9.1 Acute Pulmonary Embolism

Why Pulmonary Embolism Is a Cardiac-Unit Problem

Test-plan item II.A.1 sits inside Domain II (Non-Cardiovascular Conditions, 23% of the exam), and CMC writes it from the cardiac angle: acute pulmonary embolism (PE) kills through the right ventricle, not through the lung. Your patients are the ones who get it — the post-cardiac-catheterization patient on bedrest, the heart failure patient with low-output venous stasis, the atrial fibrillation patient whose anticoagulation was interrupted for a procedure, the patient with an indwelling central catheter or newly implanted device leads, and the post-arrest patient. The nurse who understands the right ventricular (RV) failure spiral is the one who recognizes deterioration before the arrest.

The RV Failure Spiral

Once thrombus obstructs roughly 30-50% of the pulmonary vascular bed, mechanical obstruction is amplified by hypoxic pulmonary vasoconstriction and by mediators released from activated platelets (serotonin, thromboxane A2, endothelin-1). Pulmonary vascular resistance (PVR) rises abruptly, and the sequence that follows is the whole of PE pathophysiology:

1. Acute rise in RV afterload. A previously normal, thin-walled RV (free wall 3-5 mm) cannot acutely generate a mean pulmonary artery pressure much above 40 mmHg. If the measured mean PA pressure is 55 mmHg in a patient who "just" developed PE, that RV has been chronically conditioned by something else.
2. RV dilation and rising wall tension. Tricuspid annular dilation produces functional tricuspid regurgitation, which further volume-loads the RV.
3. Interventricular septal shift toward the left ventricle (ventricular interdependence within the fixed pericardium) plus pericardial constraint.
4. LV underfilling — the left ventricle is not failing, it is empty. Stroke volume and systemic blood pressure fall.
5. Reduced RV coronary perfusion. The RV is normally perfused in both systole and diastole because RV systolic pressure is low. When RV pressure rises and aortic pressure falls, RV perfusion becomes diastole-dependent and the perfusion gradient collapses.
6. RV ischemia and infarction (this is the troponin release, not coronary occlusion), falling RV contractility, and a further drop in output. The terminal rhythm is pulseless electrical activity.

B-type natriuretic peptide rises from RV stretch; troponin rises from RV microinfarction. Both are prognostic markers, not diagnostic tests, and both drive risk stratification.

Risk Stratification Drives Everything

CMC will not ask you to choose a lytic. It will ask you to classify the patient, because classification determines monitoring intensity, unit placement, and what you escalate.

The Pulmonary Embolism Severity Index (PESI) and its simplified form (sPESI) score clinical variables, not imaging. sPESI assigns one point each for age over 80, active cancer, chronic cardiopulmonary disease, heart rate 110/min or greater, systolic BP under 100 mmHg, and arterial oxygen saturation under 90%. A score of 0 identifies a low-risk patient who may be managed at home; a score of 1 or more means the patient is not low risk, but sPESI alone never establishes intermediate-high status — you still need the echo and the troponin.

Exam trap: a normotensive patient is not a stable patient. The intermediate-high-risk patient with a dilated RV and a positive troponin is the one who arrests at 3 a.m. Normal blood pressure in acute PE is maintained by intense sympathetic vasoconstriction; when it fails, it fails suddenly and completely.

Presentation, ECG and Diagnostics

Dyspnea is the most common symptom, followed by pleuritic chest pain, tachypnea and tachycardia. Syncope is a red flag — it implies a large clot burden with transient RV output failure and carries higher mortality. Hemoptysis suggests pulmonary infarction. Physical findings that point to RV strain: elevated jugular venous pressure, a right parasternal heave, a loud pulmonic component of S2, and a tricuspid regurgitant murmur that increases with inspiration.

ECG Findings

The trap: an anterior T-wave-inversion pattern plus an elevated troponin in a hypoxemic, tachycardic patient is read as non-ST-elevation myocardial infarction and sent to the cath lab. Look at the whole picture — clear lungs, hypoxemia out of proportion to the chest radiograph, a normal or hyperdynamic left ventricle with a dilated RV, and a widened alveolar-arterial gradient point to PE. Concurrent ST elevation in aVR with anterior T-wave inversion and a dilated RV should raise PE explicitly.

Diagnostic Testing

• D-dimer. High sensitivity, poor specificity. It has value only when the pretest probability (Wells or revised Geneva) is low or intermediate. Use the age-adjusted cutoff for patients over 50: age x 10 ng/mL fibrinogen-equivalent units — a 78-year-old has a cutoff of 780 rather than 500, which safely reduces unnecessary imaging. Do not order a D-dimer when the probability is high; go straight to imaging. D-dimer is elevated by surgery, malignancy, sepsis, pregnancy, aortic dissection and heart failure — nearly every cardiac inpatient.
• CT pulmonary angiography (CTPA) is the diagnostic standard. It also gives an RV/LV diameter ratio; a ratio of 0.9 or greater on the four-chamber reconstruction defines RV dysfunction for risk stratification.
• Ventilation/perfusion (V/Q) scanning when iodinated contrast is contraindicated: significant renal impairment, severe contrast allergy, or pregnancy (perfusion-only scanning lowers the dose further). V/Q is also the screening test for chronic thromboembolic pulmonary hypertension later, not CTPA.
• Bedside echocardiography cannot rule out PE, but in a hypotensive patient a dilated, hypokinetic RV supports the diagnosis strongly enough to justify treatment when the patient is too unstable for CT. Look for McConnell sign (akinesis of the mid RV free wall with preserved apical contraction), the 60/60 sign (pulmonary acceleration time under 60 ms with a tricuspid regurgitant peak gradient under 60 mmHg), a D-shaped interventricular septum on the parasternal short-axis view, tricuspid annular plane systolic excursion (TAPSE) under 17 mm, and a dilated non-collapsing inferior vena cava. Adding a two-point lower-extremity compression ultrasound frequently finds the source clot.
• Labs. Troponin, BNP or NT-proBNP, lactate (2 mmol/L or greater predicts deterioration), and an arterial blood gas showing hypoxemia with respiratory alkalosis and a widened A-a gradient. A normal blood gas does not exclude PE.

The Crashing PE Patient: Three Things That Cause the Arrest

This is the highest-yield nursing-judgment content in the whole topic.

1. Intubation and positive-pressure ventilation. Induction agents drop preload and systemic vascular resistance; positive intrathoracic pressure reduces RV preload while raising RV afterload. In a preload-dependent, afterload-intolerant RV this is frequently fatal on induction. If intubation is unavoidable: have norepinephrine already infusing, choose a hemodynamically neutral induction agent (ketamine or etomidate rather than propofol), use low tidal volumes and the lowest workable PEEP, and avoid hypercarbia.
2. Aggressive fluid loading. A liter of crystalloid into a dilated RV worsens wall tension, worsens tricuspid regurgitation, worsens septal shift and drops cardiac output further. Give 250 mL boluses at most, only when the patient is genuinely volume-depleted, and stop if the central venous pressure rises without a rise in cardiac output.
3. Delay. The nurse anticipates, in this order: high-flow oxygen to keep SpO2 above 92% (hypoxemia raises PVR), norepinephrine 0.02-0.5 mcg/kg/min titrated to a MAP of 65 mmHg or higher, vasopressin 0.01-0.04 units/min as an adjunct because it supports systemic pressure without raising PVR, dobutamine 2-5 mcg/kg/min for RV inotropy (watch for hypotension from beta-2 vasodilation), inhaled nitric oxide 5-40 ppm or inhaled epoprostenol as selective pulmonary vasodilators, and immediate activation of the Pulmonary Embolism Response Team (PERT) with early ECMO and surgical embolectomy consultation rather than a call placed after the arrest.

Treatment

Anticoagulation

Start anticoagulation on clinical suspicion, before confirmatory imaging, unless bleeding risk prohibits it.

Reperfusion

• Systemic fibrinolysis. Alteplase 100 mg IV over 2 hours through a peripheral line is the standard regimen for high-risk (massive) PE. A reduced dose of 50 mg over 2 hours is used when bleeding risk is elevated or body weight is under 65 kg. In cardiac arrest with strongly suspected PE, alteplase 50 mg IV push (repeated once at 15 minutes) is given and CPR is continued for 60-90 minutes afterward, because the drug needs circulation to work. Fibrinolysis is not routine for intermediate-risk PE: PEITHO showed tenecteplase reduced hemodynamic decompensation but increased major extracranial bleeding roughly five-fold (6.3% vs 1.2% at 7 days) and produced about 2% intracranial hemorrhage (2.0% vs 0.2%). The intermediate-high-risk patient is monitored with a rescue-lysis plan instead.
• Absolute contraindications to systemic lysis: any prior intracranial hemorrhage, known structural cerebrovascular lesion or malignant intracranial neoplasm, ischemic stroke within 3 months, suspected aortic dissection, active bleeding, and significant closed head or facial trauma within 3 months.
• Catheter-directed thrombolysis delivers roughly 8-24 mg of alteplase over 6-24 hours (often 0.5-1 mg/h per catheter), reducing systemic exposure. Large-bore mechanical/aspiration thrombectomy removes clot with no lytic at all, which makes it the option of choice for the post-operative or post-neurosurgical patient.
• Surgical embolectomy for high-risk PE with a lysis contraindication or failed lysis, frequently with VA-ECMO as a bridge.
• IVC filter only when anticoagulation is absolutely contraindicated or PE recurs despite therapeutic anticoagulation. A retrievable filter requires a documented retrieval plan; filters left indefinitely thrombose, fracture and migrate.

Nursing Priorities

• Continuous monitoring. Rhythm, blood pressure, and a trend line rather than isolated numbers. A rising heart rate with a falling pulse pressure, a widening gap between SpO2 and end-tidal CO2, rising CVP, falling urine output, or new somnolence are the deterioration signature. New bradycardia in acute PE is a pre-arrest sign, not a vagal event.
• During thrombolysis. No intramuscular injections, no arterial or venous punctures, no invasive lines, no nasogastric tube placement, no urinary catheter insertion if avoidable. UFH is typically held during peripheral alteplase and resumed without a bolus when the aPTT falls below twice control.
• Neurologic checks every 15 minutes during the infusion and for at least 2 hours afterward. Sudden severe headache, vomiting, an acute rise in blood pressure, a change in level of consciousness, or any focal deficit means stop the infusion, notify the provider, and prepare for an emergent non-contrast head CT.
• Bleeding surveillance. Serial hemoglobin/hematocrit, fibrinogen and platelet count; access-site and groin checks every 15 minutes after catheter-directed therapy; occult gastrointestinal bleeding; and back or flank pain with an unexplained hemoglobin drop, which suggests retroperitoneal hemorrhage.
• Mobility. Once anticoagulation is therapeutic and hemodynamics are stable, early ambulation is safe and does not increase recurrence — bedrest is not a treatment for PE.
• Discharge teaching. Minimum 3 months of anticoagulation, with indefinite therapy for unprovoked or recurrent events or ongoing risk factors; strict adherence because a DOAC's protection is gone within a day of a missed dose; bleeding precautions and avoidance of NSAIDs; discontinuation of estrogen-containing contraception; recognition of recurrence; and follow-up for post-PE syndrome with an echocardiogram and V/Q scan at 3-6 months if dyspnea persists, to screen for chronic thromboembolic pulmonary hypertension.