Setting: ED
CC: “I’m having a hard time catching my breath.”
VS: BP: 108/68 mm Hg; P:108 beats/minute; T: 101°F; R: 24 breaths/minute
HPI: A 42-year-old woman, coming from India, just deplaned at the airport, feeling very short of breath, and was brought immediately to the ED. She was on a flight from Mumbai, through Dubai to New York, and started feeling dyspneic about an hour before landing. The flight stewards thought she might be having a panic attack and had her lie down on the floor in the first class cabin, but saw no improvement in her symptoms. The woman is on a stretcher in your ED with oxygen in place, and she is feeling anxious.
PMHX: ovarian cysts
Medications: none
As with most of the CCS pulmonary and dyspnea cases, order oxygen, oximeter, chest x-ray, and ABG.
PE:
General: anxious, sweating
Chest: clear to auscultation, no rales, rhonchi, or crepitations
Cardiovascular: normal
Abdomen: benign
Oxygen is considered to be administered immediately, but tests ordered at the same time are considered to be done first. It is much harder to interpret an oximeter or ABG while the person is on oxygen. It is never precisely clear how much oxygen patients are really getting except when they are on ventilator support.
Report:
Oximeter 90% room air saturation
Chest x-ray: normal
ABG: pH 7.47; PCO2 31 mm Hg; PO2 62 mm Hg
CCS is designed to assess your ability to determine just the right timing of tests versus treatments or both.
What should you do next for this person?
a. Order a ventilation-perfusion (VQ) scan.
b. Give the patient heparin.
c. Move the patient to ICU and do a CT angiogram.
d. Perform and embolectomy.
e. Order an inferior vena cava (IVC) filter.
Answer b. Give the patient heparin.
This is enough information to indicate the need to start therapy. The acute onset of shortness of breath without wheezing on examination or the rales of congestive heart failure (CHF) has a high predictive value for pulmonary embolus (PE). The number one issue in PE management is, in fact, making sure you know not to wait for specific tests like a CT angiogram, VQ scan, or lower extremity Doppler ultrasound to start therapy.
Acute Hypoxia + Normal Lung Examination and Chest X-Ray = PE
Little else besides PE causes severe desaturation and clear lungs.
Peripheral chemoreceptors:
• Aortic arch hypoxia
• Stimulation PO2 <60 mm Hg
How will you determine the need for thrombolytics?
a. Lower extremity Doppler ultrasound
b. Hypotension and right-sided heart strain on echocardiogram or electrocardiogram (ECG)
c. CT angiogram
d. VQ scan and d-dimer
Answer b. Hypotension and right-sided heart strain on echocardiogram or electrocardiogram (ECG)
Thrombolytics are used for the most severe, large clots. This question basically asks if you know how to assess the severity of the clot. Large clots block blood flow. Blocked blood flow decreases BP and causes back pressure in the heart. Clot size on CT is not as important as decreased heart function.
Severe Dangerous Clot = Hypotension and Abnormal Heart Pressure
With a large clot, which test gives the first abnormal result?
a. Right ventricular hypertrophy
b. Right bundle-branch block
c. Increased pulmonary artery (PA) pressure
d. Increased wedge pressure
e. ECG with S1Q3T3 pattern
Answer c. Increased pulmonary artery (PA) pressure
Big clots block PAs. Blocked PAs give pulmonary hypertension, which is largely saying the same thing. Right ventricular hypertension happens later. ECG findings occur after that. Wedge pressure indicates left atrial pressure. Wedge pressure is measured on a right-sided heart catheter but has nothing to do with right-sided heart pressures.
Large clots cause pulmonary hypertension.
Orders:
ECG
Echocardiogram
Activated partial thromboplastin time (aPTT), prothrombin time (PT), international normalized ratio (INR)
CT angiogram
Low molecular weight heparin has equal efficacy to IV heparin.
Heparin works by potentiating antithrombin.
It prevents clot formation, but does not destroy old clots.
The patient is on oxygen and heparin. Repeat oximeter shows the saturation largely unchanged at 91% to 92%. On a 50% facemask saturation, it is still at 93% to 94%.
When the ECG does show an abnormality, what is the most common abnormality found?
a. S1Q3T3 pattern
b. Nonspecific ST-T wave changes
c. Right bundle-branch block
d. Tall R waves in V1 and V2 (right ventricular hypertrophy)
Answer b. Nonspecific ST-T wave changes
The reason for the nonspecific ST- and T-wave changes is not precisely clear. The other findings going along with right-sided heart strain may have more specificity for a PE, but are much less common, being seen in <25% of patients.
Clots and hematomas give fever.
Coagulation Studies
Done at baseline for those patients who need anticoagulation therapy.
Reports:
ECG: sinus tachycardia with T-wave flattening in I, aVL, and V5 and V6
aPTT, PT, INR: normal
CT angiogram: large clot in PAs bilaterally
With persistent hypoxia despite increasing administration of oxygen and signs of right-sided heart strain, the patient should be placed in the ICU and thrombolytics (tissue plasminogen activator [tPA]) given.
The ventilation-to-perfusion ratio (V:Q) mismatch prevents increased oxygenation despite giving oxygen to the patient.
Report:
Echocardiogram: PA pressure 54 mm Hg (elevated); decreased right ventricular motion; enlarged right atrium
Which form of thrombophilia changes initial therapy?
a. None
b. Antiphospholipid syndrome
c. Protein C or S deficiency
d. Factor V Leiden mutation
Answer a. None
Thrombophilias make no difference in acute management. You use heparin followed by 6 months of warfarin initially with all of them. All of them get an INR of 2 to 3 with the first clot. That is why there is no point in testing for them with a first clot. They do not change management.
If a clot is found on CT, then Doppler ultrasounds of the legs do not matter.
If a clot is found on Doppler ultrasounds of the legs, then CT does not matter.
All that matters is:
Clot versus No Clot
Doppler ultrasounds are 60% to 70% sensitive for the PE source.
What is the mechanism of thrombolytics?
a. Plasmin breaks fresh clots into d-dimers.
b. Fibrinogen is activated to fibrin split products.
c. They inhibit the cascade start (factor XII and VII).
d. They break up fibrinogen after factor XIII stabilizes it.
Answer a. Plasmin breaks fresh clots into d-dimers.
Thrombolytics activate plasminogen into plasmin. Plasmin dissolves recently activated fibrin into d-dimers. Plasmin will not specifically break up clotting that has been cross-linked and stabilized by factor XIII. It is thrombin that activates fibrinogen by splitting off fibrin-split products.
Thrombin activates fibrinogen, creating split products.
Plasmin destroys fibrin, creating D-dimers.
After administering thrombolytics, both oxygenation and BP improve in the patient.
Repeat VS: P: 98 beats/minute; BP 118/74 mm Hg
Repeat ABG: pH 7.42; PCO2 38 mm Hg; PO2 74 mm Hg
Orders:
Transfer patient to ward.
Continue heparin.
Start warfarin.
Measure INR.
Do CBC.
• If heparin-induced thrombocytopenia (HIT) develops, use argatroban.
• Argatroban is a direct-acting thrombin inhibitor.
After transferring the patient to the hospital ward, repeat the physical examination. Move the clock forward 1 day at a time after moving the patient to the hospital ward. Repeat the CBC and INR each day looking for HIT and to achieve a therapeutic INR of 2 to 3. You will not see an effect of warfarin for several days and should not expect to see a fully therapeutic INR for 5 to 7 days.
Use IVC filter:
• For bleeding
• When anticoagulation cannot be used
• When there is a recurrence while fully anticoagulated
Warfarin
• Inhibits factors II, VII, IX, X
• Needs 3 days to work
After 5 days, the patient’s INR rises to 2.4. You can stop the heparin when the INR comes above 2 and discharge the patient. The length of therapy should be 6 months.