Pulmonary Embolism: Treatment and Nursing Interventions

Pulmonary Embolism (PE) Definition

• PE is the obstruction of one or more pulmonary artery branches by particulate matter originating elsewhere in the body.
• Thrombi are the most common cause of pulmonary emboli.
• Tumor fragments, amniotic fluid, air, or fat can also cause a pulmonary embolus - referred to as nonthrombotic pulmonary emboli (NTPE).
• NTPEs are very dangerous; amniotic fluid emboli (AFE) has a 17% failure to rescue rate, with the mother dying in two-thirds of cases.
• The failure to rescue rate rises above 30% when AFE occurs alongside another complication.

Epidemiology of PE

• Deep vein thrombosis (DVT) is the greatest risk factor for PE.
• Virchow's triad, consisting of venous stasis, vessel wall damage, and hypercoagulability, is the major predisposing factor for the development of DVT.
• Prolonged immobility is the most common cause of DVT.

Sources of Pulmonary Emboli

• Deep vein thrombus: A clot that breaks loose from its origin (often the deep veins of the leg or pelvis) and travels to the pulmonary vasculature.
• Fat: Typically from a long-bone fracture.
• Osteomyelitis.
• Liposuction.
• Air: From central venous catheter (CVC) insertion due to negative intrathoracic pressure allowing air entry or disconnection from a fluid source.
• Cardiopulmonary bypass.
• Hemodialysis.
• Amniotic fluid: Can enter the vascular space during delivery through placental vessels.
• Tumor: Sloughs off, and tumor particles travel to the pulmonary vasculature.

Virchow's Triad Causes

• Hypercoagulability can be caused by cancer, oral contraceptives, dehydration/hemoconcentration, sickle cell anemia, polycythemia vera, or abrupt discontinuation of anticoagulants.
• Prolonged bedrest/immobility.
• Obesity.
• Burns.
• Pregnancy.
• Vasculitis/thrombophlebitis.
• Bacterial endocarditis.
• Any postoperative patient.
• Intimal damage of vessels is caused by trauma or IV drug use.
• Atherosclerosis.

Other Risk Factors for DVT

• Obesity.
• Smoking.
• Chronic heart or vascular disease.
• Fracture (hip or leg).
• Hip or knee replacement.
• Major surgery or trauma.
• Spinal cord injury.
• History of previous venous thromboembolism.
• Malignancy.
• Age >50 years.
• Estrogen use (i.e., oral contraceptives).
• Pregnancy.

Incidence of PE

• Prior to 2020, the incidence of PE was approximately 1 to 2 per 1,000 persons in the United States; 50,000 to 100,000 patients died from PE.
• PE was a common complication of SARS-CoV-2 virus, with >15% of patients developing a PE; >40% of patients diagnosed with PE also had DVT.
• Venous thromboembolism (VTE) occurred 30 days after COVID-19 infection in 50.99 per 1,000 persons, compared to 2.37 per 1,000 persons in noninfected patients.
• PE is the third most common cause of death in hospitalized patients.
• Older adult patients are the most likely recipients of knee or hip replacement surgery with higher DVT risk due to limited mobility and aging.

Pathophysiology of PE

• A blood clot or particulate matter lodges in the pulmonary artery (PA), blocking blood flow.
• PE leads to an impaired ventilation-to-perfusion ratio (V/Q ratio), causing a V/Q mismatch with decreased blood flow to functioning alveoli.
• Prevents gas exchange at the alveolar level, leading to hypoxemia and vasoconstriction in the affected pulmonary vascular bed.
• Pulmonary vascular resistance (PVR) increases due to blood flow obstruction.
• If the right ventricle cannot overcome the increased PVR, left ventricular preload is reduced, leading to decreased oxygenation, cardiac output, and hypotension.
• Inadequate tissue perfusion and hypoxia result from decreased oxygenation and cardiac output.
• Increased PVR leads to pulmonary hypertension causing blood backflow into the right ventricle and right heart failure.
• Increased vascular obstruction exacerbates the condition.
• Classification of acute pulmonary emboli: massive (high risk), submassive (intermediate risk), or low risk.
• Massive PE: Sudden symptom onset following obstruction and can rapidly cause right ventricular heart failure and death.
  • Present if >50% of blood flow through the PA is obstructed.
• Submassive PE: Right heart dysfunction seen on echocardiogram but without hemodynamic instability.
• Low-risk PE: No indications of heart dysfunction, elevated biomarkers, or hypotension.
• Saddle PE: Straddles the bifurcation of the PA, obstructing both branches and often results in sudden death.
• Central PE: Embolus found in the main branch of the PA or its right or left branch.
• Peripheral PE: Embolism found in the peripheral or smaller branches of the pulmonary arteries.

Clinical Manifestations of Pulmonary Embolism

• Sudden onset of intense dyspnea, pleuritic chest pain, and tachypnea is indicative of an acute PE.
• Suspect PE in any postoperative patient, especially after long-bone surgeries with new shortness of breath onset; pain is attributed to inflammatory mediators released.
• Massive PE: May present with jugular venous distention (JVD) and acute right ventricular failure.
  • Decreased cardiac output may lead to hypotension and tachycardia.
  • Hypoxemia-induced tachycardia increases dead-space ventilation.
  • Compromised cerebral perfusion may cause anxiety, restlessness, and confusion.
• Pulmonary infarction: Hemoptysis (bloody sputum) may occur due to tissue hypoxia.

Pulmonary Embolism Classification and Manifestations

• Massive (High Risk)
  • Acute pulmonary embolism with prolonged hypotension requiring pharmacological support.
  • Right and left ventricular dysfunction.
  • Shock and/or cardiac arrest.
• Submassive (Intermediate Risk)
  • Acute pulmonary embolism with normal blood pressure
  • Right ventricular dysfunction evidenced by echocardiogram
  • Myocardial necrosis indicated by elevated troponin I and elevated brain natriuretic peptide (BNP)
• Low Risk
  • Acute pulmonary embolism with normal blood pressure
  • No right ventricular dysfunction
  • No elevated Biomarkers (troponin or BNP)

Common Signs and Symptoms of Pulmonary Embolism

• Dyspnea.
• Accessory muscle use.
• Pleuritic chest pain.
• Tachycardia.
• Tachypnea.
• Crackles upon auscultation.
• Cough.
• Hemoptysis.
• Unilateral lower extremity edema due to DVT, pain in extremity with redness and warmth

Diagnosis of Pulmonary Embolism

• Imaging and laboratory studies should be performed.
• If chest pain is present, an electrocardiogram (ECG) should be performed immediately to rule out myocardial infarction (MI).
  • ECG changes may be nonspecific and insensitive in massive PE, including ischemic changes (inverted T waves, ST changes) and myocardial damage (new Q waves, right bundle branch blocks).
  • ECG's predominant value is to rule out MI.
• Chest x-ray: May be done to rule out the cause of respiratory distress.
  • X-rays may show atelectatic changes.
  • Alone, a chest x-ray is not sufficient to diagnose a PE.
• Spiral computed tomography (CT) scan with IV contrast is the most ordered test to diagnose PE and can effectively identify central and peripheral emboli.
• Nuclear medicine ventilation-perfusion scan (V/Q scan) can identify ventilated but not effectively perfused areas of the lungs.
  • Phrase "high probability" indicates a V/Q mismatch.
  • V/Q scan can take up to 60 minutes
• Pulmonary angiography is the most definitive study for PE diagnosis and allows for the visualization of the pulmonary vasculature, detecting obstructions.
  • Used only if other studies are inconclusive and only in stable patients.

Additional Diagnostic tests

• Lower extremity venous ultrasound determines the presence and extent of any DVT in stabilized patients.
• A plasma D-dimer level is tested; elevated levels indicate the possibility of the presence of a thrombus in the body.
  • A negative D-dimer rules out a clot.
  • A positive D-dimer requires further testing.
• Arterial blood gas (ABG) evaluation reveals hypoxemia (PaO2 less than 80 mm Hg) and respiratory alkalosis (PaCO2 less than 35) due to increased respiratory rate.
  • As the condition progresses, ABGs may indicate metabolic acidosis.
• B-type natriuretic peptide (BNP) may be elevated due to ventricular strain, with levels above 100 pg/mL indicating heart failure.
• Troponin I and troponin T may also rise transiently, unlike in MI.

Treatment of Pulmonary Embolism

• Supportive care includes ensuring oxygenation, removing or reducing the clot, and preventing further clot growth and formation.
• Providers choose treatment based on patient presentation, risk factors, and comorbidities.
• Anticoagulation is the primary medication therapy for acute PE; it does not reduce the clot size but prevents it from enlarging and other clots from forming.
• For asymptomatic patients with a low-risk clot, anticoagulation usually consists of an oral factor Xa inhibitor and does not require hospitalization.
• Symptomatic patients are hospitalized, and IV heparin therapy is initiated for any symptomatic pulmonary embolus. This is because platelets will aggregate and adhere to the obstruction, making it larger.
• IV heparin is typically administered with a bolus, followed by a continuous drip, with weight-based dosages.
• Heparin therapy is monitored through the activated partial thromboplastin time (aPTT); therapeutic goal is 1.5 to 2.5 times the normal value, or 40 to 90 seconds.
• An additional heparin bolus may be given with an increased infusion rate if the initial aPTT is below the therapeutic level. If the aPTT is above therapeutic, the infusion rate is reduced or held.
• Once the aPTT is in the therapeutic range for two consecutive iterations, it is evaluated every 12 or 24 hours. Reaching a therapeutic level within 24 hours has been shown to have better outcomes.
• Protamine sulfate is the reversal agent to heparin.
• Subcutaneous low-molecular-weight heparin, fondaparinux, or unfractionated heparin may be prescribed instead of a weight-based heparin protocol.
• Patients need to be on anticoagulation for at least 3 months post-discharge like subcutaneous low-molecular-weight heparin, factor Xa inhibitors, or warfarin.
  • Warfarin (Coumadin) therapy is monitored using the international normalized ratio (INR), with a therapeutic anticoagulation goal of 2.0 to 3.0
  • Takes approximately 3 to 5 days to reach a therapeutic level.
• If the patient is hemodynamically compromised, thrombolytic therapy (alteplase) should be considered to lyse or remove the clot.
  • Risk of bleeding.
  • Heparin administration is discontinued during alteplase infusion and restarted after infusion completion.
  • Patients who are hemodynamically unstable may be candidates for catheter-directed thrombolysis (CDT), using a low-dose hourly infusion of tissue plasminogen activator (tPa) or urokinase which administers directly at clot site.
• IV Isotonic fluid.
  • Caution with right ventricular compromise as IV fluid may be held and dobutamine administered.
  • Hypotension can be managed with vasopressors like norepinephrine and vasopressin.

Surgical Management of PE

• Surgical is considered for acute massive PE resulting in hemodynamic instability .
• Procedure: embolectomy to remove the clot.
• Types of embolectomy: catheter or surgical.
  • Rheolytic catheter embolectomy: Pressurized saline is used to erode the clot requiring venous catheter or sheath.
  • Rotational embolectomy: Rotating tool used to break down the clot via a standard cardiac catheter.

Medications Used in the Treatment of Pulmonary Embolism

• Unfractionated Heparin - Heparin
  • Binds to antithrombin and stimulates it to inactivate factor Xa, stopping the clotting cascade
  • SQ- Used for VTE prevention, treatment for uncomplicated or asymptomatic VTE. No laboratory monitoring required.
  • IV- Used for treatment of symptomatic or unsymptomatic VTE and PE. Adjustments required to maintain a therapeutic range for aPTT. Blood draws every 4-6 hours to measure aPTT. May be used as a “bridge” to maintain anticoagulation while patient is initiating warfarin. Supratherapeutic aPTT increases the risk for bleeding complications.
    • Nursing: maintain adequate IV access, bleeding precautions, educate patient/family about bleeding risk, precautions, and s/s of bleeding, protamine sulfate is the reversal agent, monitor aPTT and platelets, and BUN/Creatinine.
• Low-Molecular Weight Heparin (LMWH)
  • Enoxaparin, Dalteparin
  • Binds to antithrombin and stimulates it to inactivate factor Xa, stopping the clotting cascade; more specific than unfractionated heparin because it does not bond to thrombin and has less activity against factor IIa; more bioavailable than unfractionated heparin
    • Nursing: Used for PE treatment, no laboratory monitoring required, initiate bleeding precautions, Educate patient/family about bleeding risk, precautions, and s/s of bleeding, protamine sulfate is the reversal agent, Monitor platelets and BUN/Creatinine, Patient/family education with teach-back if patient will be self-administering LMWH at home. -Vitamin K Antagonist - Warfarin
  • Interfere with the vitamin K synthesis needed in the clotting cascade, inhibiting factors II, VII, IX, and X
  • Given PO
    • Nursing: Takes a few days to reach therapeutic level,Monitored using INR (therapeutic level is 2-3), Routine blood testing is required, Vitamin K is reversal agent, and Educate patient/family about bleeding risk, precautions, and s/s of bleeding Xa Inhibitors -Rivaroxaban (PO), Apixaban (PO), Fondaparinux (SQ)
  • Selectively binds to factor Xa, inhibiting its role in the clotting cascade, inhibiting the generation of thrombin
    • Can be seen on a lab draw, not routinely necessary, Andexanet alfa is Reversal agent and educate patient/family about bleeding risk, precautions, and s/s of bleeding Thrombolytics - Streptokinase, Urokinase, Alteplase (rt-PA)
  • Enzymes which break down fibrin and dissolve clots
    • used for emergent, diagnosis must be confirmed prior,Higher risk of bleeding - including intracerebral, breaks down targeting including clot, Strict inclusion and exclusion criteria, Astute monitoring to assess complication

Absolute Contraindications to Thrombolytic Therapy

• History of hemorrhagic stroke.
• Active intracranial neoplasm.
• Recent surgery or trauma.
• Active or recent internal bleeding.
• Severe hypertension.
• Nonhemorrhagic stroke.
• Surgery in past 10 days.
• Thrombocytopenia.
• History of bleeding tendencies.

Surgical Management of PE

• Surgical embolectomy: Complex thoracic surgery requiring cardiopulmonary bypass which is usually when thrombolytics is contraindicated.
• Inferior vena cava (IVC) filters prevent recurrent PEs and allow for blood passage but designed to trap emoboli.
  • Indication for IVC: Active bleeding that disqualifies anticoagulation therapy, recurrent PE despite anticoagulation therapy and sever hemodynamic or dysfunction.
  • Complications: Filter migration erosion, obstruction due to thrombosis
    • Retrievable IVC filters are now able to remove when anticoagulation is advisable.

Nursing Management for PE

• Assess and Analysis
  • The manifestation is nonspecific
  • Clinical Manifestation:
    • Sudden Pleurtic chest pain/Dyspnea/Tachypnea
    • Cardiac:
      • elevated PVR indicate right ventricular such as JVD/ reduced to left side lead decrease cardiac output and Hypotension
      • Mental status (impending doom/sudden cardiac arrest)
  • Nursing Diagnoses/Problem List
    • Impaired gas exchange related to interruption of pulmonary blood flow
    • Ineffective breathing pattern: tachypnea related to pain and hypoxemia
    • Decreased cardiac output related to increased PVR
    • Risk for bleeding related to anticoagulant/thrombolytic therapy -Nursing Interventions -Assessment: is breathing effective to maintain oxygenation, pulse oximitery decline decrease from baseline, frequent vital and laboratory level

Interventions for PE

• Elevate the head of the bed.
• Administer IV fluids.
• Administer anticoagulation medications as ordered.
• Administer thrombolytic medications if ordered.
• Administer inotropic agents if ordered.
• Administer norepinephrine or vasopressin as ordered.
• Institute bleeding precautions.
• Be prepared for intubation and resuscitation.

Teaching for PE

• Disease process/lifestyle modifications
• Exercise regimen -includes aerobic exercise
• Cardiac-prudent diet that minimizes saturated fats
• Adequate fluid intake
• Smoking cessation
• Medications, mechanism, and follow up
• Bleeding precautions
• Diet: Limit foods high in vitamin K
• Signs and symptoms of a recurrent PE/DVT

Acute Respiratory Failure

• Compromised gas exchange functions of the lungs related to oxygenation and ventilation
• Two types: hypoxemia, and hypercapnic

Hypoxemic Respiratory Failure (Type I)

• Characterized by a PaO2 of less than 60 mm Hg despite increased inspired oxygen with a normal or low PaCO2

Hypercapnic Respiratory Failure (Type II)

• Characterized by respiratory acidosis, a PaCO2 greater than 50 mm Hg and pH < 7.35.

Risk factors for hypoxemic failure

• Disease processes that produce a V/Q mismatch or impair oxygen diffusion at the alveolar level such as pulmonary edema, pneumonia, or pulmonary embolus.

Risk Factors for hypercapnic failure

• Disease that impair ventilation
• Airway obstruction
• Respiratory muscle weaknedd/paralysis
• Chest-wall injury
• Anesthesia
• Opioid administration
• COPD
• Restictive lung disease Hypoxemic failure Patho- Is characterizated imparied exchanged and oxygenation because of the v/q mistmatch Hypercapnic- impaired ventailtaion occurs when there is a reduced ability of lungs adequately expand

Clinical Manifestations of Acute respiratory Failure:

• Result in (Hypercapnia/Hypoxemia) headache, confusion, somnolence/ Dizzy (Pink Colring) increase Heart rate, respiratory rate and blood pressure Effort for oxygen, restlessness, anxiety

Diagnosis of Respiratory Failure

• ABG/venous saturation: - Blood gas show adequacy for both oxygenation and ventilation in lungs
  • Check Xray and sputum culture

Treatment of Respiratory Failure

• Give Oxygen; nasal cannula or venturi mask/ Nonrebreather mask oxygen(100%), High fow- nasal (100%).
• Meds: Bronchodilators (stimulate Beta 2 Receptors help increase airflow/decrease inflamatory response, Decrease broncho constriction, and increase, diurectica (decrease pulmonmary congestion esp pulm edema: Sedation (control agitate and anxiety that oxygen consume and mechanical ventilation)

Complications of Respiratory Failure Medications

• Cardiac Failure
• Multiple orghan dysfunction
• Death

ARDS (Acute Respiratory Distress Syndrome)

• Direct damage or disruption to respiratory: caused by aspiration, chest trauma or pneumonia
• Characteristics: * acute (acute onset less than 7/Refeactory hypoxemia *Bilareal infiltrate ruling pulmonarry edema/ ratio severity-paO2/FiO2

ARDS phase process

• 3 phases:
  • Exudative: 24 to 48 after injury disruption of act
    • Interstitual edema/damage
    • Clinic Hyperventilation, respiratory output increases as attempted increase blood flow through lungs, test X-ray alvelopar increases
  • proliferative: Inflmatory mediator
• hypercardis
• Increase blood levels: -Fibrotic- Scaning/Imparied gas/change compliance decrease lead hypertension

ARDS Treatment

• X-ray for identify and guide treatment for ARDS
• ABGs
• CBC determine infection
• Mechanical Ventilation is primary treatment and oxygen decrease - Ventilation/PEEP, reduce lung

ARDS positioning/Medications

• Sedal -prone : improve Oxygen,
• Med. - antibiotic, corticosteroid, NEUROMUSCULAR BLOCKING AGENTS
  • Fluid mangement: adeq hydration avoid thickness of lungs
  • Nutrition -Complications - Ventilator: assoicaited VAE, infecion

Best interventions for ventilator and related events:

• 2022 GUIDELINE (VAP) AVOID INTUBLATION, DAY BRUSHING,

Clinical manifestations for ards:

• Pulmonary edema: lung, anxiety, altermental status

Chest Trauma Overview

• Thoracic/chest trauma acounts 1600, accounts 20 to 25% related death with MVC due to increase airbags and older Drivers
• Patho - Result: object that chest striking (steering wheels seat belt ) that cause sharp forces in bodies/tissue:

Chest trauma type

• (1Blunt injuries: ( acceleration and decerlation
  • blunt force diffuse -Penrating trauma: sharp objects /shampriel more penetrate depends on location of angle

common injuries from chest trauma

• Fractur rib
• Pneumothorax: air collect
• Hemothorax: space with blood

clinical Manifestated in Traumatic :

• decrease oxygen/Tachnpea, Comporomies, aglation, Hypoexmia, Air Under the skin, pain

Clinical test for chest trauma :

• Chect XRAY (fractur/mediistinal cheezy
• Ultra sound Chest CCT used in emergency decearl/ rib fracture

labs and analysis to include testing

test that need on emergency:

• test for abgs
• serum lactics
• CBC metabolic profile to transufions

Test for airwat?

• Evaluate airway
• Breating help

if Chect is becomes disconnected :

• submere water to prevent

if Dislodged from chest:

• applu trodium gauge

Chect test plate if:

• hemo and pneumonia occurs as results of truama: place high at midclavicular- due rise/ due gravity fluid to drain

Medications

-Medications help manage- pain -antibitoics given incress for infection

• Compomcation: Tension pneomothrax ( air collects, high level increases. MediastinalShift occur ,

Tension pneumothorax (air collect in Pleural space:

-Large bore -needle between

• 2nd/3rd innerspace( insert chest)

- Cardia tamponeade

-fluid collext in penricadail sac when heart csnnot adequately

• beck triad
• Hypertension, pulsesNarrow / Disten Neckes

surgical menagenment in Chest: Flast chest, (surgery, exicsions) Componsed:

• ** Tachypeha
• Short of breatg
• Decreae oxygenation and consciousness- abgs to include/pulse check as well

Examine the mechanisms of heparin and warfarin in treating pulmonary embolism (PE). Cover nursing interventions for patients with PE, including respiratory distress management and monitoring during embolectomy. Explore the differences between unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH).