Author:
Kai Knudsen
Granskare:
Kristina SvennerholmUpdated:
27 August, 2025
Severe cases of pulmonary embolism are characterized by hypoxia with increasing circulatory failure. Unstable hemodynamics with signs of peripheral and cerebral hypoperfusion indicate decompensation and low cardiac output (CO). Pulmonary embolism causes an acute increase in pulmonary vascular resistance (PVR), leading to right ventricular (RV) failure.
Pulmonary Embolism
Severe cases of pulmonary embolism are characterized by hypoxia with increasing circulatory failure. Unstable hemodynamics with signs of peripheral and cerebral hypoperfusion indicate decompensation and low cardiac output (CO). Pulmonary embolism causes an acute increase in pulmonary vascular resistance (PVR), leading to right ventricular (RV) failure. Wall tension rapidly rises in the pressure-loaded RV, which leads to an increased oxygen demand and decreased coronary perfusion, quickly resulting in RV ischemia. Consequently, the RV cannot maintain preload for the left ventricle, resulting in reduced CO/MAP and further decreased coronary perfusion. This quickly creates a vicious cycle with worsening circulatory collapse, eventually leading to cardiac arrest.
Since unstable patients with pulmonary embolism have acute pulmonary hypertension and RV failure, induction with typical vasodilatory agents and positive-pressure ventilation can worsen the condition. Intubation should be avoided, but if inevitable after trials of non-invasive support, the patient should be induced with Ketamine and ongoing norepinephrine infusion. For ventilatory support, lower PEEP and tidal volumes should be used. Additional fluid administration can severely worsen RV failure and should only be attempted as small boluses, evaluated each time. Pulmonary embolism is classified into low, intermediate, and high risk. Classification is determined by the level of hemodynamic impact. Intermediate risk is further subdivided into low and high intermediate risk. High intermediate risk pulmonary embolism presents with RV distension (on CT or echocardiogram) and elevated biomarkers (TNI and/or nt-proBNP). High intermediate risk patients generally do not meet criteria for thrombolysis. These patients should be closely monitored, and in the event of deterioration during anticoagulation therapy, thrombolysis (or catheter-based intervention/surgery in case of contraindication) should be considered.
High-risk pulmonary embolism is assessed as patients with hemodynamic instability.
Pulmonary embolism is classified into low, intermediate, and high risk. Classification is determined by the level of hemodynamic impact. Intermediate risk is further divided into low and high intermediate risk. High intermediate risk pulmonary embolism presents with RV distension (on CT or echocardiogram) and elevated biomarkers (TNI and/or nt-proBNP). High intermediate risk patients do not generally meet criteria for thrombolysis. These patients should be closely monitored, and in the event of deterioration during anticoagulation therapy, thrombolysis (or catheter-based intervention/surgery in case of contraindication) should be considered. In these cases, it is important to establish a plan for patient care in the event of worsening. Heart rate > 100 b/m, systolic blood pressure 90–100 mmHg, respiratory rate > 20, oxygen saturation < 90%, lactate > 2, heart failure, active cancer, and elevated troponin have been shown in post hoc analyses to correlate with increased risk of hemodynamic collapse.
Definition of Hemodynamic Instability in Pulmonary Embolism
- Systolic blood pressure <90 mm Hg or need for vasopressor to maintain systolic blood pressure >90 mm Hg (note! Syncope can indicate high-risk pulmonary embolism despite stabilized blood pressure > 90 mm Hg)
- Blood pressure drop >40 mm Hg for at least 15 min; often difficult to assess clinically
Management
First-line treatment for high-risk pulmonary embolism is intravenous thrombolysis followed by anticoagulation with Heparin infusion. The decision for thrombolysis is made by the on-call physician and ICU physician, if necessary in consultation with a coagulation specialist. Treatment should be carried out promptly in an intensive care setting.
In the case of severe contraindications to thrombolysis or failure of administered thrombolysis, catheter-based intervention, surgical embolectomy, or ECMO are alternative treatments. The choice is made in consultation with relevant specialties (on-call physician, coagulation, PCI operator, thoracic surgery, thoracic anesthesia, and intensive care) and is guided by patient history, embolus location, extent, and duration. Catheter-based intervention is performed under anesthesia monitoring. Management is also tailored to available resources and expertise in each case. In case of deterioration while awaiting intervention, additional supportive measures may be tried.
If the patient presents in severe shock or ongoing CPR, thoracic anesthesia and thoracic surgery should be contacted immediately for on-site assessment of potential ECMO use. Pending a decision, full-dose thrombolysis may be considered to buy time. ECMO may also be considered regardless of where the patient is in the treatment process, even post-thrombolysis. In rare cases, ECMO may be initiated in a relatively stable patient when RV failure makes intubation and ventilation risky. To save time, the femoral vein on the right side and the common femoral artery on the left may be catheterized by an ICU physician before the ECMO team arrives. However, catheterization in the ICU must not delay catheter-based intervention and should be coordinated with thoracic anesthesia.
Thrombolysis
Intravenous thrombolysis uses Alteplas (Actilyse®) packaged in ampoules. Ampoules I and II are mixed according to the instructions in the packaging to a concentration of 1 mg/ml. This solution is drawn directly into a 50 ml infusion syringe and can be administered via both PVK and CVK. If LMH/Heparin has been administered, start Alteplas promptly, regardless of the dose or time of LMH/Heparin administration. Any ongoing Heparin infusion is paused during thrombolysis.
- Critical situation (high vasopressor dose requirement, shock, ongoing CPR). Bolus 0.6 mg/kg (max 50 mg) iv over 5–15 min followed by 50 mg infusion over a total of 120 min. (total dose max 1.5 mg/kg if weight <65 kg)
- Hypotensive but stable patient (hypotension but adequate perfusion without inotropes or with low/moderate vasopressor dose) Bolus 10 mg iv over 2 min followed by 90 mg infusion over 120 min (standard dose). (total dose max 1.5 mg/kg if weight <65 kg)
- Patient with increased bleeding risk (absolute or relative contraindication to thrombolysis)
NOTE! In these cases, catheter-based intervention or reduced dose thrombolysis are alternatives. An acute consultation decides the best option for the individual patient! - With decision for half-dose thrombolysis: Infusion 0.6 mg/kg (max 50 mg) over 60–90 min without bolus. Then re-assess clinically:
- Upon improvement, start Heparin infusion iv or LMH sc.
- If improvement does not occur, the same dose can be repeated in 60 min.
- After thrombolysis is completed, start anticoagulation with Heparin or LMH.
The treatment regimen depends on the patient’s instability and thus the urgency of treatment. There is no difference in final outcome between bolus and continuous infusion.
Major Contraindications
- History of hemorrhagic stroke
- Ischemic stroke in the last 6 months
- CNS tumor and/or metastases
- Head trauma or CNS surgery in the last 2 months
- Surgery or major trauma in the last 3 weeks
- Lumbar/epidural puncture in the last 48 hours
- Active bleeding/known bleeding tendency
Relative Contraindications
- Current endocarditis, pericarditis
- Acute pancreatitis
- Severe liver failure
- Active peptic ulcer
- Platelet count <100 x 109/L
- Ongoing treatment with oral anticoagulants
- During childbirth and the first few weeks postpartum
- Short life expectancy, e.g., extensive cancer
Bleeding Complications During Thrombolysis Treatment
Treatment for life-threatening/severe bleeding during ongoing thrombolysis
Stop the Alteplas infusion! Administer the following medications WITHOUT awaiting test results!
- Fibrinogen concentrate 4 g iv (expected to increase fibrinogen by about 1.5–1.8 g/L). The desired fibrinogen level after treatment is >2 g/L. Alteplas has a short half-life (10 min) but fibrinogen reduction can persist for several hours, contributing to ongoing bleeding.
- Tranexamic acid (Cyklokapron® 100 mg/ml) 10 ml = 1g iv, repeat after 4 hours.
- Red blood cells as needed to maintain Hgb ≥ 10 g/dL.
- Platelet concentrate as needed to maintain platelet count ≥ 80 x109 /L.
Treatment for significant bleeding that is not life-threatening/severe
- Consider stopping the infusion
- Order blood products
- Test for a-PTT, fibrinogen, Hgb, platelet count, and thromboelastometry.
- Tranexamic acid 1 g iv.
- Consider transfusion if Hgb <10 g/dL and/or platelet count <80 x 109/L.
- See additional treatment for life-threatening bleeding below.
Minor bleeding, such as superficial hematomas and needle-site bleeding, is common/inevitable and should be managed with observation/local compression and does not require a dose adjustment of Alteplas.
Anticoagulation with Heparin
Patients who are not candidates for thrombolysis due to contraindications should initially receive a bolus of Heparin 100 IU/kg iv while awaiting further management (see algorithm).
During thrombolysis, any ongoing Heparin infusion is paused. If a patient who has received thrombolysis shows no clinical signs of bleeding, Heparin infusion is resumed without a bolus dose 60 minutes after the end of the Alteplas infusion. Target a-PTT is 70–100 s (see separate schedule).
If a patient who has received thrombolysis has severe bleeding issues, any deficiencies in coagulation factors should be corrected before resuming anticoagulation. Check Hgb, platelet count, PT (INR), a-PTT, and fibrinogen (thromboelastometry as needed). Heparin infusion affects a-PTT, other parameters should be corrected.
If the acute management ends with Heparin infusion as the only treatment, consider repeating any previously administered bolus dose if more than 2 hours have passed. The decision is made based on a-PTT. Heparin infusion follows standard anticoagulation guidelines.
Switching from Heparin infusion to LMH sc is done a day after thrombolysis is completed if the patient is hemodynamically stable and shows no significant clinical bleeding.
Anticoagulation with Low Molecular Weight Heparin (LMH)
LMH is rarely an option for an unstable patient in the ICU. However, if a stable patient received thrombolysis in the ICU and is transitioning to general ward care, it may be appropriate.
- In patients who have not received LMH, it can be started in full dose 60 min after the end of the Alteplas infusion, but initially at half daily dose every 12 hours, provided there are no clinical signs of bleeding.
- In patients who received full-dose LMH before thrombolysis, wait 12 hours from the last LMH dose before resuming (at least 2 hours), initially at half daily dose every 12 hours.
Heparin Protocol for Thromboembolic Event
Heparin, which normally occurs in the body bound to protein, is a strongly acidic, sulfated glucosaminoglycan (mucopolysaccharide) with an anticoagulant effect. In combination with the co-factor antithrombin III, heparin affects multiple steps in the coagulation mechanism, providing a blood-thinning effect. Heparin is administered in the treatment of thromboembolic events such as pulmonary embolism or deep vein thrombosis.
Dosage
- For the treatment of deep vein thrombosis, a bolus dose of 5000 IU (1 ml) iv is given if weight is under 85 kg.
- If weight is over 85 kg, a bolus dose of 7500 IU (1.5 ml) iv is given.
- For the treatment of pulmonary embolism, a bolus dose of 7500 IU (1.5 ml) iv is given.
- In cases of massive DVT/PE: larger bolus (100-150 IU/kg).
- In patients with increased bleeding risk, a bolus dose of 2500 IU iv is given, except in cases of massive pulmonary embolism/DVT. If pulmonary embolism is suspected, bolus and infusion are started while awaiting diagnosis confirmation. A continuous infusion of heparin (heparin drip) is then administered. 15000 IU (3 ml) is added to 500 ml of 0.9% NaCl or 7500 IU (1.5 ml) to 250 ml of 0.9% NaCl. The infusion is started simultaneously with the bolus dose.
- For patients weighing > 60 kg and aged < 65 years, the rate is 42 ml/hour. For other adults, it is 36 ml/hour. The treatment effect is monitored with a-PTT tests. The first a-PTT test is done after 6 hours. a-PTT should be 1.5-3 times the reference value, i.e., 60-120 seconds (increased bleeding risk: 50-80 seconds).
Heparin Dosing Schedule
Correction measurements according to APTT values
| aPTT value without increased bleeding risk (target value 60-120 sec) | aPTT value at increased bleeding risk (target value 50-80 sec) | Primary action | Adjust the drop rate | New sample checked |
|---|---|---|---|---|
| > 200 sec | >160 sec | Check the infusion mixture. Take a new test APTT sample, turn off the drop for 1 hour (not the first APTT after drip start) | Reduce at 9 ml/h | New test after 4 hours |
| 181-200 sec | 141-160 sec | Reduce at 9 ml/h | New test after 6 hours | |
| 141-180 sec | 111-140 sec | Reduce at 6 ml/h | New test after 6 hours | |
| 121-140 sec | 81-110 sec | Reduce at 3 ml/h | New test after 6 hours | |
| 60-120 sec | 50-80 sec | Unchanged infusion rate | If the first value after drip start, take a new test after 6 hours, or after 12 hours. | |
| 50-59 sec | 40-49 sec | Increase at 2 drops/min (= 6 ml/h) | New test after 6 hours | |
| < 50 sec | < 40 sec | Give 2500 E of Heparin i.v. and | Increase infusion rate at 9 ml/h | New test after 6 hours |
Indications
Anticoagulation. Deep vein thrombosis (DVT), pulmonary embolism. Intravascular coagulation, peritendinitis crepitans. Extracorporeal circulation in cardiac surgery and hemodialysis.
Side Effects
Bleeding, thrombocytopenia, transient liver effects.
Concentration
5000 IU/ml, 25,000 IU/ml.
Warning
Heparin is contraindicated in cases of high bleeding risk. Caution is recommended in patients with thrombocytopenia and platelet function defects (including medication-induced) as well as in severe liver and kidney failure.
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