Cerebrovascular Events & Pulmonary Embolism
Cerebrovascular Events (Stroke)
Concepts
Priority Concepts:
Perfusion
Cognition
Interrelated Concepts:
Mobility
Sensory Perception
Transient Ischemic Attack (TIA)
Definition: Often called a “warning sign” of stroke, it is a temporary neurological dysfunction resulting from a brief interruption in cerebral blood flow. It is a medical emergency.
Symptoms:
Usually resolve within minutes.
May last as long as hours.
Blurred vision
Diplopia (double vision)
Facial droop
Weakness
Numbness
Vertigo
Aphasia (speech problems)
Causes: Often caused by carotid stenosis (narrowing of the carotid artery) and atrial fibrillation.
Diagnostics:
Blood clotting studies
ECG (electrocardiogram)
CT head without contrast
Carotid Ultrasound (US)
ABCD Assessment Tool: Used to evaluate TIA and determine recurrent stroke risk.
A: Age greater than years
B: Blood pressure greater than
C: Clinical TIA features (e.g., unilateral weakness, speech disturbance)
D: Duration of symptoms and Diabetes history
Clinical Management for TIA
Treating the Cause:
Surgery to remove atherosclerotic plaque in the carotid artery (carotid endarterectomy).
Carotid angioplasty with stenting.
Pharmacologic Interventions:
Antiplatelet drugs (e.g., aspirin, clopidogrel) to prevent stroke.
Antihypertensive drugs to lower blood pressure.
Lifestyle Modifications:
Controlling hyperglycemia and diabetes.
Smoking cessation.
Diet improvements.
Stroke
Pathophysiology: An interruption of perfusion to any part of the brain that results in infarction (cell death).
Significance: Leading cause of death, disability, dementia, and depression worldwide. It is a medical emergency requiring immediate treatment to reduce or prevent permanent disability.
Types of Stroke:
Ischemic Stroke:
Thrombotic: Caused by a thrombus (blood clot) forming in a cerebral or carotid artery, often due to atherosclerosis.
Embolic: Caused by an embolus (dislodged clot) that travels from another part of the body, usually the heart (e.g., from atrial fibrillation), to the brain.
Hemorrhagic Stroke: Caused by bleeding into the brain tissue or surrounding spaces.
Intracerebral Hemorrhage (ICH): Bleeding occurs directly into the brain tissue.
Subarachnoid Hemorrhage (SAH): Bleeding occurs into the subarachnoid space, the area between the brain and the tissues covering the brain.
Aneurysm: An abnormal ballooning or outpouching of a blood vessel, creating a weak spot in the artery wall that can rupture and bleed.
Arteriovenous Malformation (AVM): An angled collection of malformed, thin, and dilated vessels that directly connect arteries and veins, bypassing the capillary system, and are prone to rupture.
Etiology and Genetic Risk for Stroke
Genetic Predisposition:
First-degree relatives with a history of stroke.
Family history of aneurysms.
Leading Causes/Risk Factors:
Smoking
Obesity
Hypertension (high blood pressure)
Diabetes mellitus
Elevated cholesterol
Illicit drug use (contributing to increased incidence in younger adults/middle age)
Incidence and Prevalence of Stroke
Fifth leading cause of death in the U.S.
Women have a higher incidence than men, likely due to women living longer.
High prevalence in the “Stroke belt” region in the southeastern United States.
More than million stroke survivors.
Numbers in younger adults/middle-aged individuals are increasing, partly attributed to illicit drug use.
Health Promotion and Disease Prevention for Stroke
Healthy People 2030 Goals: Reduce deaths from stroke and increase stroke survivors participating in stroke rehabilitation.
ABCS Strategy:
Aspirin use when appropriate.
Blood pressure control.
Cholesterol management.
Smoking cessation.
Assessment (Recognize Cues): Stroke
Priority: Ensure the patient is transported to a designated stroke center offering diagnostic imaging, therapy with IV fibrinolytic therapy, and a specialized stroke team.
Focused History:
Determine any recent bleeding events or current anticoagulant use.
Inquire about:
Symptom onset (crucial for treatment windows).
Activities at the time of onset.
Symptom progression or worsening.
Individual medical history.
Current medications.
Social history.
Sensory or motor deficits.
Rapid Assessment (within minutes of arrival):
Neurologic Examination: Utilize the National Institutes of Health Stroke Scale (NIHSS).
Level of Consciousness (LOC) and Glasgow Coma Scale (GCS): Frequent assessments for acute changes.
Five most common symptoms of stroke:
Sudden confusion with trouble speaking and difficulty understanding speech (aphasia).
Sudden numbness or weakness of the face, arm, or leg (hemiparesis/hemiplegia).
Sudden visual changes (e.g., blurred vision, diplopia, hemianopsia).
Sudden dizziness, trouble walking, or loss of balance/coordination (ataxia, vertigo).
Sudden severe headache with no known cause (often associated with hemorrhagic stroke).
NIHSS (National Institutes of Health Stroke Scale):
A primary clinical assessment tool for stroke severity.
Scoring range: to points. Higher scores indicate greater severity.
Item Titles and Scores:
. Level of Consciousness (LOC): (alert) to (coma/unresponsive).
. Orientation questions (): (both correct) to (neither correct).
. Response to commands (): (both tasks correct) to (neither correct).
. Gaze: (normal horizontal) to (complete gaze palsy).
. Visual fields: (no defect) to (bilateral hemianopia).
. Facial movement: (normal) to (complete unilateral palsy).
. Motor function (Arm) (a. Left, b. Right): (no drift) to (no movement).
. Motor function (Leg) (a. Left, b. Right): (no drift) to (no movement).
. Limb ataxia: (no ataxia) to (ataxia in limbs).
. Sensory: (no loss) to (severe loss).
. Language: (normal) to (mute or global aphasia).
. Articulation: (normal) to (severe dysarthria).
. Extinction or inattention: (absent) to (severe loss).
Stroke Severity Scores:
: No stroke symptoms.
: Minor stroke.
: Moderate stroke.
: Moderate to severe stroke.
: Severe stroke.
BEFAST Acronym for Stroke Signs:
Balance: Loss of balance.
Eyes: Lost vision.
Face: Face drooping.
Arm: Arm weakness.
Speech: Speech difficulty.
Time: Time to call (an ambulance).
More Specific Stroke Symptoms by Hemisphere:
Right Hemisphere Stroke:
Visual and spatial awareness issues.
Unaware of deficits (anosognosia); disoriented to place and time.
Personality changes; impulsivity; poor judgment.
Left-sided motor deficits (hemiplegia or hemiparesis).
Tends to minimize problems.
Short attention span.
Impaired time concept.
Left Hemisphere Stroke:
Speech and language difficulties (aphasia, often expressive or receptive).
Mathematic and analytical thinking issues.
Right-sided motor deficits (hemiplegia or hemiparesis).
Slow performance.
Aware of deficits (leading to depression, anxiety).
Impaired comprehension.
Psychosocial Assessment:
Assess patient's reaction to illness, body image, self-concept, and ability to perform Activities of Daily Living (ADLs).
Screen and treat for depression.
Address financial status and occupational issues.
Consult social services/case management.
Assess for emotional lability (uncontrollable emotional states).
Laboratory Assessment:
Elevated Hemoglobin (H&H) and White Blood Cell count (WBC).
Blood glucose (to rule out hypoglycemia as a stroke mimic).
Hemoglobin A1C (for diabetes management).
PT (Prothrombin Time), INR (International Normalized Ratio), aPTT (activated Partial Thromboplastin Time) (for clotting status, especially if considering fibrinolytics or anticoagulants).
Imaging Assessment:
CT head without contrast (initial scan to rule out hemorrhage).
CT perfusion and/or CT angiography (to assess cerebral blood flow and vessel patency).
MRA (Magnetic Resonance Angiography).
Ultrasound (US) (e.g., carotid US).
Analyze Cues & Prioritize Hypotheses for Stroke
Inadequate perfusion to the brain due to interruption of arterial blood flow and a possible increase in Intracranial Pressure (ICP).
Decreased mobility and possible need for assistance to perform ADLs due to impaired cognition or motor deficits.
Aphasia (speech problems due to decreased circulation in the brain) and/or dysarthria (facial muscle weakness impacting speech).
Sensory perception deficits due to altered neurologic reception and transmission.
Planning and Implementation for Stroke
Improving Cerebral Perfusion:
IV Fibrinolytic Therapy (e.g., Alteplase):
Purpose: To dissolve artery occlusion in acute ischemic strokes.
Time Window: Determined by the time frame from symptom onset, typically a hour window.
Drug: Alteplase is currently used.
Dosage: total dose, administered over minutes, with of the dose given as a bolus infusion over minute.
Blood Pressure Requirement: Must be below for administration.
“Door to Needle” Time: Newest target is minutes for administration.
Monitoring: Carefully monitor for signs of intracerebral hemorrhage or other bleeding during infusion.
Discontinuation: Discontinue infusion immediately for severe headache, severe hypertension ( > 185/110 \text{ mm Hg}), bleeding, nausea, or vomiting.
Endovascular Interventions:
Intraarterial thrombolysis: May be used for patients with ischemic stroke outside the time window for IV Alteplase.
Mechanical embolectomy: Surgical blood clot removal.
Carotid stent placement: Used to prevent or manage acute ischemic strokes caused by carotid artery narrowing.
Hemorrhagic Stroke Management: Methods are evaluated based on stopping active bleeding (e.g., coiling for aneurysms, surgical clipping, managing AVMs).
Monitoring for Increased Intracranial Pressure (ICP):
Normal ICP: .
Risk: Highest risk of cerebral edema in the first hours after stroke onset. Neurologic status may worsen hours after endovascular procedures.
Assessment: Assess patients with acute stroke and after treatment every hours, depending on the severity.
Reporting: Report any signs of neurologic deterioration to the provider; the first sign of increased ICP is declining level of consciousness (LOC).
Key Features of Increased ICP:
Decreased LOC
Behavioral changes, restlessness
Headache
Nausea and vomiting
Change in speech patterns
Pupillary changes
Cranial nerve dysfunction
Ataxia
Seizures
Abnormal posturing (decorticate, decerebrate)
Cushing's triad: Severe hypertension (), wide pulse pressure (difference between systolic and diastolic BP), and bradycardia.
Aphasia
Best Practices for Managing Increased ICP:
Maintain head in midline, neutral position to promote venous drainage.
Avoid sudden hip/neck flexion.
Avoid clustering nursing interventions/procedures, allowing for rest periods.
Hyperoxygenation before and after suctioning.
Provide airway management to prevent frequent suctioning and coughing (which can increase ICP).
Keep lights low to decrease photophobia.
Closely monitor Blood Pressure (BP), heart rhythm, oxygen saturation (), Blood Glucose (BG), and body temperature to prevent secondary brain injury.
Medical Treatment for Increased ICP:
Intravenous Mannitol (osmotic diuretic).
Hyperventilation (short-term to cause vasoconstriction).
Elevation of the head (head of bed at degrees).
Additional medications (e.g., corticosteroids for edema, sedatives).
Draining extra cerebrospinal fluid (CSF) via ventriculostomy.
Craniotomy (rarely, to decompress the brain).
Cerebral Perfusion Pressure (CPP):
Closely linked to ICP.
Formula: (where MAP is Mean Arterial Pressure).
Normal CPP: .
Implication: CPP less than results in permanent neurologic damage.
Ongoing Drug Therapy (to prevent further events and protect neurons):
Antiplatelet drugs (e.g., aspirin, clopidogrel) are standard of care following ischemic strokes; not given within hours of IV Alteplase to prevent bleeding.
Anticoagulants (e.g., heparin, warfarin, rivaroxaban, apixaban) for patients with cardiopulmonary issues like atrial fibrillation.
Calcium channel blockers (e.g., nimodipine) to prevent cerebral vasospasm, especially after subarachnoid hemorrhage.
Symptom management: Stool softeners (to prevent straining), analgesics, and anxiety medications.
Promoting Mobility and ADL Ability:
Assess patient’s functional ability (ambulation, feeding, bathing, dressing).
Maintain NPO (nothing by mouth) status until swallowing ability is assessed by speech pathology.
Develop a collaborative plan to prevent aspiration and support nutrition.
Ensure proper positioning of flaccid extremities to prevent injury (e.g., shoulder subluxation, foot drop).
Referrals for rehabilitation (physical therapy, occupational therapy) to prevent complications of immobility (pneumonia, atelectasis, venous thromboembolism, pressure wounds).
Promoting Effective Communication:
Speech and language problems can result from aphasia or dysarthria.
Expressive Aphasia (Broca's aphasia): Patient understands what is said but cannot speak clearly or form words. Patient is often aware of the deficit and may become frustrated or angry.
Receptive Aphasia (Wernicke's aphasia): Patient cannot understand spoken or written words. Patient is usually able to talk, but the language used is often meaningless or nonsensical (word salad). They may be unaware of their deficit.
Consult speech pathology for specialized knowledge and intervention.
Managing Changes in Sensory Perception:
Patients often have difficulty with visual perceptual tasks and problems differentiating left from right.
Approach: Always approach the patient on their unaffected side.
Unilateral Neglect: Most commonly seen in patients with right cerebral strokes; the patient neglects the left side of their body and environment. Nursing interventions include reminding patients to turn their heads and scan the environment, placing objects within their field of vision, and approaching from the neglected side initially to gain their attention.
Homonymous Hemianopsia: Visual field of the same half of each eye is affected (e.g., loss of left visual field in both eyes). Teach the patient to turn their head side to side to scan and expand their visual field.
Apraxia: Inability to perform learned movements despite having the desire and physical ability to do so. Consult physical therapy and occupational therapy to assist with this cautious, slow behavioral style.
Care Coordination and Transition Management for Stroke
Eight Core Measures:
Venous thromboembolism (VTE) prophylaxis.
Antithrombotic therapy at discharge.
Anticoagulation therapy for atrial fibrillation at discharge.
Thrombolytic therapy as indicated (within optimal window).
Antithrombotic therapy reevaluated by the end of hospital day .
Statin medication at discharge.
Stroke education provided and documented.
Assessment for rehabilitation.
Patient and Family Education:
Lifestyle changes (diet, exercise, smoking cessation).
Drug therapy (medication names, dosages, purpose, side effects, administration).
Mobility skills (how to use assistive devices, safe transfer techniques).
Nutritional management (dietary restrictions, dysphagia strategies).
Communication skills (strategies for aphasia).
Depression monitoring and screening.
Counseling services.
Palliative care (if appropriate).
Evaluate Outcomes for Stroke
The patient has adequate cerebral perfusion to avoid long-term disability.
The patient maintains blood pressure and blood glucose within a safe, prescribed range.
The patient performs self-care and mobility activities independently, with or without assistive devices.
The patient learns to adapt to sensory perception changes, if present.
The patient communicates effectively or develops strategies for effective communication as needed.
The patient has adequate nutrition and avoids aspiration.
Pulmonary Embolism (PE)
Concepts
Priority Concepts:
Gas Exchange
Interrelated Concepts:
Perfusion
Clotting
Pathophysiology Overview of PE
Definition: A collection of particulate matter (solids, liquids, air) that enters venous circulation and lodges in a pulmonary vessel.
Common Cause: While any substance can cause an embolism, a blood clot is the most common.
Impact: Large emboli in the lung vessels obstruct pulmonary blood flow, leading to:
Reduced gas exchange.
Reduced oxygenation.
Pulmonary tissue hypoxia.
Decreased perfusion.
Potential death.
Connection to DVT: Most often, a PE develops because of a Deep Vein Thrombosis (DVT), where a clot forms in the deep veins, usually of the leg.
Venous Thromboembolism (VTE): DVT combined with PE is termed VTE.
Mechanism: When a clot breaks off from deep veins, it travels through the bloodstream to the right side of the heart, then into the pulmonary artery, where it lodges.
Consequence: This obstruction results in impaired alveolar perfusion and outflow, increasing alveolar dead space and creating a ventilation-perfusion () mismatch, meaning areas of the lung are ventilated but not perfused, leading to inefficient gas exchange.
Major Risk Factors for PE
Prolonged immobility
Central venous catheters
Surgery (especially abdominal and orthopedic)
Pregnancy
Obesity
Advancing age
Conditions that increase blood clotting (hypercoagulable states)
History of thromboembolism
COVID-$19$
Infection
Additional Risk Factors for PE
Smoking
Estrogen therapy (e.g., oral contraceptives, hormone replacement therapy)
Heart failure
Stroke
Cancer (many cancers increase clotting risk)
Chemotherapy
Trauma
Hip replacement
Knee replacement
Heparin-induced thrombocytopenia (HIT)
Lifestyle Changes to Prevent PE
Encourage smoking cessation, especially if using hormone therapy.
Reducing weight and becoming more physically active.
Drink plenty of water, change positions often, avoid crossing legs, and get up from a sitting position for at least minutes each hour when traveling.
Avoid the use of tight garters, girdles, and constricting clothing.
Refrain from massaging leg muscles to prevent dislodgement of potential clots.
Nursing Care to Prevent PE
Start passive and active range-of-motion exercises for the extremities of immobilized and postoperative patients.
Ambulate patients as soon as possible after surgery.
Use pneumatic compression devices (e.g., sequential compression devices, SCDs) after surgery as ordered.
Evaluate patients for criteria indicating the need for anticoagulant therapy.
Administer prophylactic low-dose anticoagulant or antiplatelet drugs after specific surgical procedures as ordered.
Prevent pressure under the popliteal space (do not place a pillow directly under the knee, as this can impede venous return).
Perform a comprehensive assessment of peripheral circulation at least once per shift.
Elevate the affected limb degrees or more above the level of the heart to improve venous return, as appropriate.
Reposition the patient every hours or ambulate as tolerated.
Assessment (Recognize Cues): PE
Physical Assessment/Signs and Symptoms:
Respiratory:
Dyspnea (sudden onset is common)
Pleuritic chest pain (sharp, stabbing pain on inspiration)
Crackles (rales), wheezes
Pleural friction rub (rare)
Cough
Hemoptysis (bloody sputum)
Tachypnea (increased respiratory rate)
Cardiac:
Tachycardia (fast heart rate)
Distended neck veins (jugular venous distention)
Syncope (fainting)
Cyanosis (bluish discoloration of skin/mucous membranes)
Hypotension (low blood pressure)
or heart sounds (indicative of heart strain)
Psychosocial Assessment:
Anxiety
Restlessness
Apprehension
Sense of impending doom
Laboratory Assessment:
Arterial Blood Gas (ABG): Initially, decreased PaCO and PaO due to hyperventilation and poor gas exchange. PaCO may then increase later due to shunting of blood and respiratory fatigue.
General metabolic panel.
Troponin (to assess for myocardial injury due to right heart strain).
Brain Natriuretic Peptide (BNP) (to assess for cardiac strain/failure).
D-dimer: A blood test that measures a fibrin degradation product. Elevated D-dimer suggests the presence of a clot but is not specific for PE (it can be elevated in many conditions). A normal D-dimer can help rule out PE in low-risk patients.
Imaging Assessment:
Computed Tomography Pulmonary Angiography (CTPA): The standard for diagnosing a PE. It is a highly sensitive and specific test.
Lung Scintigraphy (Ventilation/Perfusion Scan or V/Q scan): Can be used if a CTPA is contraindicated (e.g., pregnancy, kidney disease or failure, contrast allergy). It compares lung ventilation with perfusion to identify areas of mismatch.
Analyze Cues & Prioritize Hypotheses for PE
Hypoxemia due to mismatch of lung perfusion and alveolar gas exchange with oxygenation.
Hypotension due to right ventricular failure (from increased pulmonary vascular resistance).
Potential for excessive bleeding due to anticoagulation or fibrinolytic therapy.
Planning & Implementation for PE
Managing Hypoxemia:
Oxygen Therapy: May be applied by nasal cannula, mask, or require mechanical ventilation, depending on the severity of hypoxemia. Use pulse oximetry to monitor oxygen saturation and hypoxemia.
Anticoagulation or Fibrinolytic Therapy:
Initial Anticoagulation: Unfractionated heparin infusion, low-molecular-weight heparin (LMWH) injection (e.g., enoxaparin), or fondaparinux injection are used initially to prevent further clot formation.
Fibrinolytic Drugs: Used for treatment when specific criteria are met, such as in massive PE with shock, hemodynamic collapse, or instability. Alteplase (the same drug used for ischemic stroke) is an example.
Bridge Therapy: From IV to oral anticoagulation is typically started on day of heparin infusion.
Oral Anticoagulants: Use continues for at least months, but patients at continued high risk for PE may require lifelong therapy (e.g., warfarin, direct oral anticoagulants like rivaroxaban, apixaban, dabigatran).
Monitoring Responses:
Check vital signs, lung sounds, and cardiac and respiratory status at least every hours.
Document increasing dyspnea, dysrhythmias, distended neck veins, and pedal or sacral edema.
Assess for crackles and other abnormal lung sounds along with cyanosis of the lips, conjunctiva, oral mucosa, and nail beds.
Psychosocial Support: Stay with the patient and speak calmly and clearly, providing assurances that appropriate measures are being taken to help manage their anxiety and apprehension.
Managing Hypotension:
IV Fluid Therapy: Infusing crystalloid solutions (e.g., normal saline) to restore plasma volume and prevent shock, especially if hypovolemia is contributing. Monitor indicators of fluid adequacy (urine output, skin turgor, mucous membranes).
Drug Therapy: Vasoactive drugs (vasopressors like norepinephrine, dopamine) are used when hypotension persists despite fluid resuscitation to improve blood pressure and tissue perfusion. Assess the patient’s cardiac status closely during therapy with any of these drugs due to their potent effects.
Minimizing Bleeding:
Drug Therapy Impact: Anticoagulant and fibrinolytic drugs for PE impair the patient’s ability to start and continue the clotting cascade, increasing the risk of bleeding.
Antidotes: Ensure specific antidotes for anticoagulants (e.g., protamine for heparin, vitamin K for warfarin) are available on the nursing unit.
Assessment: Assess for evidence of bleeding (e.g., petechiae, purpura, ecchymoses, epistaxis, hematuria, melena) and examine all output for blood. Assess the patient’s abdomen for increasing distention or tenderness, which could indicate internal bleeding.
Laboratory Monitoring: Monitor laboratory values such as Complete Blood Count (CBC, especially hemoglobin and hematocrit), blood clotting studies (PT, INR, aPTT), and platelet count.
Care Coordination and Transition Management for PE
Home Care Management:
Address activity intolerance resulting from heart or lung damage.
Assess for assistance needed with ADLs and consider modified living arrangements.
Self-Management Education:
Patients may continue anticoagulation for months or years, depending on their risk and extent of PE.
Teach patient and family bleeding precautions (e.g., avoid razor blades, use a soft toothbrush, avoid contact sports, recognize signs of bleeding).
Provide instructions for follow-up for lab monitoring (e.g., INR checks if on warfarin).
Evaluate Outcomes for PE
The patient attains and maintains adequate gas exchange and oxygenation.
The patient does not experience hypovolemia and shock.
The patient remains free from bleeding episodes.