Neuro Assessments and Intracranial Pressure

Module 6 Neuro

• Assessment includes identifying/monitoring neuro deterioration.
• Serial Neuro Assessments every 1-2 hours are a priority, along with SpO2, temperature, ICP monitoring, I&O's every 1-2 hours, cardiac rhythm and markers, serum electrolytes, BUN/CREA, ABG's, and End tidal CO2.
• Know CN V for trigeminal sensation from the upper and lower face, and chewing.
• Hyponatremia S/S includes N/V, headache, confusion, fatigue, restlessness, muscle weakness, spams/cramps, seizures, and coma.
• Use the Glasgow Coma Scale for LOC and the Romberg test for balance.
• Check for Babinski sign reflexes.

Intracranial pressure

• Headaches are a concerned finding: Restlessness, confusion, changes in LOC, vomiting, seizures, and widening pulse pressure.
• In late stages (Cushing's Triad), widening systolic pulse pressure (systolic HTN), increased systolic BP, bradycardia, irregular respirations, pupillary changes (unilateral fixed & dilated pupil due to uncal herniation compressing CNI 3), Posturing, and positive Babinski reflex occur.
• Cerebral edema involves swelling of the brain.
• Hyperventilate to decrease ICP with hypercapnia (CO2 is a vasoconstrictor).
• ICP is measured using an intraventricular catheter, also known as an external ventricular drain.
• Monitor airways, I & O's, skin for infection, and BM.
• Increase HOB- semi fowlers, give stool softener, and check for nasal drainage (check BG).
• Complications include cerebral herniation, infection, and over drainage which can lead to subdural hematomas.
• Assess A&O before educating.
• Causes of Increased ICP includes tumors, hematomas, hemorrhages, and abscesses.
• Diagnosing ICP is done via CT scans and Lumbar punctures.
• Monitoring medications consist of Osmotic diuretics, high concentration sodium chloride (hypertonic saline), and Sedatives for pain and anxiety (Morphine, midazolam, fentanyl, and propofol).
• A ventriculostomy is a cerebrospinal fluid drainage system using an external ventricular drainage system.
• Interventions: Raise HOB 30-45 degrees to decrease ICP via gravity.
• Hyperventilation decreases ICP with hypercapnia (CO2 is a vasoconstrictor), and drainage of CSF.
• Perform endotracheal suctioning prn, administer meds as prescribed (osmotic agents and sedatives), and monitor CSF drainage.
• Avoid hip flexion.
• Brain tumor post-op complications include increased ICP, bleeding, cerebral edema, seizures, and VTE.
• Osmotic Diuretics- Mannitol decreases ICP (most effective diuretic for ICP).
• Use Sedative, paralytic, and analgesic for intubated patients.
• Prior to SX, hold meds like aspirin and blood thinners.
• Rt-PA dissolves blood clots and restores blood flow.
• Sedatives: Morphine, midazolam, fentanyl, and propofol, are for pain and anxiety.
• Thrombolytics: Alteplase, Tenecteplase are contraindicated in hemorrhagic strokes.
• Antiadrenergic- Clonidine lowers BP by relaxing blood vessels making it easier for the heart to beat.
• Antihypertensives: Labetalol, Hydralazine, and Nicardipine.
• Antiplatelets: Aspirin and Clopidogrel are contraindicated in hemorrhagic strokes
• Anticoagulants: Heparin and Warfarin for atrial fibrillation are contraindicated in hemorrhagic strokes.
• Oral Sympathomimetics: Midodrine increases BP by affecting alpha-1 receptors.

Stroke

• Risk factors: HTN, smoking, hypercholesterolemia, drugs, >55 years of age.
• Exclusion from tPA: GI bleed, recent trauma, or recent SX.
• Hemiopia is vision loss due to stroke resulting in a fall risk.
• Scan the environment or surroundings for Patient Education.

Stroke Diagnosis and Treatment

• DX: A CT helps identify any bleeds.
• An MRI, carotid duplex, echo, and labs (cbc, electrolytes, bun/crea, chol, and hypercoagulable states) also help identify strokes.
• The primary goal is catheterization for reperfusion and endovascular thrombectomy to retrieve the clot.
• The primary goal for stroke is reperfusion.
• NIHSS (Stroke scale) is an important tool to quantify stroke severity.
• For ventilated patients, use sedation vacation to check their neuro assessments.

Ischemic Stroke

• Pathophysiology: Sudden blockage of the cerebral blood vessels leads to reduced bleeding.
• Symptoms occur suddenly.
• Left MCA causes weakness of the R face, arm, and leg, R hemianopia, decreased sensation of the R side of the body, dysphasia, difficulty expressing thoughts, and inability to process speech input.
• Right MCA causes weakness of the L face, arm, and leg, left hemianopia, inattention, or neglect of the L side.
• Loss of vision in the L temporal field and R nasal field of vision.
• Requires you to scan the area to visualize objects on the L side.
• Basilar Artery syndrome is dizziness, ataxia, tinnitus, n/v, unilateral weakness on one side of the body, difficulty in articulation of speech, swallowing, and managing oral secretions.
• TX: IV rt-PA administered within 3-4.5 hours of symptoms, and Endovascular Thrombectomy up to 24 hours after onset.
• Meds: Thrombolytics, antihypertensives, antiplatelets, and anticoagulants.
• Prevention: Manage BP, antiplatelet therapy if indicated, lipid-lowering therapy, and lifestyle modifications.
• Neuro assessments every 1-2 hours, monitor LOC and pupil activity, VS (BP, HR, Spo2), monitor ICP, I&O's, Serum Sodium and osmolality, and monitor for MI.
• BEFAST (Balance, eyes, face, arm, speech, Time!) is an acronym to teach the public.
• A compilation of strokes is herniation.
• CM of Herniation: Bradycardia, Positive Babinski, dilated pupil, and High systolic BP.
• A late sign of herniation is abnormal posturing.
• Aspiration is due to swallowing and reduced consciousness.
• Chronic complications include hemorrhage, cytotoxic edema, weakness, and paralysis.
• Homonymous hemianopia requires scanning techniques.
• Other complications includes Dysphasia, apraxia, and depression.
• Interventions: HOB 30-45 degrees, maintain neck neutral, suction to minimize ICP, meds (Osmotic, sedatives, and antipyretics).
• Evaluation: Monitor and report early signs of increased ICP and preserve neuro function.

Hemorrhagic Stroke

• Risk factors: HTN, smoking, heavy alcohol use, and sympathetic nervous system stimulants.
• Traumatic or nontraumatic hemorrhage, ruptured aneurysm, and arteriovenous malformation can cause hemorrhagic stroke.
• Subtypes: Nontraumatic Subarachnoid hemorrhage (SAH), Intracerebral Hemorrhage (ICH - most common cause is HTN or caused by anticoagulant use), Intraventricular Hemorrhage (IVH).
• CM: for SAH- severe headaches and altered LOC.
• For ICH- weakness, numbness, difficulty speaking, and altered consciousness.
• For IVH-increased ICP.
• The goal is to prevent and mitigate complications, and secure cerebral aneurysms by Aneurysm clipping or aneurysm coiling.
• Contraindications for meds: no t-PA, No NSAIDs, antiplatelets, or anticoagulation for hemorrhagic stroke, Trauma/head injury, and aspirin.
• Complications: Delayed cerebral Ischemia (DCI), hyper/ hyponatremia, MI, and neuro deterioration due to rebleeding or increased ICP.
• Diagnosis: 1st CT scan to detect hemorrhage, labs: CBC, coagulation profile, and electrolytes.
• For ICH- control BP, reverse coagulopathy if on anticoagulants, and manage ICP with osmotic therapy and drainage.
• Diagnoses include Impaired swallowing, a High risk for impaired gas exchange related to aspiration, Sensory perceptual alterations, Impaired physical mobility related to hemiparesis.
• Diagnoses can also include Impaired verbal communication related to decreased perfusion to the speech centers in the brain (Broca's [motor speech] and Wernicke's [sensory speech]).
• Diagnoses may also include Impaired family coping related to catastrophic illness and uncertain outcome.
• Perform serial neuro assessments, VS, neurovascular assessments, assess puncture site (arteriogram), ECG (A-fib), serum electrolytes, and I&O's.
• Interventions: give rt-PA within 3-4.5 hours, perform bedside swallow screen, elevate HOB, positioning of HOB, place feeding tube, aspiration precautions, bleeding precautions, and frequent repositioning.
• Educate on stroke diagnosis, activate of EMS, warning S/S of stroke, risk factors, smoking cessation, and medication education.

3- GBS (Acute inflammatory demyelinating polyneuropathy)

• Patho: Autoimmune response destroys myelin of peripheral nerves.
• Destruction at nodes of Ranvier, Cranial, motor, sensory nerves are affected causing lower extremity weakness and is usually precipitated by infection 1 month prior.
• CM: Difficulty swallowing, accessory muscle use with breathing, ascending pathway that starts on the feet and moves up.
• Areflexia, cardiac dysrhythmias, hypotension, paralytic ileus, urinary retention, and SIADH can result.
• Stage 1: Acute stage includes demyelination, edema, and inflammation which can last up to 4 weeks.
• Stage 2: Plateau phase where demyelination ceases, and stabilization occurs.
• Stage 3: Recovery

GBS Priorities for Care

• ABCs are the main priority and mechanical ventilation may be required
• The diagnosis is progressive weakness of two or more limbs caused by neuropathy, areflexia + hx of recent viral or bacterial infection.
• A lumbar puncture will present with the CSF + for protein.
• Electromyography shows slowed nerve conduction.
• TX: IVIG and plasmapheresis.
• VII, IX, X, XI, and XII cranial nerve assessment should be performed to identify deficits.
• Look at facial expression, speech, gag, and swallow.
• Complications; Resp failure, risk for VTE, pressure injuries, pneumonia, and autonomic dysfunction.
• Interventions: Elevate HOB to prevent aspiration, provide mobility, IVIG, VTE prophylaxis, give comfort, and establish communication.
• Recovery can take weeks up to months.

ALS (Amyotrophic Lateral Sclerosis)

• ALS Pathophysiology: It is a rapidly progressing fatal CNS dz that affects voluntary muscle control.
• Causes muscle weakness and atrophy without impairing senses or cognitive function.
• ALS affects both upper motor neurons (in brain/ Spasticity) and lower neurons (spinal cord/Flaccidity) leading to muscle weakness, atrophy, and twitching.
• With progression- the brain loses the ability to control muscle movement leading to paralysis.
• In bulbar ALS, it affects muscles with speech, swallowing, tongue movement, and eventually respiratory failure.
• CM: Progressive weakness, muscle cramps, dysphagia, spasticity, flaccidity, difficulty breathing, speech problems, voice changes, twitching, head drop, uncontrolled periods of laughing/crying, weight loss, and tongue atrophy.
• Education: Report difficulty swallowing or breathing.
• Medication: Riluzole slows Progressive Dz, provides no curative TX, and only helps relieve symptoms.
• The brain loses the ability to use its muscles.
• Concerns: Airways, Breathing, Circulation, difficulty swallowing, cyanosis, dusty skin, and skin integrity.
• Diagnosis: testing for muscle strength, spasticity, atrophy, and hyperreflexia.

ALS Diagnostics and Treatments

• Diagnostics: Electromyography, swallow studies, and lumbar puncture.
• Meds provide Symptomatic relief (Baclofen, laxatives, analeptics, and tricyclic antidepressants).
• There's No curative treatment.
• Therapies: PT, OT, ST, assistive devices for mobility/breathing, and nutrition.
• Assessments: Airways, oxygen, motor strength, swallowing ability, skin, and coping skills.
• Interventions: ROM exercises, give meds, repositioning, respiratory care, and emotional support.

Brain Tumors

• CM: Papilledema, dysphagia, hemiparesis, vertigo, increased ICP, headache, n/v, decreased alertness, cognitive impairment, personality changes, ataxia, abnormal reflexes, cranial nerve palsies, elevated BP with widening pulse pressure, bradycardia, n/v, numbness/tingling, and new onset of seizure activity.
• Tumors can cause an increase of ICP.
• Complications: increased ICP, bleeding (do frequent neuro assessments), Cerebral edema (managed with glucocorticoids, osmotic diuretics, hyperventilation, head positioning), seizures, and VTE (prevent with mechanical devices and pharmacological measures).
• Assessment: Neuro assessment, VS, sodium electrolytes, I&O's, urine sg and osmolality (monitor for DI), and pain.
• Actions: Give steroids, replaces fluid loss, elevate HOB, Give stool softeners/ antiepileptic meds, and apply VTE prophylaxis.
• TEACH to tapper steroids/ monitor BG/ med adherence, Fall preventions, head covering, and mouth care.

Myasthenia Gravis

• (Autoimmune neuromuscular junction disorder)
• Higher in Men over 50 years old with result in respiratory failure.
• Characterized by Skeletal Muscle Weakness and a high risk for aspiration related to bulbar weakness.
• Know Patho: Anti-acetylcholine receptor antibodies prevent binding of acetylcholine.
• Destruction of the postsynaptic membrane.
• Binds to AChR, leads to the destruction of receptor sites in Membranes.
• ACh binding becomes blocked and affects the skull and muscle, causing weakness.
• ACh sensitivity is diminished, with a reduction In depolarization and muscle contraction causing weakness and fragility.
• CM: Trunk and limb weakness, progressively worsening, significantly affects their ADLs.
• Ocular issues include Ptosis (droopy eyelid) and diplopia (double vision).
• Bulbar: Cranial nerves 9, 10, 11 (phonation, chewing, swallowing).
• Assess for CM of respiratory deterioration or muscular weakness.
• Diagnosis: AChR antibodies, Electromyography, Edrophonium (Tensilon) test, and Chest CT scan for thymoma.
• Meds: Pyridostigmine (Mestinon), Prednisone, immunosuppressants, and Eculizumab.
• Therapies: IV immunoglobulin and Plasmapheresis.
• Management: Respiratory assessment, +/_ intubation, give meds, elevate HOB, establish communication, offer a soft diet, plan rest periods, and safety measure.

Trigeminal neuralgia

• (Chronic pain condition affecting trigeminal nerve CN V)
• Risk factors: HTN, MS, demyelination of the trigeminal nerve. Patho: Usually unilateral, severe/brief/stabbing/recurrent pain, distribution of one or more branches of the trigeminal nerve, etiology is unknown. CM: Triggers: Touching skin, brushing teeth, drinking, Smiling, talking.
• Attacks vary in frequency with up to 15 attacks/hr.
• Avoid caffeine and hot foods.
• Meds: Antiepileptics, and Baclofen (muscle relaxant).
• Sx: Microvascular decompression providing pain relief within 24-48 hours.
• Assessment: Pain, oral intake, weight, and hx of exacerbations.
• Interventions: give meds, nonpharmacological strategies, and avoid triggers.

Subdural/ Epidural Hematomas

• Both Caused by Traumatic head injuries.
• Epidural Hematoma: Blood collects between the skull and dura mater which is common with the talk & die phenomenon.
• Imaging is a convex appearance
• Subdural Hematoma: Blood collects between the arachnoid mater and dura mater which causes subdural injury to a vein with a primary cause of Venous bleed
• Traumatic Subarachnoid Hemorrhage: is typically focal in location and occurs because of disruption to veins and arteries traversing the arachnoid layer.
• Management: prevent secondary brain injury, manage ICP, and promote perfusion.
• TBI Diagnostics: CT, MRI, transcranial doppler, and serum sodium & osmolality.
• Craniotomy: opening of the skull to remove blood accumulation.
• Priority assessment: Serial neuro assessments, monitor for increased ICP and ensure effective cerebral perfusion.
• ECG & cardiac biomarkers for MI, VS, and implement seizure precautions.
• Complications: Increased ICP, herniating syndrome, meningitis, dural tears, seizures, GI bleeding, DI, and SIADH (low sodium/low serum osmo).
• Assessment: Serial neuro assessment, ECG & cardiac biomarkers, VS (Cushing's Triad), and seizure activity.
• Interventions: HOB > 30 degrees, head midline, avoid sharp hip flexion, management of CSF leak, Avoid NG tube placement (orogastric tube is an alternative).
• Initiate enteral nutrition, maintain normothermic temperature, implement seizure precautions, and ensure VTE prophylaxis (compression devices or socks).

SHOCK & SEPSIS

• Assessment: Restlessness, confusion, irritability, lethargy, and coma.
• Cardiovascular: Assess BP (hypotension), HR (tachy first then brady), skin color, peripheral pulses, CRT. Related to decreased blood to tissues, decreased perfusion, decreased volume Respiratory: RR (tachypnea), ABGS, and SPo2.
• Renal: Oliguria then anuria and increased CREA progression to renal failure.
• GI: decreased gut perfusion.
• Hypoactive Bowl sounds, N/V.
• Hemodynamic monitoring: Art line, pulmonary artery catheter, central venous catheter.

Stages of Shock

• Initial- hypoxia with subtle changes in HR and decreased CO.
• Compensation Vasoconstriction Restlessness, confusion, Tachycardia, low but normal BP, tachypnea, resp alkalosis, oliguria, hyperglycemia, decreased bowel sounds, weak pulses, and cool moist skin.
• Progressive: Failure to compensate causes extensive shunting of blood to vital organs. Profound hypoperfusion, hypotension, lethargy, coma, dysrhythmias, anuria, absent bowel sounds, electrolyte imbalances, worsening metabolic acidosis, and respiratory acidosis, cold extremities, weak or absent pulses.
• Refractory: Prolonged inadequate blood supply to cells = cell death = Multisystem organ failure, Shock irreversible in this stage.
• Circulatory system unable to supply adequate oxygen to tissues to meet metabolic demand resulting in Tissue hypoxia, organ failure, and death.

Sepsis/Septic Shock

• Sepsis (Most Common): Excessive release of proinflammatory cytokines and Organ dysfunction is caused by a deregulated response to infection, circulatory and metabolic abnormalities which increase mortality.
• Prevention: Hand washing and aseptic technique for procedures and early identification of sepsis.
• Early Stage: Tachycardia, bounding pulses, and fever.
• Late Stage: cool/pale skin, weak/ thready pulses, tachycardia, and profound hypotension.
• Labs: Serum lactate, blood cultures, CBC, lactic acid, coagulation studies, Liver function test, ABG's.
• Management: ABX w/i 1 hr after cultures, Fluid resuscitation (Crystalloids), and Vasopressors (norepi) to maintain MAP of >65 after fluid resuscitation fails.
• Corticosteroid therapy and ongoing monitoring are also important.
• Complications: DIC, MODS, and stress ulcers
• Assessment: Neuro status, VS (hypotension/tachycardia), hemodynamic readings (CO increased/ decreased venous return), urine output (decreased), skin color/temp (late: cold/ DIC: tissue necrosis), bleeding (excessive with DIC).
• Interventions: handwashing/ aseptic technique, oxygenation, prepare for intubation, lactate levels, blood cultures, administer ABXs, fluid replacement, vasoactive support, and mouth care.

Disseminated Intravascular Coagulopathy

(DIC)

• Consumptive thrombocytopenia.
• Release of inflammatory mediators cause excessive clotting which lodges in microvasculature causing ischemia and necrosis.
• Exhaust clotting factors cause the release of fibrinolytics reducing clotting which results in excessive bleeding.
• Managed with vigorous tx of underlying sepsis, volume replacement, blood products (Fresh frozen plasma), and replacement of clotting factors.
• Education: Bleeding precautions, soft toothbrush, no IM injections, and no peripheral blood draws.

Multi Organ System Failure

• MODS : Excessive inflammation and decreased end-organ perfusion causes organ dysfunction and then death.
• Sepsis and Neurogenic shock lead to MODS (refractory stage).
• Concerning Lab findings: Kidney failure.

Hypovolemic Shock

• Assessment: Neuro status (LOC), VS, CRT, hemodynamic readings (decreasing CVP/ PAOP), urine output, and skin color/temp (cold/clammy).
• Causes: acute blood loss (Trauma/ GI bleed) and/or Rapid fluid loss (V/D/burns).
• EARLY/Initial- may compensate with no symptoms.
• Later/Progressive- Lethargy, hypotension, metabolic/respiratory acidosis, anuria, pale, cold/cyanotic skin, weak/absent pulses, and dysrhythmia occur. Refractory stage -Coma, hypotension, ischemic and necrotic cold extremities, renal failure, and hepatic failure. Management: Oxygen (100% nonrebreather mask) may need to prepare for intubation, IV access and fluids resuscitation (ISOTONIC FLUIDS), identify & treat cause (fluids/ blood).

Cardiogenic Shock

• Inadequate pumping of heart leads to cardiogenic shock.
• Risk factors: End Stage HF, cardiomyopathy, HTN, DM, multi-vessel dz, and acute MI.
• CM: Initial- chest pain, diaphoresis, n/v, decreased cardiac output, and metabolic acidosis.
• As shock progresses: Hypotension, bradycardia, crackles, organ failure, and coma.
• Management: 12 lead ECG, cardiac enzymes, CXR, oxygen, emergency revascularization (PCI), mechanical circulatory support (IABP), Vasopressors, and inotropes (dobutamine).
• Assessment: Neuro status (LOC), VS (hypotension, tachycardia, increased RR, decreased SPO2), hemodynamic parameters (increased preload with low contractility), Breath sounds (crackles r/o Pulmonary edema), decreased U/O, and skin (cool/clammy).
• Labs: ABG's (resp alk), venous oxygen saturation (decreased SvO2/Scv02), metabolic panel (renal/liver failure), lactate (increased-poor perfusion).
• Interventions: Oxygen (100% nonrebreather mask), prepare for intubation, administer meds (norepinephrine/ dopamine, dobutamine, diuretics, morphine, IVF, and restrict activity.

Distributive Shock

• Distributive shock includes blood/fluid in the wrong place, with relative hypovolemia, and inadequate venous return. Can be caused by Septic shock!
• Anaphylaxis : Release of histamine causing severe systemic hypersensitive reaction.
• Common triggers: Seafood and ABXs.
• Management: removal of trigger, IM epinephrine, NRB 100% or intubate, and IVF.
• Labs look for IgE
• Meds: Antihistamine, corticosteroids, inhaled bronchodilation.
• CM: SOB, tachypnea, wheezing, stridor, cyanosis, confusion, urticaria, hypotension, tachycardia, and skin which presents with urticaria and angioedema.
• Assessment: VS, resp assessment, skin/ peripheral perfusion
• Interventions: remove trigger, epi IM, oxygen, IV access, and give meds.
• Educate on avoiding triggers & Epi pen administrations.

Neurogenic Shock

• Sympathetic nervous system disruption = loss of vasomotor tone and is caused by disruption of SNS due to spinal cord injury, regional spinal anesthesia, or brain injury.
• Only one shock presenting with bradycardia.
• Spinal cord injuries are above T6.
• CM: Warm/dry skin, flushed appearance.
• Profound Bradycardia, hypotension, peripheral vasodilation, decreased LOC, and decreased urine output.
• Management: treat cause, fluid resuscitation, vasoactive meds (epi/norepi/phenylephrine, atropine for bradycardia), and ventilatory support. Assessment: VS (low BP/HR), hemodynamic parameters (low CO/CVP/PAOP/SVR), RR and SpO2, and I&o's
• Interventions: IVF, IV meds (vasoactive drips and atropine), raise HОВ slowly, and apply VTE prophylaxis.
• Monitor serum Lactate levels and ABGs, and ensure the arterial line for continuous BP readings.

Obstructive Shock

• Adequate volume with inadequate delivery which occurs from a mechanical barrier decreasing cardiac output which results in decreased cardiac output and impaired tissue perfusion.
• Risk factors: Increased Right afterload = Acute pulmonary embolism. Impaired filling = cardiac tamponade, and tension pneumothorax. Complications: decreased LOC & u/o, poor pulses, pale/cool skin, decreased bowl sounds, chest pain, n/v, and SOB. Management: treat the cause, give oxygen, and vasoactive infusion with Cardiac tamponade- pericardiocentesis for PE- thrombolytic therapy.
• Assessment: Neuro status, VS (hypotension, tachycardia, tachypnea), hemodynamic parameters, u/o (decreased), skin color/temp, and breath sounds (crackles).
• Interventions: Oxygen (100% nonrebreather), prepare for intubation, administer meds (norepinephrine or dopamine, heparin or thrombolytic if the cause is PE.
• Education: PE prevention. Bleeding precautions with anticoagulants.

Shock Medications

• Adrenergic/Inotropic- Dobutamine is used to increase contractility and cardiac output. Vasopressor medications like norepinephrine or dopamine cause vasoconstriction, increasing blood pressure.
• Morphine sulfate relieves pain, decreases myocardial O2 demand, and decreases venous return through vasodilation Diuretics are used cautiously to decrease fluid overload and preload and to lower BP.
• Anticoagulation via heparin can be used for administration if the cause of obstructive shock is PE
• Thrombolytic therapy can be used if the cause of obstructive shock is PE
• Atropine- for bradycardia
• Nitrates- Nitroglycerin -Vasodilator is used to treat or prevent chest pain.