permeability of pulmonary membranes sepsis or septic shock inhalation injuries drugs and toxins aspiration syndromes neurogenic causes high altitude
cardiogenic: elevated pulmonary capillary hydrostatic pressure acute myocardial ischemia or infarction cardiomyopathy valvular heart disease hypertensive emergency diastolic dysfunction
COPD
typically an acute exacerbation of chronic condition so get the PMHx
look for classic presentation:
- big blue boater
- skinny pink puffer
What are the physical findings of COPD?
tachypnea increased phlegm/purulent phlegm inspiratory and expiratory wheeze decreased air movement use of excessory muscles pursed lip breathing somnolence or confusion left ventricular dysfunction
Signs of hypoxemia
tachypnea cyanosis agitation tachycardia HTN increased work of breathing creates CO2 not compensated for by alveolar ventilation --> hypercarbia and respiratory acidosis --> to confusion, stupor, hypopnea, apnea
What is the work up for a COPD pt?
ask the pt about their home oxygen and baseline O2 saturation
medications
hx of steroids, intubation, recent illness
always get a CXR!
EKG - hypoxia can lead to ischemic changes
your most valuable tool to measure response to medication or decline is the pulmonary function test or peak flow
consider ABG if you suspect respiratory acidosis
What is the treatment for COPD?
oxygen to O2 saturation of 90-92%
correct hypoexemia to Pa02 >60mmHg
–effects of supplemental O2 may take up to 30 minutes to see
Warming:
balance the need for increase PaO2 against the possibility of producing hypercapnia
Pts with chronic respiratory acidosis rely on hypoxia for respiratory driver
Smooth muscle relaxants:
Albuterol: Ipratropium (atrovent) 2:1 x 1
Steroids
prednisone 60mg PO or methylprednisolone 125 mg IV
ABX are standard of care for COPD exacerbation even in absence of infiltrate of CXR
When should you consider intubating a COPD pt with acute exacerbation?
altered mental status
respiratory fatigue
respiratory distress, agitation
Acute CP lateralizing to one side, with unilateral or absent breath sounds
Pneumothorax
RR >24
HR >120
Subcutaneous emphysema
Hyper-resonance
Hypotension
