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Exam 3


Stable Angina occurs predictably with exertion and is relieved by rest and nitro
Variable Angina occurs unpredictable, often at night, and is caused by coronary artery spasm
Unstable Angina occurs with increasing frequency and intensity. Pain may occur at rest. High risk of MI
ECG changes with angina ST depression and T-wave depression
Criteria for stent use for cardiac complications 75% or greater stenosis
Use of nitro for angina up to 3 times 5 minutes apart, if not relieved call 911
Considerations for beta blockers do not use with asthma patients; cause vasodilation and decreased O2 demand
Long-term medication for angina calcium-channel blockers
Primary Goal for angina or AMI Reduce O2 demand and improve O2 supply
Cardiac cripple when patients change their ADLs due to fear of developing chest pain
Acute Coronary Syndrome chest pain that lasts 10-20 minutes at rest and is not relieved by nitro. Near-complete occlusion of the artery.
Difference between acute coronary syndrome and AMI ACS is near-complete occlusion with some blood flow; AMI is complete occlusion of the artery
Diagnostic tests for AMI and ACS Troponin and CK-MB
Fibrinolytic drug action used with AMI/ACS to break up clots causing occlusion
Arthrectomy procedure removal of the arthrosclerosis build up in the arteries
CABG procedure bypass the occluded area with a vessel graft from another area
Stable MI vs unstable MI stable occurs progress slowly gradually leading from angina to MI; unstable occurs suddenly from rupture/spasm/clots
EKG changes with AMI ST elevation and developed Q wave
MONA for AMI morphine, oxygen, nitro, aspirin
infarct extension cells around the infarct dying due to the release of toxins from the nearby dying cells
Intra-aortic balloon pump (IABP) action temporary balloon pump in the heart to provide muscle rest
ventricular assist device (LVAD) action temporary or permanent placement to decrease cardiac workload and aid with cardiac healing
sudden cardiac death unexpected death within 1 hour of cardiac symptoms usually caused by V-fib
Heart failure heart can't meet demands of the body
symptoms of heart failure SOB, peripheral edema, ascites, loss of appetite, fatigue, cough with sputum, confusion
Systolic heart failure The ventricles do not CONTRACT and PUMP blood effectively leading to DECREASED CO
Diastolic heart failure The ventricles do not RELAX and FILL effectively
Left-sided heart failure Fluid backs up in the LUNGS causing SOB, crackles, dyspnea, fatigue, cyanosis, and syncope
Right-sided heart failure Fluid backs up in the BODY causing peripheral edema, DJV, liver enlargement, anorexia, ascites, and nausea
Causes of left-sided heart failure HTN and CAD
Low-output heart failure The heart has low cardiac output and cannot meet the demands of the body; Caused by CAD and HTN
High-output heart failure The heart has normal cardiac output, but the body has especially high O2 demands, so the heart cannot meet the demand; Caused by hypermetabolic states
Classify the stages of heart failure A = at risk; B = disease with no symptoms; C = disease with past/current symptoms; D = disease with symptoms at rest
Diagnosing heart failure renal function; LFT with right-sided; ABGs with left-sided; thyroid function with high-output
A-lines for hemodynamic monitoring usually in jugular vein; monitors pressures within vessels; risk of infection a bleeding
A-line normal rang for hemodynamic monitoring 70-90 mmHg
Medications for heart failure vasodilators and diuretics
Signs of pulmonary edema SOB, cyanosis, PINK FROTHY SPUTUM
Treating Pulmonary edema INTUBATION; Morphine causes vasodilation and pain control; diuretics, oxygen, and suctioning. Constant monitoring with assessment at least q 30minutes since changes occur rapidly
Infective endocarditis inflammation of the endocardium; primary risk factor is DENTAL WORK
S&S of infective endocarditis flu-like symptoms, malaise, heart murmur, petichiae
Diagnosing infective endocarditis Blood culture (identify agent) and TEE (visualize heart valves)
Treating Endocarditis antibiotics; EDUCATION & PREVENTION
Risks associated with endocarditis vegetation on the valves accumulates and dislodges it can cause mobile emboli and be very dangerous
Myocarditis inflammation of the myocardium heart muscle; most at risk are immunocompromised patients
Diagnosing myocarditis EKG, heart ECHO, and biopsy to detect agent
Treating myocarditis immune-suppressants to decrease inflammation; bed rest and O2
Pericarditis inflammation, fibrosis, and scarring of the pericardial sac. Constricts the heart causing impaired pumping ability
Signs of pericarditis friction rub, tachycardia, fever, and chest pain
Complications of pericarditis pericardial effusion: fills with fluid pericardial tamponade: fills with blood
Pericardial Tamponade LIFE THREATENING: hallmark is pulsus paradoxus (decreased BP with inhalation; increased with exhale)
Treating pericarditis Pericardiocentesis; pericardial window
Valvular heart diseases valve stenosis: the valves fuse together and cannot fully open/close; valve regurgitation: the valves do not close completely and allow backflow of blood
Treatment of valve diseases valvuloplasty for stenosis (cut fusion of the valves); valve replacement; symptomatic management with diuretics, anticoagulants, and vasodilators
Types of cardiomyopathy Dilated: enlarged heart causing L&R HF; hypertrophic: left side is too large causing L-sided HF and a-fib; restrictive: heart becomes rigid causing diastolic HF
MODS impairment of two or more organ systems as a result of uncontrolled inflammatory response to severe trauma or illness
Treatment of MODS treat the underlying cause and the organ system affected
Shock different types of shock caused by systemic imbalance between oxygen supply and demand
Calculating CO HR x Stroke Volume = CO
Calculating MAP (mean arterial pressure) CO x SVR (systemic vascular resistance) = MAP
normal MAP value 70-110mmHg
Stage 1: Early Shock uncompensated and reversible: HR may be elevated and VS changes will be slight. Blood loss of <500mL drop in MAP of <10mmHg
Stage 1: Compensated Shock body releases epinephrine and norepinephrine causing casoconstriction; RAA pathway causes sodium and water retention to conserve fluids. Blood loss of 1000mL and drop in MAP by 10-15mmHg
Stage 2: Intermediate shock MAP drops >20mmHg; fluid loss of 35-50% Pulse will be tachy and thready, body becomes hypoxic causing release of lactic acid causing ACIDOSIS and HYPERKALEMIA
Stage 3: Irreversible Shock MAP is <60mmHg with >2000mL blood loss; Pulse is absent with critically low BP and CO. Tissue damage is irreversible and death is likely.
Neurologic changes during shock Early: restless and anxious; Intermediate: lethargic and confused; Late: coma
Manifestations of Hypovolemic shock decreased BP; increased HR, thready Pulse, RR increased, skin pallor and edema, decrease urine output, slowed cap refill
Cardiogenic Shock there is no fluid loss, but the heart is unable to pump blood effectively
Causes of cardiogenic shock AMI, restrictive pericarditis, cardiac tamponade
Manifestations of Cardiogenic shock and Obstructive shock hyper-hypotension, HR rapid with distended veins, resp. crackles and labored, skin cyanotic and cold, dependent edema and distended veins due to increased venous pressure
Obstructive shock obstruction in the heart or great vessels causing decreased blood flow throughout body despite enough fluid. Manifestations are the same as cardiogenic
Distributive Shock several kinds of shock including sepsis, neurogenic, and anaphylaxis, where there is uncontrolled peripheral vasodilation
Septic Shock Manifestations decreased BP, increased and thready pulse, RR deep and rapid, skin warm and flushed, decreased urine output, fever, chills, and weakness
Manifestations of Toxic Shock Syndrome widespread inflammation, headache, hypotension, confusion, VD, rash, DIC, platelet aggregation and decreased blood flow
Neurogenic Shock CNS disturbance causes uncontrolled vasodilation and venous blood pooling
Causes of neurogenic shock *Anesthesia, CNS depressants, spinal cord injury, head trauma
Anaphylactic Shock widespread hypersensitivity reaction that causes uncontrolled vasodilation and blood pooling
Manifestations of anaphylaxis respiratory distress, dyspnea, bronchospasm, abdominal cramping, swelling of the hands and face, drop in BP
Treating SHOCK initially Oxygen, Fluids (NS/LR), Blood products
Lactated Ringers Solution used to replace plasma volume, same concentration as plasma, frequently used with burns and shock
Medications for treating shock Vasoconstrictors (norepinephrine) to increase BP, Inotropes (Dopamine) to increase CO, Colloid Solutions (increase fluid volume)
Considerations for norepinephrine It is infiltrates it will cause tissue necrosis
Considerations for inotropes Monitor patient on telemetry, monitor I&Os, and triple check IV pump settings
Use of vasodilators with shock Used with cardiogenic shock to decrease O2 demand of the heart; run IV with D5W and monitor for hypotension
Colloid Solutions for treating shock (Hetastarch and Dextran) Plasma expanders to increase plasma volume; Give with LARGE-gauge needle and have EPI at bedside increase of allergic reaction
Things that affect burn degree temperature, duration, and skin thickness
Primary concern in burn patients in the first 48 hours Fluid Loss due to increased capillary permeability and third spacing of fluid --> HYPOVOLEMIC SHOCK
Layers of the skin Epidermis (top) Dermis (nerve endings and hair follicles), under that is fat, muscle, then bone.
Superficial burns damage to the epidermis; Red, tender, with NO Blistering; likely to heal on it's own
Partial-thickness burns the epidermis is destroyed and there is damage to the dermis; Blistering, peeling, sloughing
Full-thickness burns The epidermis and the dermis are destroyed and there is damage to underlying tissues. SKIN does NOT stretch; non-blanching, loss of feeling in area.
Zones of burn damage Zone of coagulation (cell death), Zone of Stasis (cells have potential to heal/die), Zone of Hyperemia (cells will likely heal)
Cold water or ice burns This causes vasoconstriction to the area and increases the area of cells that are likely to die. NEVER put ice on a burn
Difference between superficial partial and deep partial burns Color and Blanching: red with fast color return = superficial partial; pale/pink with slower color return = deep partial
Edema r/t Burns Small burns will lead to localized swelling; Burns >20-30% will lead to systemic swelling
Lab changes in burn patients increased K+ --> HYPERKALEMIA; Na+ shift into the third space --> HYPONATREMIA
Primary survey of burn patients ABCs: airway, breathing, circulation
Types of burn inhalation injury above the glottis (oral and nasal); below the glottis (usually prolonged exposure to smoke and chemicals)
Signs of inhalation injury SOB, wheezing,black/ashy sputum, singed nasal/facial hair, stridor, decreased LOC
Treating inhalation injury 15L of Oxygen by non-rebreather, and prophylactic intubation with pulsing to replace cilia action
Considerations for carbon monoxide poisoning pulse ox cannot tell the difference between O2 and CO (if O2 is reading 100% you should be concerned). Bright red conjunctiva is a sign of CO poisoning
Diagnosing CO poisoning ABGs
CO poising treatment non-rebreather on 100%, Vent with 100%, hyperbaric chamber (potentially, but has drawbacks)
Circumferential full-thickness burns impairs circulation to limbs or torso (causing impaired respirations)
Diagnosing complications from circumferential burns Check PULSES every hour; by palpation or Doppler. Increased respiratory effort, SOB, chest tightness; or diminished pulses and pale extremity
Treating complications from circumferential burns Loosen ACE wraps, if not resolved within 15 minutes. Escharotomy (specific cuts in the eschar to allow increased blood flow and decrease the restrictive nature of eschar)
Rule of Palm each palm is 1% TBSA
Rule of nines arms, and head are 9% each, torso top/bottom & front/back and legs are 18% each
Most accurate way to determine burn surface area Lund & Browder chart
Fluid resuscitation for burns in adults and children >40kg 2mL x kg x %TBSA = mL/24h
Fluid resuscitation for burns in children <40kg 3mL x kg x TBSA = mL/24h
Fluid resuscitation for electrical burn patients 4mL x kg x TBSA = mL/24h
Measuring response to fluid therapy Urine Output should be 30-50mL/h
AMPLE Tool Quick history assessment: Allergies, Medications, Past hx, Last meal/drink, Events surrounding injury
Treating partial thickness skin burns Biograin or Porcine (pig skin that should stick to the burn and allow for healing while providing protection)
Treating Full-thickness burns removal of dead eschar and skin graft onto affected area (skin graft can be sheet or meshed)
Treating chemical burns initially protect yourself; remove affected clothes, FLUSH with water,
Morgan Lenses lenses that are hooked p to tubing which flushes the eyes with normal saline
Diagnosing electrical injuries There will be definitive entrance and exit injuries from electrical current; there may be concurrent flame burn from a sparked fire,
Treating electrical injuries If no contact injuries and no EKG changes then the patient can be discharged; if EKG changes monitor for 24 hours, if burn injuries, treat burns. Muscle fascia may need deep escharotomy to treat diminished pulses
Urine output with electrical injuries urine may be red or tea colored (indicating myoglobin in the urine from muscle damage). UOP should be 50-75ml/h.
Sulfamylon, Silva, and Bacitracin Sulfamylon (painful) and Silva used on full-thickness; Silva and Bacitracin used on partial-thickness
Caring for burns Must be washed and debris BID with applied medications and bandages
Pain with burns medicate the pain, but the patient has to be alert enough to accomplish therapy and rehab which will start on day 1.
Area of the brain the controls breathing and HR Brain stem
ANS Sympathetic response fight or flight
ANS parasympathetic response rest and relax response
Cranial nerves 12 cranial nerves that control sensory/motor/both
Nail bed test press pen down on the nail bed on the toe or finger and measure patient response to pain
What is the lowest Glascow coma scale number 3 (patient is in a coma)
Neuro assessment Pupils, muscle strength, balance, orientation, LOC, pain response
AEIOU for assessment Series of things causing changes in LOC: Alcohol, Epilepsy, Insulin, Opiates, Uremia (presentation of UTI)
TIPSS for assessment Series of things causing changes in LOC: Tumor, Injury, Psych, Sepsis, Stroke
Normal Intracranial Pressure 0-15mmHg
Complications of ICP decreased cerebral blood flow, altered LOC, and herniation (brain herniates out the bottom of the skull)
Treating ICP Manitol: diuretic to decrease ICP. Measure if it's working by monitoring I&Os and LOC; low-stimuli environment, managing HR, BP, and Temp.
Causes of ICP cerebral edema (increased fluid due to injury or infection) and hydrocephalus (over production of cerebral fluid)
Treating hydrocephalus VP shunt to drain excess fluid
Cushing's Triad sign of ICP: increased systolic BP, widening pulse pressure, and decreased HR
Signs of ICP Cushings Triad, spiked fever, headache, and projectile vomiting
ICP monitoring hole in the skull with probe inserted to monitor the ICP
Seizure threshold all people have a certain seizure threshold, some is higher or lower than others
Epilepsy reoccurring seizures that are self-resolving
Simple Partial Seizure NO altered consciousness, causes hallucinations and altered sensations. The patient will generally know when these seizures are coming on.
Complex Partial Seizure IMPAIRED consciousness, characterized by REPETITIVE nonproduction activity, Amnesia is common, and may have aura
Generalized Absence Seizures There WILL BE altered consciousness, Sudden, brief cessation of motor activity (lasting 5-15 seconds)
Tonic-Clonic Seizures Consciousness is IMPAIRED, sudden loss of consciousness, characterized by sharp muscle contractions lasting 60-90 seconds
Tonic phase Breathing may stop, pupils will be fixed and dilated.
Clonic phase Hyperventilation, with altering contraction and relaxation of the muscles
Status Epilepticus recurrent seizures with very short periods between seizures = MEDICAL EMERGENCY
Complications of Status Epilepticus Hypoxia, Hypoglycemia, Hyperthermia, and exhaustion
Treating Status Epilepticus Airway, IV Dextrose, Valium/Ativan (during seizure), Dilantin (long-term control)
Managing seizures do not restrain, do not put anything in the mouth. Turn to the side if they vomit, suction if needed to clear the airway, SAFETY is the priority. Keep oxygen and suction at bedside, and pad the bed rails.
Antiepileptic drugs Neurontin, Lamictal, Topamax
When to call a squad for seizures first-time seizure, pregnant, or diabetic patients
Monitoring a seizure what precipitated the event, how long did each phase last, what did the seizure look like?
TIA mini-strokes that are self-resolving and leave no long-term damage. They are a HUGE warning sign for stroke
Ischemic Stroke Occlusion of the blood supply to the brain (clots)
Hemorrhagic Stroke Bleeding/rupture decreasing blood flow to the brain
Manifestations of Stroke one-sided weakness, facial droop, altered LOC, sudden onset
FAST Facial droop with smile, Arm drop when holding up, Slurred speech, and Time to act
Treating strokes Act quickly. Clot-busters, aspirin, Fibrinolytics, surgery, and REHAB
TPA considerations Clot-buster. You MUST KNOW what kind of stroke the pt is having before you give this. NEVER give to a bleeding patient
Focal TBI affects a specific area of the brain; contusions and hematomas
TBI Hematomas Focal injury; Epideral (outside the dural sac), Subderal (within the dural sac), Intracerebral (within the brain)
Treating TBI hematomas Burr hole to drain blood and relieve pressure; intracranial are difficult to treat
Diffuse TBI affects the entire brain; shaking, accel-decel, and rotation injuries, and concussions
TBI Contact phenomena direct injury to the brain: hitting your head, falling injuries.
TBI acceleration-deceleration injury MVA or shaking injuries; causes damage to the front and back of the brain as it hits the skull
TBI rotation injuries The head rotates quickly causing whiplash and damage within the brain.
Manifestations of TBI Symptoms will be related to the area of the brain affected: changes in LOC, vision changes, motor/speech/behavior changes, loss of consciousness
Diagnosing TBI CT/MRI, Toxicology report, ICP monitoring
Treating TBI Burr hole to relieve pressure and drain fluid, Mannitol to decrease ICP
Symptoms of Brain Tumors symptoms dependent of location: headaches, seizures, vomiting
Diagnosing Brain Tumors MRI, EEG, Arteriogram (detects blood supply to the tumor)
Treating Brain Tumors surgery (if possible), chemo, radiation, rehab
Considerations for ALL neuro patients SAFETY and Risk of Falls
Headaches Tension (usually mild), Migraines (usually more severe), Cluster (usually severe targeted area)
Treatment for severe headaches Calcium channel and Beta blockers, pain control (non-narcotic), decrease stimulation (dark, quiet rooms), treat nausea
Spinal Cord injuries Accel-Decel injury, Hyperflexion (chin to chest), Hyperextension (backward), Axial loading (crushing injury), Rotation injury
Autonomic Dysreflexia CNS signals cannot climb the spinal cord
Symptoms of autonomic dysreflexia red & hot above the injury, white & cool below the injury; Severe HTN, Bradycardia, pounding headache
Causes of autonomic dysreflexia pressure ulcer, fecal impaction, clogged catheter, full bladder
Treating autonomic dysreflexia unkinked catheter, empty bladder, treat fecal impaction, treat pressure ulcers. TREAT UNDERLYING CAUSE
Consideration of spinal cord injury height The higher up the injury the more severe the symptoms
Treating spinal cord injuries initially ABCs, immobilize, steroids (decrease inflammation), vasopressors (increase BP). antispasmotics (pain and spasms), antiemetics (prevent vomiting), surgery, and traction
Treating spinal cord injuries long-term Rehab, assistive devices, analgesics, stool softeners, anticoagulants
Meningitis (Bacterial/Viral) Symptoms neck pain, fever, chills, nucal rigidity (stiff neck), Brudzinski's sign, Kernig's sign, ICP
Brudzinski's sign when the pt puts their chin to chest; the knee will pop up
Kernig's sign pt lays flat on back, flex hip at 90 degree angle and the pt cannot kick their foot out
Encephalitis Infection of the covering of the spinal cord
Encephalitis Arbovirus Caused by mosquitos and ticks
Diagnosing CNS infections Spinal tap or Lumbar Puncture with culture of cerebral spinal fluid
Treating CNS infections antibiotics/antivirals, anticonvulsants (risk of seizure), antipyretic (fever), antiemetics (nausea from ICP), treat symptoms.
Considerations for treating CNS infections medications MUST cross the blood-brain barrier. ALWAY draw blood for cultures before starting antibiotics. Always start with broad abx and move more narrow.
Dementia progressive degenerative disease that interferes with daily life. Treat with supportive care and SAFETY measures.
Alzheimer's Disease Progressive form of dementia; manage depression, supportive and emotional care; SAFETY
Multiple Sclerosis (MS) demyelinating of CNS causing DIPLOPIA, weakness, sensory loss, vision changes, and fatigue
Treating MS immunosuppresants (fight autoimmune process), ACTH hormones, Rehab, and maintain as much function as possible
Parkinson's Disease Decrease in Dopamine causing progressive degeneration: tremor, rigidity, facial "mask", impaired swallowing, impaired walking, and depression
Treating Parkinson's Disease Dopamine agonists (Levadopa), anticholinergics (help with swallowing), Rehab to maintain function
Myasthenia Gravis autoimmune disease causing chronic muscle weakness: works from EYES DOWN, weakness, tachycardia, and respiratory distress
Myasthenia Crisis Due to skipping medication: causes acute exacerbation of symptoms
Cholinergic Crisis Due to over-medicating: causing GI symptoms, muscle weakness, resp. distress
Diagnosing Myasthenia Gravis Tensilon Test
Treating Myasthenia Gravis immunosuppresants, glucocorticosteroids, anticholinesterases
Guillaine-Barre Disease Demyelinating of the peripheral nervous system causing rapid ascending paralysis *EMERGENCY; The paralysis will resolve once it's treated
Considerations for Guillaine-Barre Disease as the paralysis moves upward it will interfere with breathing and heart. Patient may end up intubated. Use a marker to mark the progression of the paralysis.
Trigeminal Neuralgia chronic unilateral facial pain; treat with Tegretol and surgery
Bell's Palsy Disorder of the 7th cranial nerve causing facial droop, and unilateral weakness; Treat with PT
Created by: jperrault9941
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