NUR212 Final Exam

Cerebral Perfusion Pressure (CPP)

-Pressure needed to maintain adequate blood flow to the brain-CPP=MAP-ICP-Normal CPP 70-100mmHg-CPP <50mmHG is associated with ischemia and neuronal death (TIA or Stroke)-As CPP decreases, autoregulation will fail and cerebral blood flow will decrease-MAP brings blood into the brain-ICP draws blood out of the brain

Auto Regulation

the brain's ability to regulate its own blood flow in response to metabolic needs, despite systemic blood flow

Skull Components

-10% CSF-12% Intravascular Blood-78% Brain Tissue

Acute Head Injury

-Head trauma leading to increased ICP, ICP leading to a TIA, TIA leading to stroke-Classifications: open/closed, mild/moderate/severe (Depending on GCS and length of time unconscious)

Glasgow Coma Scale

-Normal= 15-Decrease in GCS = decrease in LOC

Closed Head Injuries

-Coup-Contrecoup-Concussion-Contusion-Diffuse Axonal Injury (Rotational Injury)-Intracranial Hemorrhage

Coup

-Blunt object strikes the head-Acceleration injury-The actual impact/trauma to the outer skull

Contrecoup

-Head strikes an immovable object-Deceleration Injury-Injury to the brain due to coup injury-Brian injury occurs at the opposite side of impact

Concussion

-Mild TBI-Blunt head trauma resulting in a change in neurological function, but no identifiable brain damage-Typically lasts 72 hours-Cerebral damage is at a microscopic level-Damage is undetected by radiography-Transient unconsciousness <20 mins

Signs/Symptoms of Concussion

Transient unconsciousness, memory difficulties, amnesia, dazed/confused, headache, vertigo, vomiting, bothered by light, sleep disturbances, slurred speech

Post-Concussion Syndrome

-Includes persistence of cognitive and physical manifestations for an unknown period of time-Can occur 3+ months after injury-Usually occurs with multiple concussions

Contusion

-Occurs when the brain is bruised-May have a period of unconsciousness associated with stupor and or confusion-Bruising of cerebral soft tissue-Macroscopic tissue/vessel damage seen on CT/MRI-Associated with longer periods of unconsciousness and has a more guarded prognosis-Occurs often from older adults falling with accompanying blood thinner use

Diffuse Axonal Injury (Rotational Injury)

-Rapid spinning of the head and contents that causes tears of the axons-Widespread injury to the brain that results in a coma (for 6-24hrs).-Seen with severe head trauma-Abnormal posture, increased ICP

Intracranial Hemorrhage

-Can occur in epidural, subdural, or intracerebral space-It is a collection of blood in brain spaces that follows head trauma

Manifestations of Head Trauma

Amnesia, loss of consciousness, CSF leakage from the nose or ears, manifestations of increased ICP

Decorticate Posturing

-flexed wrists, elbows and feet-Adducted arms-Internally rotated hips

Decerebrate Posturing

-Flexed wrists and feet-Extended, pronated and adducted arms

Manifestations of Increased ICP

Severe headache, N/V, deteriorating LOC, restlessness, irritability, dilated pupils, non-reactive pupils, cranial nerve dysfunction, Cheyne-Stokes respirations, decorticate/decerebrate/flaccid posturing, seizures, Crushing's Triad

Crushing's Triad

-Late finding of increased ICP-Severe HTN with a widening pulse pressure (systolic-diastolic), and bradycardia-Increased SBP, Decreased DBP, Bradycardia

Monitoring ICP

-Monitored by placing a screw/catheter/sensor through a burr hole into the ventricle/subarachnoid/epidural/subdural space within the brain-Indications: GCS<8, or those with abnormal CT/MRI

Intracranial Pressure (ICP)

-The pressure within the cranial vault.-Normal= 10-15-With ICP of >30mmHG, the brain will fail

Reasons for Increased ICP

-a rise in arterial/venous pressures-increase in body temp-hypercarbia leading to cerebral vasodilation-endotracheal/oral suctioning-coughing-extreme head flexion/extension-increasing intra-thoracic or intra-abdominal pressures

Increased ICP Treatment

-Level 1) least aggressive, initiate if pt at risk for increased ICP, patient positioning, maintain normothermia, pain control, sedation, reduce environmental stimuli-Level 2) Drain CSF, osmotic diuretic (Mannitol), fluid volume maintenance, mechanical ventilation to maintain PaCO2 of 30-35 with no cerebral hypoxia, administer anti-seizure meds (Barbiturates), repeat CT scan-Level 3) most aggressive, Indicated for ICP>20, Mild hyperventilation, produce mild hypothermia, administer a neuromuscular blockade to stop shivering (hypothermia will decreased metabolic need, so block the shivering that will increased metabolic demands), preform craniotomy which will allow the brain to swell without hypoxic event

Complications of Increased ICP

-Seizures-Diabetes Insipidus-Syndrome of Inappropriate Antidiuretic Hormone-Brain Herniation-Brain Death

-Seizure Activity

-Electrical system of the brain fires in a disorganized fashion-Seizures are a critical event casing increased ICP, hypoxia, increased metabolic demand, and secondary injuries-Treatment) safety, ABCs, timely anticonvulsants, continuous EKG monitoring, administer IV lorazepam/phenytoin/fosphenytoin to lower seizure threshold

Diabetes Insipidus

-antidiuretic hormone is not secreted adequately, or the kidney is resistant to its effect-Will see large amounts of dilute urine and hypotension-TBI causes pressure on the pituitary gland, the pressure impairs ADH secretion which leads to diuresis, polyuria/polydipsia-increased serum sodium

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

-opposite of Diabetes Insipidus-Increase of total body water (fluid volume excess) due to increase in ADH. -Excess ADH causes water retention-Will see small amounts of concentrated urine-Decreased serum sodium will cause intracranial swelling-Treatment) fluid restriction, monitor I&Os, neuro checks

Brain Herniation

-Catastrophic complication of increased ICP-As pressure increases, brain tissue shifts to an area of less pressure, this will push the brain out of its normal position and slide down into the brainstem, causing death-Prevention/Tx) close monitoring, controlling ICP, craniotomy

Brain Death

-Irreversible complication-Brain/brainstem function is not evident for 24 hours-Will have an inability to maintain adequate BP, profound bradycardia, a loss of basic neurological functioning, fixed/dilated pupils, and a lack of reflexes

Cerebral Hematoma

-Occurs when blood accumulates in cranial vault-Result of injury to cerebral vein/artery-High-impact injury: multiple hematomas possible-Named by location: subdural, epidural, intracerebral

Subdural Hematoma

-Blood accumulates between the dura and arachnoid layers-Usually secondary to venous injury-Develops slowly (time between injury and onset of manifestation-Manifestations: (acute, within 48 hours) drowsiness, headache, hemiparesis, confusion, agitation (subacute within 48hours-2weeks) neurological deterioration possibly delayed, increased ICP, drowsiness and headache(chronic, greater than 2weeks) vague manifestation, often misattributed, personality changes, headache, anxiety, ataxia, incontinence-Management: surgical evacuation, placement of subdural drain-Nursing: monitor LOC, frequent neuro checks

Epidural Hematoma

-High impact transfer force, small arteries sheer, blood accumulates rapidly between skull and dura mater-Manifestations: brief unconsciousness, alert and oriented, fixed/dilated pupils, headaches, n/v, -Treatment: surgical evacuation, placement of ICP monitoring, ICU admission-Nursing: neuro checks, identify any reoccurring bleeding

Stroke (CVA)

-Acute neurologic deficit occurring when blood flow is impaired to a localized area of the brain.-Due to the ischemia/reduced blood flow/injury to neurological tissue, death can occur-Risk Factors: age, gender, ethnicity, race, heredity, family history, certain diseases, HTN, CAD, hyperlipidemia, smoking, excess alcohol use, obesity, sleep apnea, metabolic syndrome, poor diet, drug abuse, high blood sugars, lack of exercise-Prevention: reduce weight, increase exercise, decrease alcohol intake , stop smoking-Recognition: (BEFAST) balance, eyes, face, arms speech, timeWill see initial hyporeflexia then hyperreflexia-Diagnostics: done to confirm a stroke, identify cause, determine the type. History, neuro exam, GCS, NIH Stroke Scale, CT within the frit 25 minutes, cranial nerve reflexes, MRI, CT, MRA, cerebral angiography, transcranial doppler ultrasound, lumbar puncture, TEE, cardiac imaging

Transient Ischemic Attack (TIA)

-Interruption of cerebral blood flow, brief episodes of focal neurological deficits-Warning sign that a stroke is most likely to occur-Associated with increased risk for stroke-Transient episode of neurologic dysfunction caused by focal brain/spinal cord/retinal ischemia, but without acute infarction of the brain-Symptoms typically last <1 hour-1/3 will progress to a stroke

Classifications of Strokes

-Ischemic Stroke (thrombotic, embolic, TIA)-Hemorrhagic Stroke

Ischemic Stroke

-Thrombotic: Caused by a blood clot that obstructs arterial blood flow to an area of the brain-Embolic: caused by an emboli that travels from its original site outside of the brain and becomes lodged in an artery that feeds the brain-TIA-Treatment: Keep BP 140/90 to compensate for the compromised cerebral blood flow (labetalol). Control F/E balance (DI/SIADH), keep hydrated to promote perfusion to the brain, manage ICP, TPA-Surgical: if TIA/stroke caused by CAD preform a carotid endarterectomy, stenting, and transluminal angioplasty

TPA Protocol

-Recombinant tissue plasminogen activator.-Used to reestablish blood flow through a blocked artery to prevent cell death-Start within 3-4.5 hours of s/s onset-IV TPA within 6 hours-After-care: prevent further clot formation with anticoagulants and antiplatelets in combination-Weight based-10% initial bolus-Other 90% infused over 60 minutes

Hemorrhagic Stroke

-When there is bleeding into the brain tissue/cranial vault, due to increase in ICP, trauma, aneurysms, arteriovenous malformations, and hypertension-Caused by a hemorrhagic aneurysm within the brain. Subarachnoid hemorrhage, bleeding between the brain and the skull, intracranial hemorrhage, blockage of the carotid artery-Manifestations: memory/judgement impairment, affected side weakness or paralysis, unilateral neglect, agnosia (inability to recognize things), homonymous hemianopsia (visual deficit on both sides of each eye), elimination deficits

Right-sided Brain Injury

-Right sided stroke injury will affect the left side of the body-S/S: paralyzed, left sided hemiplegia, left sided neglect, spatial-perceptual deficits, tendency to deny/minimize problems, rapid performance, short attention span, impulsivity, impaired judgment, impaired sense of time

Left-sided Brain Injury

-Left sided stroke will affect the right side of the body-Paralyzed right sided hemiplegia, impaired speech and language, impaired right and left discrimination, slow performance, cautious, aware of deficits, anxiety, depression, impaired comprehension for language and math.

Dysarthria

disturbance in muscular control of speech

Aphasia

-occurs when stroke damages the dominant hemisphere of the brain that affects language-Receptive: Loss of comprehension-Expressive: loss of language production-Global: total loss of ability to communicate

Affect

-Difficulty controlling emotions-Emotional responses may be exaggerated/unpredictable-May be magnified by depression, change in body image, and loss of function

Agnosia

-Inability to recognize/interpret things even if they are familiar-Cannot recognize things by touch

Apraxia

-Inability to carry out purposeful movements-Not paralyzed or flaccid, but as if the limb doesn't belong to them

Intracerebral Hemorrhage

-Bleeding in the brain-Cerebral blood vessel ruptures causing bleeding into the brain (NO WARNING SIGNS)-More common in older adults experiencing sustained increase in SBP-Most common of fatal stroke

Subarachnoid Hemorrhage

-Rupture of aneurysm or trauma-Likely to occur with activity-Result of HTN-NO WARNING SIGNS-Treatment: No anticoagulants, keep BP high to normal range, seizure prophylaxis, manage ICP, resection/clipping/evacuation of hematomas

Obstructive Emergencies

- Spinal cord compression- Superior vena cava syndrome- Third spacing-Cancer patients are at increased risk for clots due to hyper-coagulopathy, they can develop clots faster and more frequently because of uncontrolled cell proliferation

Spinal Cord Compression

-Life threatening emergency if located above C3-Will lose the ability of the phrenic nerve which controls bleeding-S/S: intense and localized back pain due to compression, motor weakness, paresthesia below the level of injury, sensory loss, changes in the bladder and bowel function (S2 and up overflow incontinence, S3 and S4 flaccidity incontinence)-Diagnostics: abnormal reflexes, sensory and motor abnormalities, percussion tenderness at compression site, MRI, myelogram, X-ray, bone scan, CT to find the primary tumor site in cancer patients.-Treatment: corticosteroids(decreasing inflammation/relieve compression symptoms), narcotic analgesics for pain control, Radiation to shrink tumor, laminectomy/spinal fusion if the tumor has invaded the vertebrae. -Nursing: prevent immobility complications, control pain, PT/OT, neuro checks, manage bowel and bladder.

Superior Vena Cava Syndrome (SVCS)

-Often the first sign for a cancer patient-Tumor compressing the superior vena cava causing increased venous pressure due to inadequate outflow of venous blood to the head, neck, face, chest, upper arms.-Dilation of superficial veins due to blood flow obstruction impairing drainage-S/S: facial/upper body edema, dyspnea, cough, stridor, tachypnea, headache, lethargy, disturbed vision, dizziness, stupor/coma, red skin, JVD-Diagnostics: CXR, CT, bronchoscopy, tissue biopsy-Treatment: depends on the cause of obstruction (tumor, side effect of radiation, or DVT), radiation, corticosteroids, anticoagulants/thrombolytics, diuretics, chemo, stent replacement-Nursing: monitor respiration status, O2 sats, administer O2, avoid R-arm venipuncture, elevate HOB, remove restrictive clothing, daily weights, I&Os, assess for dysphasia.

Third Spacing

-Shift of fluid form vascular to interstitial space-Can be secondary to surgery, immunotherapy, or septic shock-S/S: hypovolemia signs, hypotension, tachycardia, decreased CVP, decreased urinary output-Treatment: F/E replacement, fluid bolus to increase vascular perfusion, CO, and urinary output-Albumin may increase ICP, therefore contraindicated with brain tumors

Metabolic Emergencies

-Caused by production of ectopic hormones directly from the tumors or secondary to metabolic alterations caused by the tumor or cancer treatment-Neutropenic Sepsis-Tumor Lysis Syndrome-Hypercalcemia-Aplastic Anemia-SIADH

Hypercalcemia

-Due to osteoclastic activity decreasing calcium in bone and releasing the calcium into serum.-Bone destruction by tumor cells release of calcium-Most common metabolic crisis in cancer treatment-Can be due to tumors producing parathyroid-like substances which promote calcium release-S/S: serum Ca>10.5, confusion, hyporeflexia, impaired renal function, frequent urination, excessive thirst, renal calculi, renal failure, EKG showing shortened QT interval, arrythmias, bradycardia, cardiac arrest, N/V, constipation, fatigue, depression, muscle weakness, anorexia-Treatment: aggressive hydration (3L/day), diuretics (furosemide 40-80mg IVP Q4-6 hours), calcitonin (to increase ca and phosphorus in bone deposits, corticosteroids, bisphosphonate (fracture prevention), dialysis-Nursing: monitor Ca levels, electrolytes levels, teach s/s of hypercalcemia, monitor EKG, prevent fractures, mental status, encourage mobilization, Hypercalcemia enhances digoxin!!!!!

Tumor Lysis Syndrome (TLS)

-Cell death causes the release of intracellular contents causing hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia, resulting in renal failure/cardiac arrest-Caused by trauma, burns, crush injuries, and cancer treatment-S/S: dependent upon which abnormal value is measured (look for a specific electrolyte imbalance), fatigue, weakness, memory loss, muscle cramps, altered mental status, tetany, paresthesia, seizures, elevated BP, wide QRS with hypercalcemia, dysrhythmias, cardiac arrest, anorexia, N/V, abdominal cramping, diarrhea, flank pain, oliguria, anuria, renal failure-Treatment: Aggressive hydration 48 hours before and after chemo, diuretic to flush toxins, kayexalate for hyperkalemia (contraindicated for N/V/D), Albumin hydroxide to promote phosphate excretion, hemodialysis. -Nursing: daily weights, I&Os, renal status, preventative measures, recognize high risk chemo patient's, monitor for electrolyte imbalances

Neutropenic Sepsis

-Emergency-ANC <500 cells/mm3-fever may be the only symptom-can die in 24-48 hours without ABX-Diagnostics: S/S of infection, physical assessment, culture for PICC and central line, urinalysis, x-ray-Treatment: IV fluids, broad spectrum ABX within 1 hour of neutropenic fever, isolation, antifungals-Prevention: hand hygiene, vaccines, myeloid growth factors (filgrastim and pegfilgrastim), neupagen

Aplastic Anemia

-Insufficient production of blood cells related to antineoplastics.-Causes: chemo, cytotoxins, radiation-Bone marrow and blood stem cells are damaged-Pancytopenia: decrease in all types of blood cellsS/S: lack of mature blood cells, ecchymosis, petechiae, bleeding , GI bleed, increased risk for infections.-Treatment: transfusions of blood and platelets, bone marrow transplant, erythropoietin, neupagen, Neulasta-Nursing Care: supportive care, manage symptoms, prevent injury, monitor labs, monitor pulmonary, renal, neuro, and cardio status

Infiltrative Emergencies

-Malignant tumors may invade major organs, or secondary to cancer treatments-Damage to major organs caused by infiltrating cancer-Cardiac Tamponade or Carotid Artery Rupture

Cardiac Tamponade

-Malignant tumors may invade the pericardium directly or through the blood/lymph system.-All blood is filtered though the heart-Cancer in blood will cause cardiac tamponade-Causes: high radiation dose-S/S: retrosternal chest pain, SOB, JVD, muffled S1 and S2 heart sounds, pericardial friction rub sounds, (Beck's Triad) narrowed pulse pressure due to low arterial blood flow/JVD/muffled heart sounds, (paradoxical pulse) marked drop in pulse amplitude and SBP of >10mmHG upon inspiration-Diagnostics: echo, CT, CXR, EKG (low QRS voltage), hemodynamic instability-Treatment: pericardiocentesis, pericardiectomy

Carotid Artery Rupture

-Rupture of carotid artery secondary to invasion of the arterial wall by tumor or erosion following surgery or radiation.-S/S: bleeding (minor oozing to major spurting)-Treatment: apply pressure to the site, IVF, blood products, surgical ligation of the carotid artery

Chemotherapy Complications

-Expected outcomes from chemo, not so much crisis complications-Results due to chemo treatment, not considered emergencies, but they can become emergencies-Febrile neutropenia-Neutropenic sepsis-Nephrotoxicity-Enterotoxicity-F/E Imbalances

Neutropenia

-Abnormally low WBC count-Can be caused by damage to bone marrow, infections, meds/chemo-Febrile Neutropenia: ANC <500 and fever is present-Neutropenic Sepsis: due to bone marrow suppression, neutrophils are at their lowest level 10-14 days after chemo, <1000 (500 if recent chemo treatment). Will have fever >100.4

Nephrotoxicity

-High amounts of drugs/antibiotics increase renal damage resulting in nephrotoxicity-Risk Factors: FVD, advanced age, pre-existing renal dysfunction, concomitant use with NSAIDS, aminoglycosides, ionated contrast material-Comorbidities: high drug doses of chemo or antibiotics, urinary tract obstructions-Alkylating Agents: Carboplatin, Cisplatin, Cyclophosphamide, Ifosfamide, Melphalan-Antimetabolics: Azacitidint, Methotrexate, Cytotoxic antibiotics (Mitomycin C), Vinca Alkaloids (Vincristine)

Renal Failure Classification

-Prerenal: depends on fluid volume status, what is coming into the kidneys, dehydration, sepsis, and NSAID use-Intrarenal: How well the kidneys managing the fluid that's coming in, electrolyte imbalances, infection, nephrotoxicity, pre-existing renal damage, genetic damage, chronic UTI/damage, tumor lysis syndrome-Postrenal: how well the fluids that came/come in are being managed, and how well it is being excreted, bladder outlet obstructions, urethral obstructions.-Nursing Care: determine FVD, FVE, keep fluids going in and out, I&Os, assess for urinary retention, daily weights, vitals, assess for oliguria, polyuria, nocturia, hematuria, flank pain, monitor CMP.

Enterotoxicity

-Very common, can occur with chemo treatment-CINV: chemo induced nausea and vomiting-Female>Male-Young>Old-Mucositis: inflammation of mucous lining in the GI tract-Nursing: start assessment in the mouth, IV hydration, monitor electrolytes, manage N/V, anti-diarrheal meds, oral hygiene-Oral yeast infections, cryptococcus, candida. Mucous membranes in the GI tract start in the mouth-Resistance to "azole" drugs is growing in presence of these infections

Chemo Brian

-Related to the effects of chemo.-Short-term, will resolve-S/S: decreased ability to multitask, minor forgetfulness, decrease in concentration, memory issues-Treatment: antioxidants, cognitive behavioral therapy, erythropoietin for decreased blood cell count, methylphenidate

Alzheimer's Medications

-Cholinesterase Inhibitors : slow the progression of AD (Aricept, Exelon), NMDA receptor agonists (Namenda), SSRIs (zoloft, celexa, prozac), Tricyclic Antidepressants (Nortriptyline, Amitriptyline), Antipsychotics (Haldol), Benzodiazepines

Normal Physiologic Adaptations to Pregnancy

-Blood volume increases 40-50%-Physiologic (dilutional) anemiaPulse Increases (about 10%)-Increased cardiac output-Increase glomerular filtration rate-Decreased peripheral vascular resistance-Slightly decreased or unchanged blood pressure-Physiologic edema-Increased clotting factors

Preeclampsia

-Development of hypertension and at least one major organ system involvement in normotensive patient after 20 weeks (very rare type may develop in first postpartum days)-BP of ≥ 140/90 (2 readings, 4-6 hours apart)-Proteinuria of > 3 gms on a 24 hour specimen-Thrombocytopenia-Impaired liver function studies-Impaired Renal function (creatinine above 1.1)-Pulmonary EdemaCerebral or visual disturbances-Develops in about 8% of normal pregnancies-Develops in 25% of women with chronic hypertension or renal disease-Chronic hypertension with superimposed preeclampsia

Preeclampsia Risk Factors

-Age- < 19; >40-Parity- primigravida-African Descent-Multiple pregnancy-Preeclampsia in a previous pregnancy-Obesity-Renal disease-Pre Gestational Hypertension-Diabetes - pre gestational or gestational

Preeclampsia Pathophysiology

-Cause is unknown-Vasospasm is responsible for complications-BP rises - normally falls slightly in 2nd trimester-GFR decreases -proteinuria, oliguria-Plasma volume decreases as albumin levels fall & fluid moves from intravascular compartment to tissues (edema)-Liver function may be altered - epigastric pain & elevated liver function tests-Poor tissue perfusion of many organs-Endothelial cell dysfunction-CNS Irritation - Headaches, visual disturbances, & hyperreflexia-Uteroplacental insufficiency-IUGR & Placental Abruption may occur

Manifestations of Preeclampsia

-Pathology related to vasospasm & endothelial cell irritation (cerebral & visual symptoms)-Diminished blood flow to kidneys, liver, brain-BP of ≥ 140/90-At least 20 weeks gestation-Elevated liver enzymes, creatinine-Thrombocytopenia-Proteinuria X 2 (at least +1); do 24 hr. urine (not necessary for diagnosis)-Edema/ Weight gain - Significant weight gain in short time period (example - 5lb /2.5 KG in one week, but look at pattern of weight gain)-Dependent edema is normal-Assess for edema of hands, face, and abdomen after 12 hours of rest-Assess for pulmonary edema

Manifestations of Severe Preeclampsia

Must be present to meet criteria:-BP of ≥ 160/110Some of these will be present:-Massive Proteinuria (5 grams or more)-Persistent Headache-Epigastric pain-Hyperreflexia of ≥ +2 or + 3-Visual disturbances-Irritability-Generalized edema-Pulmonary Edema-Thrombocytopenia-Elevated liver enzymes, BUN, and Creatinine-Increased H & H-Decreased urine output

Management of Preeclampsia

-Early identification of high risk women -careful monitoring at all prenatal visits-No proven prevention strategies; low dose aspirin may help in women with preeclampsia history-Home care unless progressing to severe preeclampsia-Daily weight, BP, and urine testing (24 hr. collection at regular intervals)-Activity restrictions -rest with positioning on L side as much as possible-Regular diet - no added salt, adequate protein-Daily Fetal Kick Counts-Use of antihypertensives is controversial; diuretics are not used-Fetal monitoring - NST, BPP, & ultrasounds-Frequent monitoring of lab work (Platelets, liver function tests, BUN, creatinine, CBC)-Deliver at 37-40 wks if stable, sooner if worsening-Monitor BP during PP period, may need meds for several days or weeks

Management of Severe Preeclampsia

-Hospitalization - rest in quiet environment, monitor, prevent complications, & stabilize for delivery if at least 34 weeks-Assess for worsening:Edema, especially facial-DTR's /CNS symptoms - Headache, visual disturbances-Liver function tests & platelet counts-Strict I&O; measurement of urine protein & function-Fetal monitoring - Look for decelerations & decreased variability. (BPP & NST)-Steroids for lung maturity if ≤ 34 wks-Hydralazine, Labetalol, or Nifedipine-keep BP less than 160/110 to minimize risk of stroke (not agreed on by all providers)-Magnesium sulfateInduction of labor or C Section when safe-Benefits of delivery usually outweigh risks after 34 wks

Maternal Complications of Preeclampsia

-Severe Preeclampsia-HELLP Syndrome-Eclampsia-DIC-Abruptio Placenta-Renal Failure-Hepatic Failure-Cerebral Hemorrhage/Stroke

Fetal Complications of Preeclampsia

-PREMATURITY / DEATH-Both can be related to planned delivery before 37 weeks as treatment for maternal hypertensive disorders-IUGR (intrauterine growth restriction-Hypoxia

Magnesium Sulfate

-Used to prevent seizures (eclampsia) by ↓ CNS irritability-Smooth muscle relaxation may result in slight lowering of BP-Increases uterine perfusion; Decreases contractions-Initial loading dose 4-6 gms over 30 min.-Continuous infusion of 1-3 gms./ hour-Assess renal function prior to and during infusion-Foley catheter with strict I & O-May cause significant decrease or loss of reflexes, sedation, & inadequate respirations-Blood levels must be monitored

HELLP Syndrome

-Hepatic Dysfunction characterized byHemolysis (H); Elevated Liver Enzymes(EL);Low Platelets (LP)-Variant of severe preeclampsia, but some women progress from mild to HELLP without symptoms of severe preeclampsia-Laboratory, not clinical diagnosis-Occurs in only 1/500-1000 pregnancies-Platelet count < 100,000, elevated AST & ALT, and hemolysis-Usually have preeclampsia; may be worsening-Epigastric pain /Malaise-Bruising, petechiae, bleeding from IV site-All women with pre-eclampsia should be assessed regularly for HELLP-Increases risk for adverse perinatal outcomes-Evidence of HELLP is used to determine need to begin delivery even if preterm-Arteriolar vasospasm, endothelial damage, & platelet aggregation-May lead to liver, kidney and placental damage

Eclampsia

-Seizure activity (tonic/clonic) in a woman with preeclampsia (usually severe)-Usually preceded by headache, blurred vision, & epigastric pain-Apnea during the seizure results in hypoxic injuries for mother and fetus-Seizure care:-Maintain airway - side lying position; aspiration is a leading cause of maternal mortality-Prevent injury-IV Valium (use of this drug is controversial)-Suction and Oxygen when seizure activity is over-Initiate or maintain Magnesium infusion-Evaluate mental status-Prepare for delivery when stabilized

DIC

-Abnormal overstimulation of the clotting process secondary to disease and stimulated by release of large amounts of tissue thromboplastin:-Abruptio Placenta-Severe preeclampsia-Sepsis ( stillbirth)-Consumes large amounts of clotting factors (Platelets, Fibrinogen, Prothrombin)-Results in External bleeding, Internal bleeding, Occlusion of small vessels by fibrin clots-Laboratory Findings and Assessment:-Spontaneous bleeding from gums, nose, IV sites, incisions, Foley, injection sites-Petechiae (around blood pressure cuff)-V.S. consistent with ↓ fluid volume-↓ levels of platelets & other factors used for coagulation (fibrinogen, factor V, factor VII)-fibrin split products-Hemolysis-Prolonged clotting times - PT & APTT-Treatment:-Correction of underlying pathology-Careful monitoring of lab values & assessment of blood loss / fluid volume (Monitor urine output)-Administer fluids to replace volume-Blood components to replace clotting factors-Oxygenation-Emotional/Family support /Grief counseling

Abruptio Placentae

-Premature separation of placenta-Partial / complete-1% of all pregnancies-15% of all perinatal deaths-RISK FACTORS:Maternal Hypertension, Cocaine, Smoking, Abdominal Trauma, Multiple Gestation-Manifestations:Abdominal pain, Vaginal bleeding, Hypovolemic symptoms-Treatment:Maintain oxygenation & fluid volume, Fetal Monitoring, Ultrasound may determine degree of abruption; hematology and coagulation studies may be abnormal, Delivery unless abruption is small & stable-Neonatal OutcomeDepends on gestational age, degree of abruption, & speed of delivery-Perinatal loss support if needed-Mortality is 10 - 20%-Maternal OutcomeDepends on degree of blood loss and speed of replacement-Renal failure may result-1% mortality rate - Significant cause of maternal death

Prolapsed Umbilical Chord

-Umbilical cord lies below presenting part-Most commonly seen after AROM-Cord may be longer than normal (30- 90 cm.)-Very small / Very large fetus-Occurs when cord is lower than presenting part-Prevention- No AROM until head engaged-Nursing responsibilities during/after any ROM include fetal monitoring and observation of color & character of fluid.-Prompt recognition - Fetal Monitoring-Cord may be prolapsing from vagina-Trendelenburg or Knee Chest position-Keep pressure off cord with sterile gloved hand until delivery-Oxygen and Fluids-Keep cord moist with saline if protruding-Stat C-Section unless close to fully dilated

Precipitous Labor

-Precipitous labor is less than 3 hrs-Woman may be very anxious about not being in a hospital-DO NOT PANIC-Do not try to stop the delivery-Lateral position may be best-Vaginal/perineal trauma from rapid descent & expulsion of fetus-Gloves, clean material under buttocks-Support head to prevent trauma-Check for nuchal cord-Gentle downward pressure to deliver shoulders-Body will be slippery-Clear airway-Dry baby & keep warm-Keep baby at level of uterus-Allow placenta to deliver on its own-Clamp & cut cord if sterile items available; wrap baby & placenta together if not-Allow baby to nurse; increased risk for hemorrhage

Cardinal Movements: Mechanisms of Labor

-Engagement-Decent & Flexion-Internal Rotation-Extension-External Rotation or Restitution-Expulsion

Triage System

-Nursing assessments to differentiate between emergent care and urgent care-Over triage wastes resources-Lack of triage, patient's do not receive care

Emergent Care

threats to airway, circulation, and breathing

Urgent Care

Needs attention, but it is not life threatening

Primary Survey

1-Airway): airway blockage or C-spine injury2-Breathing): pneumothorax, bronchospasm, PE3-Circulation): Shock4-Disability): Seizure, Hypoglycemia, Meningitis, Intracranial hemorrhage, Infarction, Intoxication5-Exposure): hypo/hypernatremia, critical skin conditions

Primary Survey Questions

-SAMPLE: s/s, allergies, PMH, last oral intake, events and mechanism of injury

Secondary Survey

-completed one stable-vitals, history, head to toe assessment, inspect the posterior surface

Sudden Death

-verify with family organ donation status-Call Gift of Life for further info regarding measures-Post-Mortem Care

Good Samaritan Law

-Protects nurses in public if attempting lifesaving measures without proper equipment

Legal Aspects

-All hospitals have a duty to treat regardless of insurance status

Advanced Directives

-living will/ code status-Durable Power of Attorney (medical and financial)

Search and Seizure

-May search for ID and medications-If weapons are found or illegal drugs, place in locked area and call police or security

Calling a Code

-Check ABCs, if responsive-Call for help, a code-Start compressions-When help arrives, ask them to get more help and crash cart-When they return, have them switch to compressions, you must start the ambu-bag-Next person, attaches the defibrillator if no pulse is found

Post Code Evaluation

-How did it run-Where there any issues-Is follow-up review needed-Does staff need counselling-Were other patient's cared for

Heart Conduction

1. Sinoatrial node 2. Atrioventricular node 3. Atrioventricular bundle of HIS 4. Right and left bundle branches 5. Purkinje fibers

Ventricular Tachycardia (V-tach)

-QRS Complex: distorted-Ectopic foci fires consistently-Rate: 110-250 BPM-Symptoms: dizziness, fatigue, fainting, chest pain, SOB, hypotension, decreased CO-Causes: cardiomyopathy, structural changes, ischemia, heart failure, myocarditis, electrolyte imbalances (MG or K), acid-base imbalances-Pulseless Treatment: compressions, Defib (120-200 joules), epi 1mg every 3-5 mins, amio 300mg, then 10 min later 150mg dose, then ween with amio or lido drip-Treatment with pulse: attach defib to evaluate rhythm, 150 mg amio over 10 minutes, followed by a drip, synchronized cardioversion if meds fail

Torsade's de Pointe

Caused from a Mg deficiency-give mag sulfate 2g

Ventricular Fibrillation (V-fib)

-Multiple firing from ectopic foci in the ventricle (quivering ventricle)-No Pulse, therefore no CO-Causes: MI, ischemia, CAD, post-cath, TPA-Treatment: (same as pulseless v-tach) compressions, Defib (120-200 joules), epi 1mg every 3-5 mins, amio 300mg, then 10 min later 150mg dose, then ween with amio or lido drip

Supraventricular Tachycardia (SVT)

-electrical signals re-entering the atria from the ventricles-Looks like a QRS followed by a T-wave, no distinguishable P-wave-Causes: genetics, stimulants, heart failure, heart disease, pregnancy, thyroid disease, medications (asthma and cold)-Symptoms: tachy, palpitations, chest pain, SOB, fatigue, dizziness, sweating, syncope-Treatment: -Adenosine: start with 6mg then 12mg, then another 12mg if no improvement give an IV bolus (avoid use in respiratory pts)-Verapamil-If unstable synchronized cardioversion-Non-invasive: Valsalva maneuver, carotid sinus massage-Long-term Management:-Beta-blockers, Ca channel blockers, amiodarone-Radiofrequency ablation

Asystole/ PEA

-Ventricular standstill-Poor prognosis-Causes: advanced cardiac disease, end-stage cardiac failure-Treatment: CPR, attach defibrillator and check rhythm in different leads (if different treat for PEA)-NO DEFIBRILLATION

PEA Treatment

-Treat what may apply to the patient.5 H's-Hypoxia: 15L of O2-Hypovolemia: fluids-Hydrogen Ions (acidosis): bicarb-Hyper/hypokalemia or glycemia: potassium, calcium, sugar, insulin-Hemorrhage: fluids and blood products5 T's-Tension Pneumothorax: chest tube-Tamponade: pericardiocentesis-Thrombosis (MI): cardiac cath, antiplatelets-Toxins-Thrombosis (PE): heparin, thrombolytics

Transcutaneous Pacing

-At apex and L-scapula area for pads-Rate: 60-80-MA: 70-100 (energy needed to capture)-Sedate if BP is stable-noninvasive-Painful

Pediatric Physiologic Differences

-Smaller airway, therefore easier for obstruction-Nose Breath first 6 months, clean nose-Higher Metabolic Rate, therefore higher O2 demand-Proportionally larger head-Smaller blood volume-Greater Body Surface Area, hypothermia-Flexible bones, less protection of thoracic cavity

Assessing a Child

-LOC-ABC-D: (neuro check) AVPU Scale-Alert, responds to verbal stimuli, to painful stimuli, or unresponsive-E: expose the child to examine other injuries

Pediatric Circulation Compromise

-Keep the child warm-Bleeding: elevate above the heart, apply direct pressure, leave impaled object in place-Compensate: 25% of total blood volume before the BP is affected, give fluids and blood products

Near Drowning

-Call 911-Open Airway, assume spinal cord injury-Rescue breathing-CPR (15 compressions, two breaths, one hand)-Cut off wet clothes-100% survival rate if at hospital awake

Anaphylaxis

-Causes: insect stings, drugs, nuts, latex-S/S: itchy eyes, lip swelling, wheezing, dyspnea, laryngeal edema, stridor, hypotensive shock, respiratory arrest-Treatment: Epi 1:1000 0.3 mg-Emergency trach if airway is closed

Toxic Ingestion

-Toxins: meds, pesticides, kerosene, alcohol, antifreeze, cleaning agents, daffodils, lily of the valley, English ivy-Rx: activated charcoal or mag citrate

Fractures

-Assess: ABCs, cervical precautions, quality of pulse distal to fracture, cap refill, control of movement/sensation-Interventions: teach about prevention, fluid volume replacement, splint above and below the injury, remove jewelry/clothing

Burns

-Edema: obstructed airway-Hypovolemic shock-S/S of Smoke Inhalation: lethargic, confusion, metabolic acidosis, tachy, seizures, coma-Carbon Monoxide Poisoning: skin is cherry red, treatment is 100% O2

Hypothermia

-S/S: dilated pupils, rigid muscles, bradycardia, amnesia, slurred speech, cold skin-Interventions: warm blankets, remove wet clothing, call 911-Passive Warming in ER: blankets, booties, head cover, warm IV, gastric lavage

Hyperthermia

-S/S: change in LOC, rapid pulse, skin warm and dry, thirsty, faint, muscle cramps-Call 911, open cloths, cool towels to head, groin, and axilla-Monitor: IV (isotonic), O2, SpO2, Cardiac Monitor,

Delerium

-Triggered by underlying conditions-S/S: decrease in cognition, disoriented, decreased attention, poor judgments, restless, altered perception, memory loss-Assessments: Hx from relative, recent stressors/illness, medications-Interventions: keep calm and safe, keep quite, avoid bright lights, temperature extremes, startling movements, sounds

Functions of Skin

-barrier-vitamin D synthesis-cutaneous absorption-sensory functions-thermoregulation-psychological and social functions

Burns: Determining Severity

-Depth of Tissue Damage-% of Body Surface Area to determine amount of fluid to give them-Areas of increased risk for infection-Other Trauma-Age-Type of Burn: chemical, inhalation, electrical

First Degree Burns

-Epidermal layer damaged-Characteristics: dry, no blisters, minimal to no edema, erythematous, painful, rapid heart loss, heals within 2-5 days without scarring-Emergent if it involves high risk areas or covers 99% of the body

Second Degree Burns

-Partial thickness skin loss-Epidermis destroyed and dermis is injured-Characteristics: blisters, weeping, good cap refill, painful, rapid heat loss, heals within 5-21 days with no grafting, white, cherry red, or mottled-If infection, can turn into a full thickness wound

Third Degree Burns

-Full thickness-Complete destruction of epidermis, dermis, involves subcutaneous tissue-Characteristics: Dull, red, leathery, eschar, mixed white, waxy or pearly, soot stained (electrical or inhalation burn), less heat loss due to dryness, may include the facia, muscle and bone-Large areas need to be grafted takes months to heal-Smaller areas will heal form the outside, inward and will take weeks-Pain, less sensation, nerve endings burnt

Calculating a Burn

-Lund and Browder scale

Parkland Formula

Volume LR = 4mL x BSA% x kg-1st 50% of total fluid volume in the first 8 hours-2nd 50% of total fluid volume in the following 16 hours-Lactated Ringers: an isotonic solution that will help expand the intravascular compartment

Thermal Burns

-Involves scalding, flame, heat contact or steam-contact burns-Immersion scald

Electrical Burns

-Entrance and Exit wounds-Severity of tissue damage-Current follows the path of least resistance: blood vessels, muscle, skin, tendons, bone-Types: electrocuted, arch, electrical flame-Burn damage is worse under the skin

Burn Scene Care

-Determine power source, turn it off-Assess for cardiac/respiratory arrest (usually vtach or vfib), LOC, entrance and exit wounds, keep warm-Immediate complications: cardiac/respiratory arrest, fractures from falls or tetanic contractures, extensive muscle damage, look at urine output (myoglobin in the urine, thick dark, must flush to prevent AKI-Long-term Complications: neurologic impairment, demyelination of nerves thus possible amputation, cataracts, impotence (no sexual activity)

Chemical Burns

-strength of the chemical, quantity of the chemical, manor/duration, mechanisms of the chemical-Acids: causes coagulation necrosis, cell damage in heart, kidneys, and spleen-Skin is dry-household cleaning products products-Alkalis: liquid vacation necrosis leads to tissues transferred into gelatins-Moist, slippery, grey-Common cause: drain/oven cleaners, cement, fertilizer-Organic Compounds: coagulation necrosis-Common cause: phenol, chemical disinfectants, petroleum-Immediate Complications: standard precautions, remove clothing, powder chemical must be brushed off, eye burns must be flushed, look for hidden burns

Inhalation Burns

-3 Types: carbon monoxide poisoning, injury above the glottis (possible trach), injury below the glottis (trach)-15-40% O2 neuro damage-40-50% abundant-60-70% fatal-200x more attracted to Hgb than O2-Treatment 100% O2 emergency trach

Burn Questions

-Where did the injury occur-What was burning-Were noxious chemicals involved-Did they lose consciousness

Burn Assessments

-Hypoxia: agitation, anxiety, cyanosis, stupor-Breath sounds, accessory muscle use, dyspnea, tachycardia, voice, brassy, cough, grunting, swallowing, sputum, singed nasal hair, erythema and edema of oral/nasopharynx, vital signs

Burn Treatments

-Maintain Airway-Possible intubation-100% O2-ABG-Suctioning-Prone if on ventilator-Stop burn/ cool burn-Primary ABC Assessment-Assess neuro status-Exposure-Compartment syndrome (third spacing)-Vitamin C resuscitation to reduce edema-A-line blood pressure-Can start IV line at burn site-Check all pulses-LR based on body surface area-Time when burn started

Preload

the amount of blood coming in to the heart-restore by volume, give fluids and blood products

Burn Shock

a form of nonhemorrhagic hypovolemic shock resulting from a burn injury-Capillary permeability, loss of plasma-Protein and electrolytes, high potassium-Edema, fluid shifts, worse in the first 24 hours-Intravascular volume, hypovolemic-Fluid released, pulled into interstitial space, causes dehydration-Vascular Space, third spacing-Hemolysis of RBC

Consensus Formula

-Used to determine how much volume to give back in the first 24 hours-Adult: volume LR = 2mL x % of burn x Kg-Child: volume LR = 3mL x % of burn x Kg-Monitoring Fluid Resuscitation (Hourly I&O)-Adults: 0.5 mL/Kg/hr or 30-50 mL/hr-Child <30kg: 1 mL/Kg/hr-Child >30kg: expect 30-50 mL/hr

Circumferential Burns

-Lead to compartment syndrome if around extremities or chest-Compartment syndrome = EMERGENCY-Escharotomy must be preformed

Fasciotomy

-Can be done at the bedside in emergency situations-Surgical incision down to the muscle, releases pressure and fluid comes out of tissue-Color, pulses, and sensation should come back to extremity immediately-Used for electrical burns, and deep burns-Dressing changes Q8hrs-Maintain sterility

Burns: Nutrition

-High carb and high protein-Supplement protein-20% burn or more increase the PO intake + tube feed-Vitamins and antioxidants

Burns: Complications

-Muscle wasting, constipation from pain meds, need a lot of rest, electrolyte imbalances (Mg, K, Phosphorus), maintain strict glucose control (80-110mg/dL), risk for stress ulcers, monitor VS

Temporary Wound Coverage

-Can graft with minimal to no infection-Xenograft: animal-Allograft: human-Bio-synthetic: nylon fabric with silicon film + collagen

Permanent Wound Closure

-Skin grafting: do not itch, 30-50SPF forever-dermal replacement: layers of collagen and silicon-Autogleus: regenerating cells for grafting, expensive, extra fragile-Monitor donor sites

Burn Center Referral Criteria

1. Partial thickness burns greater than 10% TBSA2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints3. Third degree burns in any age group4. Electrical burns, including lightning injury5. Chemical Burns6. Inhalation injury7. Burn injury in patients with pre-existing conditions8. Any patient with burns and concomitant trauma9. Burned children in hospital without qualified personal10.Burn injury in patients who will require long-term rehabilitative intervention

Oxygenation Lab Ranges

CO: 4-8CVP: 2-12PCWP: 8-15pH: 7.35-7.45CO2: 45-35HCO3: 22-26

Types of Artificial Airways

OropharyngealNasopharyngealOral endotrachealNasal endotrachealTracheostomy

Why intubate?

-Neuromuscular Diseases: Guillain-Barre, Multiple Sclerosis, Myasthenia Gravis, ALS-Pneumonia-Anesthesia-Hypoxia-Airway Obstructions: Neck trauma, inhalation burns, malignancy, anaphylaxis

Why trach?

-ET tube exceeds 2 weeks (excluding Covid patients)-Easier to ween patient off-Comfort-Management of secretions-Long-term ventilation-Does the patient understand what this means and do they want it?

Equipment needed for Endotracheal tubes

ET tube (sizes: 7, 7.5, 8)StyletLubricationSedation10cc syringeLaryngoscopeRestraintstape/stabilization productSuctionO2

Insertion of ET Tube

-Explain procedure-Sedation, if hemodynamically stable-Document-In PA, nurses are unable to intubate, unless a nurse anesthetist-Nurses are responsible for the tube after it had been placed-Every 1-2 hours-Long-term every 4 hours-Check placement of tube with a chest xray-Pt lay flat, no pillow, restrain (with new orders every 24 hours)-Hyperextend the neck, pull jaw forward and up-Push tube down-Listen for equal breath sounds-Tape in place-Continuous SpO2-Orders for sedation and pain management: Pentanol, Propofol (liver function test, triglycerides), Ketamine-Nursing Assessment for ET Tube: Neurologic, Respiratory, Lung sounds, secretions, distress, Anxiety, Skin Integrity, Mouth care every 4 hours to prevent Ventilator Acquired Pneumonia (VAPs), Gas Exchange, Monitor ABGs

Management of Artificial Airways

Maintain the correct placement of the tube-CXR: document the position of the tube-Auscultate for bilateral breath soundsMaintain proper cuff inflation (taunt)-Minimal leak technique (add 1cc of air at a time)Maintain and monitor ventilation and oxygenation-ABGs, SpO2, Clinical conditionMaintain tube patency-Suctioning, 3x down, 10 seconds per insertion-Mouth care and endotracheal repositioningFoster comfort and communication by talking with the patient

Extubation

Need a 10cc syringe, suction, and substitute high flow O2Need and order, respiratory will be involvedPt must be maintained at a 90 degree angleMonitor the patient carefullyExtubation failure: age, secretions, diseases, obesity, aspiration

Tracheostomy Tubes

Advantages:-More comfortable, pt can talk, can eat and swallow (must deflate the balloon), can ween fasterComplications:-Hemorrhage, pneumothorax, laryngeal nerve damage, subcutaneous emphysema, trach comes out, infection from poor suctioning, tracheal collapse, stoma does not closePts at Risk for Complications:-Smokers, diabetes, alcoholics, immunocompromised, COPD, steroid use, newborns and infants

Trach Equipment

Trach tube with inner cannula and cuffTrach tiesObturator-Use to plug stoma if the trach comes out-Must document its location each shiftSuctionOxygenSedationRestraintsDressings

Tracheostomy Procedure

Procedure in OR-Only at bedside in absolute emergency-Incision between the 2nd and 3rd tracheal rings, insert trach tube-Sutured and stays in for 5 daysTrach: Post-Op Assessments-Check behind neck for gravity-dependent drainage, Maintain an obturator and trach tube at bedside, Neurologic, Respiratory, Lung sounds, secretions, distress, Anxiety, Skin Integrity, Mouth care every 4 hours to prevent Ventilator Acquired Pneumonia (VAPs), Gas Exchange, Monitor ABGs, Check ties to ensure 1 finger fits under on each sideRemoving a Tracheostomy-Need an order to decannulate-Can clear own secretions, can breath, can eat/swallow-Usually wait one week to ensure no repercussions

Mechanical Ventilation

-Provides 100% oxygen and controls breathing-Maintains normal CO2 if unable to maintain: MS or thoracic trauma-Indications for Mechanical Ventilation-PaCO2 greater than 55 mmHg-PaCO2 less than 50 mmHg with FIO2 greater than 60%OR...-PaO2 greater than 50 mmHg with pH less than 7.25-Tidal Volume 5mL/kg-Respiratory Rate greater than 35 breaths per minute

Positive Pressure Ventilators

Primary method used in acutely ill patientsDuring inspiration the ventilator pushes air into the lungs under positive pressureVolume cycled ventilators are the most common typePreset pressure and Preset volumeInspired O2 concentration remains consistent

Settings on a Ventillator

-Rate: amount of breaths given in one minute-Tidal Volume (TV): volume of gas given in one minute-Fraction Inspired Oxygen (FIO2): 21%-100%, must keep pt O2 level above 90%-Positive End Expiratory Pressure (PEEP): allows the alveoli to stay open and inflated, thus allowing for better gas exchange.-Start at 5cm and shouldn't go higher than 15cm-The higher the PEEP the more risk for pneumothorax and decreased CO-Airway Pressure Limits: high and low-High pressure: Pt bites the ET tube, coughing, or with suctioning-Low pressure: vent tube may be disconnected from the pt or vent-Continuous Positive Airway Pressure (CPAP)Constant flow of pressure-Used for sleep apnea or spontaneous breathing trials-Pressure Support (PS)

Modes of Mechanical Ventilation

-Selected based on the patient's ventilatory status, respiratory drive, and ABGs-Three basic modes:CMV: Controlled Mechanical VentilationACV: Assist Control VentilationSIMV: Synchronized Intermittent Mandatory Ventilation

Controlled Mechanical Ventilation

-Breaths are delivered regularly and independent of the patient's ventilatory effort-Used when the patient has no drive to breath (anesthetized patient)-Used when the patient is unable to breath spontaneously (paralyzed patient)-Patient cannot breath on their own

Assist Control Mechanical Ventilation

-Delivery of breath is triggered by inspiratory effort of the patient after preselected time interval has elapsed-If the patient fails to breath, the ventilator cycles in-Patients can initiate their own breathing-Used when patients are spontaneously breathing, but have ventilator failure or gas exchange insufficiency-Respiratory failure, COPD, pulmonary edema, CNS dysfunction-Patient can ventilate faster, but not slower than the present rate-The patient gets a number of set breaths, but can also take their own additional breaths

Synchronized Intermittent Mechanical Ventilation

-Patient breathe spontaneously at own TV and Rate-Ventilator delivers a preset tidal volume at a preset frequency-Between ventilator delivered breaths, the patient is able to breathe spontaneously through the ventilator circuit-Preset inspired oxygen concentration with each spontaneous breath-Used when weaning pt from ventilator

Weaning from Ventilator

-Reduce the FIO2 to 30-40%-Decrease or Eliminate PEEP-IMV: allows for gradual conditioning of the diaphragm weakened by disuse-RSBI: is a tool that is used in the weaning of mechanical ventilation in the ICU.-The ratio of respiratory frequency to tidal volumef/vt

Criteria for a Successful Ween

-Respiratory Rate is less than 35 breaths per minute-Good tolerance to spontaneous breathing trials-HR less than 140 bpm or heart rate variability of greater than 20%-Arterial O2 saturation greater than 90% or PaCO2 greater than 60 mmHg on FIO2 less than 0.4-Systolic BP greater than 80mmHg and less than 180mmHg or a less than 20% change from baseline-No signs of increased work of breathing or distress

Rapid Shallow Breathing Index (RSBI)

RSBI = Respiratory rate (f) / Tidal Volume (vt)-RSBI less than 105, successful ween predicted-RSBI greater than 105, failure to wean predicted-Terminal Weaning: need and order and DNR/DNI activated

Suctioning

-Need an order-For secretions-Intermittent-In-line suction is continuous-Assess for: Increased anxiety, Deceased SpO2, Circumoral cyanosis, Abnormal lung sounds, Prolonged Cap Refill, Explain procedure, Conscious with a functional gag, Semi-fowlers, Look into nares for any trauma, Lateral position if unconscious-Post-SuctionRe-assess the respiratory systemEnsure pt is breathing, normal color, no bradycardia

Acute Respiratory Failure

-PaO2 less than or equal to 60mmHg-PaCO2 greater than 45 mmHg-Arterial pH less than 7.35

Type I Respiratory Failure: Hypoxemia

-Affects every organ and tissue-Results from abnormal oxygen transport-Causes of Hypoxemia-Pulmonary edema-Pneumonia-Pleural effusions-Atelectasis-Alveolar hemorrhage-Pulmonary infarction-Asthma/ chronic lung disease

Type II Respiratory Failure: Hypercapnia

-Inadequate alveolar ventilation-Marked elevation of CO2-Due to decreased ventilatory drive, respiratory muscle fatigue or failure and increased work of breathing-Causes of hypercapnia: medications/drugs, brain-stem lesions, hypo/hyperthyroidism, Obesity, sleep apnea

Combined Hypoxic and Hypercapnic Respiratory Failure

Combination of inadequate alveolar ventilation and abnormal gas transport

Respiratory Distress Assessment

DyspneaRestlessnessConfusionAnxietyDeliriumTachypneaTachycardiaHypertensionTremorCardiac dysrhythmiasPeripheral cyanosisAccessory muscle useDiaphragmatic weakness and fatigue

Diagnostics/ Management of Early Respiratory Distress

ABG analysisChest X-rayPulmonary Function, if not on a ventilatorManagement:Controlled O2 therapyConsider reason they came inConsider ventilationSpO2 greater than 90% with O2 therapy

Acute Respiratory Distress Syndrome (ARDS)

-It is a sudden and progressive form of respiratory failure.-Alveoli become too damaged, increased -permeability of fluid-Alveoli fill with fluid and this decreases O2 availability-Increased infiltrates, decreased lung capacity, therefore hypoxia-50% mortality rate-Gram Negative Sepsis and ARDS is a 75% mortality rate

Predisposing Factors to ARDS

Direct Injury-1) aspiration-2) viral/bacterial pneumonia-Chest trauma-Fat, air, or amniotic fluid emboli-Toxic inhalation-Near Drowning-O2 Toxicity-Radiation PneumonitisIndirect Injury-1) sepsis-2) severe massive trauma-Acute pancreatitis-Anaphylaxis-DIC-Severe head trauma-Shock state-Cardiopulmonary bypass-Multiple blood transfusions-Narcotic OD: Heroin-Non-pulmonary systemic disease

Pathophysiologic Phases of ARDS

1: Injury (Exudate)-Occurs 1-7 days after host invasion or injury-Permeability and engorgement occurs-Fluid shifts from interstitial to alveolar epithelium-Blood passing through cannot be oxygenated-Alveoli Cell type I and II produce surfactant, these are damaged due to ARDS-Dysfunctional surfactant therefore the alveoli become weak from fluid buildup and they collapse2: Reparative Phase (Proliferative)-Occurs 1-2 weeks after the injury-Influx of neutrophils, monocytes, fibroblasts, and lymphocytes due to inflammation-Lungs can easily regenerate-When there is dense fibrous tissue then this stage is complete, therefore can not further recover once the tissue becomes fibrotic3: Fibrotic-2-3 weeks after injury-chronic/late phase-Decreased lung compliance leads to permanent ventilation to survive-Poor gas exchange, hypoxic without ventilator

Clinical Manifestations of EARLY Respiratory Distress

Dyspnea, tachypnea, cough, and restlessnessFine rales scattered throughoutABG: respiratory alkalosis because of compensationCXR: clear chest x ray

Heart Failure vs ARDS

Heart failure: will see an enlarged heart on chest x rayARDS: will see a white out on chest x ray

Clinical Manifestations of LATE Respiratory Distress

Retractions, confused, tachypneic, diaphoretic, change in mentation, agitated, restless, pale, cyanotic, coarse rhonchi/ cracklesABG: respiratory acidosis b/c increased CO2 and decreased O2

Complications of ARDS

Cardiac arrhythmias from decreased CO from decreased O2 in the bloodMonitor electrolytes (K, Mg)V-tach and V-fibARDS put on PEEP, more pressure on heartOral IntubationAt risk for HAI (maintain sterility)Risk for aspiration w/ feedings or suctioningVolu-pressure trauma: tidal volume too high on ventStress ulcersRenal failureMonitor urine output (BUN and creatinine)Antibiotics are nephrotoxicMonitor ET tubeSeptic Shock from stressDIC: correct with heparinThrombocytopenia

Nursing Care of ARDS

Treat underlying causeCritical Care bundles: VS, heart pressures, pulses, heart sounds, chest x ray, lung sounds, equal chest expansion, color, ABG results, bowel sounds, urine outputSedation: propofol, ativan, chromiumOxygen: suctioning 80-100 mmHgHandwashingProningChecking placementTube feeding, are they tolerating it?Check blood sugarsABX, pressors, epi, anti-ulcerMAP: greater than 65

Labs to Evaluate with ARDS

CBCCMP: albumins and proteinsBNPPT/PTT/INRD-dimerFSPABGLactic AcidCXRCPK/troponinCulturesUrine: culture + drug screen

Proning

16% reduction in mortality with proningMoves the heart forward, lungs expand more, decreased O2 demandProne for 16 hours, supinate them for 8Complications:Facial edemaPressure injury woundsMepilex bony prominencesNeed 5 people, need respiratory therapistCan loose lines, if not carefulContracturesWound dehiscenceAutomatic and manual proningContraindicated with:Obesity 114kg or less114-150kg automatic

ARDS Pharmacology

Antibiotic therapy in known infectionsBronchodilatorsCorticosteroids (controversial)Surfactant replacementAntioxidants: nitric oxideRelaxes smooth muscles in lungs (titrate up and down)ECMO therapy: lung bypassSedationNeuromuscular blocking agentsFurosemide/ AlbuminNutrition

Cardiogenic Shock

Heart cannot maintain a normal CO because:1) Systolic Dysfunction: less than 90-Heart is unable to pump blood forward-Decreased cardiac index-CO is less than 2L/min2) Diastolic Dysfunction-Right or left ventricles do not fill properly during diastolate-One or the other (systolic or diastolic)-Secondary to MI (anterior MI), valve disease, cardiomyopathy, cardiac tamponade, brady or tachy-Early Signs and Symptoms: Cyanosis, pale, moist, decreased urine output, anxiousness, confusion, tachycardic, hypotension, crackles, SOB, increased pulmonary-capillary wedge pressure (PCWP), narrowing pulse pressure, increased SVR, increased heart workload, increase in myocardial O2 consumptionClinical Manifestations: Confusion, hypotension, what are the root causes?-Treatments:O2 therapyIV fluidsPositive inotropic drugs (dopamine), titrate upIncrease preload and afterloadMimics SNSTrendelenburg positioning

Compensatory Mechanisms for Shock

-Baroreceptors: sense decreased pressure, secrete epinephrine and norepinephrine to increase PVR, increase arterial pressures, therefore increases myocardial contractility-Fluid shifts:-Renin-Angiotensin: (BP and Fluid Balance) Renin form kidneys when BP decreases, converts angiotensin I into II, increase in Na+ reabsorption by the kidney tubules, therefore increasing the BP-ADH-Aldosterone: (BP, fluids, electrolytes, and SVR) Adrenal cortex releases aldosterone, causes the kidneys to increase Na+ and fluid retention, it releases ADH, which is vasopressin from the pituitary, which causes an increase in fluid retention in the kidneys, therefore increasing BP

Hypovolemic Shock

-"Cold shock"-Loss of intravascular fluid volume, 15%-20% volume deficit, can be compensated in adults-750 mL out of 5L of blood-2 types:-Absolute hypovolemia-Loss of arterial blood: Hemorrhage, GI loss, Fistula, diabetes insipidus, diuretics-Relative hypovolemia: Fluid moves from vascular to interstitial from increased capillary permeabilityDecreased volume, Decreased venous return to heart, therefore decreased preload and CO-Decreased perfusion, impaired because metabolic needs-Vascular space is the same, decrease in volume from fluid shifts-Fractures, burns, sepsis, bowel obstruction, ascites=Clinical manifestations: Increased HR, increased RR, increased CO, increased stroke volume, Decreased pulmonary-capillary wedge pressure-Greater than 30%, initiate blood transfusion and IV fluids-Assessments: Decreased preload, drop in BP, prolonged cap-refill, orthostatic BP, tachypneic, decreased urine output, pale, cool, clammy, confused, anxious, absent BS, arterial pressure low=Diagnostics: CBC, H/H, BUN, creatinine, increased urine specific gravity, increase in lactate, increase in glucose, Xray, CT-Treatment:Correct the cause, stop the bleedingAdminister blood products, fluids (NSS, LR), albumin, volume expanders, vasopressor, give back the volume, O2 at 15 L/minMonitor vitals, lab work

Anaphylactic Shock

-Life threatening vasoactive mediators, released and increases permeability-Third-spacing and fluid shifts-Signs/ Symptoms: Decreased BP, chest pain, wheezing, stridor, swelling of the lips and tongue, flushed skin, itching, anxiety, and impending sense of doom-Treatment:Intubate to keep airway openGive epi 1:1000, Benadryl, IV fluids, steroids

Septic Shock

-The body's response to an infection-Medical emergency due to the disruption of O2 and nutrients to tissues and organs-Client's at Risk: Very young, elderly, immunocompromised, trauma/burns, alcohol/drug use, invasive procedures, drug-resistant bacteriaTypes of Sepsis:-Sepsis (uncomplicated: flu-viral infection)Does not need to be in hospital-Complicated, need to be hospitalizedSeptic ShockNeeds hospitalization in ICUSystolic BP <90, MAP <65, 1 or more organs are involved-Septic Shock Assessment: Fever, rigor, chills, fatigue, malaise, n/v, increased WBCs, hyperventilation/ changes in breathing, respiratory alkalosis, anxiety/ confusion-Shock Assessment: Glasgow Coma Scale, acidosis, SBP <90, MAP <65, CVP >8, CVP >12-15 if vented with PEEP

Diagnostics for Sepsis

WBCsPlatelets (DIC)Lactate levels every 6 hrsPositive blood culturesChest x rayC-reactive protein

Sources of Sepsis

Lungs: pneumoniaAbdominal: gallbladder, peritonitis, bowel perforation, appendix ruptureKidney/bladder: foley, urosepsisSkin/Wounds: Iv sites, central linesBone marrow aspirate/ transplantCNS: meningitis, encephalitis

Treatment of Septic Shock

-Mechanical ventilation (VAPs Precautions), frequent mouth care-Treat in bundles1) Within the first 3hrs of severe sepsis-Lactate level-Cultures: aerobic/anaerobic x2-30mL/kg of crystalloid fluids: NSS, LR-3L in emergent situations-Antibiotics, broad spectrum2) Within 6hrs of initial s/s of septic shock-Placement of central line-CVP monitoring 8-12 mmHg-Maintain MAP greater than 65-To maintain:-1: norepinephrine-2: vasopressin 0.03 units/min-3: dopamine-4: dobutamine up to 20 mcg/kg/min-5: PRCB-Urine output should be greater than 0.5mL/kg/hr-Mixed venous o2 saturation 65% (less than 80% is good)-Vasopressors if not responsive to IV fluids-Continue to monitor lactate levels3) Mechanical ventilation-PEEP-Proning-Evaluate HOB: 30-45 degrees-sedation/ neuromuscular blockers-Weaning protocols-Mouth Care Q4hrs-Suctioning-Initiate ABCDE Bundle: Awakening, breathing, coordination, delirium, early mobilizationOther Guidelines include:-Glucose control: below 180-Continuous renal replacement therapy (CRRT)-DVT prophylaxis-Stress Ulcer prevention-Nutrition, tube feeds

Multiple Organ Dysfunction Syndrome: MODS

-Failure of more than one organ in an acutely ill patient where homeostasis cannot be maintained without interventionOrgan and tissue changes:-Renal: Ischemia, tissue necrosis, decreased blood perfusion, releases angiotensin I and II-CNS: Changes with LOC-Pulmonary: Ischemia, ARDS, hypoxia, acidosis, pulmonary edema-GI: Ischemia, loss of protective mucosa, increased ulcers and bleeding-Cardiac: Decreased preload, failure, decreased blood volume, vasodilation, decreased SVR-IV Clotting: DICPharmacology:-Adrenergic Drugs-Norepinephrine (levophed)-Epinephrine-Neo-synephrine (phenylephrine)-Vasopressin-Dobutamine (dobutrex): + inotrope, increases CO only-Cardiac Glycosides-Digitalis: + inotrope, increases CO and decreases HR

Stroke Volume

Preload: amount of blood coming into the heart-Filling pressures-Can be altered by not enough volume-Decreases with vasodilationAfterload: amount of force needed to get the fluid out of the heart

Spinal Cord Injury

-Damage to any part of the spinal cord or nerves that end at the spinal canal.-It may cause a lack of sensation, change in strength, and movement below the site of the injury-Complete: total loss of all motor and sensory activity below the site of the injury-Incomplete: some nerves are preserved and some sensory and motor function occurs below the level of the injury-Assess for secondary injury: hemorrhage, hypoxia, ischemia, edema-Multifaceted, complex care-Requires knowledge of acute assessments/ interventions as well as rehabilitation-Recovery is roughly 6mos-1yr

SCI Classification

Extent of the injury/ severityLevel of the injuryCervical, 7Thoracic, 12Lumbar, 5

Causes of SCI

Motor vehicle accident, falls, violence, sports, alcohol impairment, arthritis, cancer, infection, fluid accumulation/ inflammation around the chord

Risk factors for SCI

Male (16-30 y/o)65+ from fallingImpulsive behaviorsbone/joint disorders

Upper Motor Neuron Lesions

Essential for voluntary movementInvolves neurons in the cerebral cortex, thalamus, brain stem, and spinal cord tracts, modified by the basal ganglia and the cerebellumDysfunction causes:Spasticity and paralysis, loss of voluntary muscle control, hyper-reflexive (continuous incontinence)

Lower Motor Neuron Lesions

Essential for muscle contractionInvolves neurons in the brain stem, the cranial nerves, the anterior-horn cell of the spinal cordInjury causes:Flaccid paralysis, areflexia, hypoactivity in bowel and bladder, sexual dysfunction

Pathophysiology of SCI

-Resulting hypoxia reduced the oxygen tension below the level that meets the metabolic needs of the chord-Lactate = the metabolites-The lactate level builds up and causes acidosis and vasoactive substances are automatically released into the body (norepinephrine, serotonin, and dopamine), high levels of these hormones cause vasospasms, therefore causing increased hypoxia, eventually leading to necrosisOnce the injury has occurred...-The spinal cord has minimal ability to adapt to vasospasms-By 24hrs, permanent damage has occurred due to edema-Treatment starts at the time of the injuryMechanisms of SCI-Hyperflexion-Hyperextension-hyper-rotation/flexion

Spinal Shock

-State of transient psychologic reflex depression of chord function below the level of injury with associated loss of all sensorimotor functions-Temporary loss or depression of almost all of the spinal reflexes below the level of injury-Decrease in reflexes, decrease in sensation, flaccid30-60 minutes after injury, full-effect sets in after hours, lasts 4-6 weeks-Sympathetic nerves have lost normal connection to CNS-Spinal Shock has ended when...-Deep tendon reflexes, spasticity, and increase in muscle tone-Rehabilitation begins as soon as the pt is stabilized-Symptoms depend upon the level of the injury-Quadriplegia, occurs in the cervical spine-Paraplegia, occurs in the thoracic and lumbar regions

Neurogenic Shock

Hemodynamic changes due to the loss of the autonomic tone, due to the spinal cord injuryHypotensive, bradycardic, change in LOC

SCI Assessments

RespiratoryC-spine injury above C4 presents loss of respiratory functionPt requires mechanical ventilation foreverAt risk for pneumonia, atelectasis, and respiratory failureCardiovascularAbove T5 generally decreases the influence of SNS1: bradycardia2: vasodilationDecreased CO, venous pooling, minimal perfusionKeep MAP of 85+ for the first 7 days after the injuryUrinaryNeurogenic bladder, lower motor neuron injuryPt requires catheterizationGastrointestinalAbove T5 = hypomotilityPt at risk for paralytic ileus + bowel perforationPt needs an NG tube to decompressIntegumentaryAt risk for pressure ulcers, due to immobilityInability to sweat (thermoregulation), PoikilothermismMetabolicAcid-base imbalancesMonitor electrolytesPeripheral VascularAt risk for DVTs, PEs

Diagnostics for a SCI

Complete neurological exam every 4hrs for 7 daysABGsCMP/CBCUrine: drug screen, kidney functionRadiology studies: xray, CT, MRI

Medical Treatment for SCI

-Antispasmodicsbaclofen/ lioresaltizanidine/ zanaflexdantrolene/ dantrium: interferes with Ca release, need Ca supplementDiazepam/ valium: inhibits sensory pathway-Hypothermia: to decrease inflammation to the spinal chordCool pt then warm slowly-Cholinergics: for neurogenic bladder causing urinary retentionLower motor neuron injuryUrecholine-Urinary antispasmodic: delays voidingoxybutynin/ ditropan-Antihypertensives: after the first 7 dayshydralazine/ apresolineNifedipine/ Procardia: ca channel blocker-VasopressorsNorepinephrine

Surgical Treatment for SCI

-Indications: fracture is unstable, penetrating injury, cord compression, decreased mental status progression-Skeletal traction-Cervical tongs: screws into either side of head to stabilize c-spine-Halo traction: a vest that holds a halo traction around the head, best for a mobile patient (thoracic/lumbar)Types of procedures:-Osteoplasty: cement the vertebrae together, dries within 30 minutes-Spinal Fusion: fuse the spine together, using a piece of bone from the iliac crest, fibular, from a cadaver-Laminectomy: removing a piece of the vertebrae to help with spinal cord decompression

Autonomic Dysreflexia

-Life-threatening, must be treated immediately-Chord-injury above T6-Mostly with cervical injury-Reflex response to simulation of SNS-Develops after spinal shock-Abnormal response below the level of the spinal cord injury-If not treated immediately: Stroke, MR, Epileptic seizureCauses:-Bladder distension, bowel distention, skin stimulation, decubitus, painSigns/Symptoms-Hypertensive (20-40 mmHg more than normal, acute headache, bradycardic, flushed face and upper chest, cold and clammy below the lesion, diaphoretic, nasal congestion, blurred vision, convulsions, feeling of impending doomTreatment-Raise HOB to 90 degrees-Foley kinked?, drain the bladder-Bowel disimpaction-Loosen clothing-Take off socks and braces-Blood pressure medications

Gillian Barre

An autoimmune disorder that attacks the body's nervesCauses:Covid-19, Zika virus, recent surgery or vaccination, respiratory or digestive tract infectionSigns/Symptoms:pins and needles in extremities, weakness in legs that spreads to the upper body, unsteady gait or inability to walk or climb stairs, difficulty with facial expressions and talking, double vision or inability to move eyes, severe pain, difficulty with continence, rapid HR, low or high BP, difficulty breathingDiagnostics:Tentalon, spinal tap, electromyography, nerve conduction studiesTreatment:Immunoglobulin therapy, plasma exchange, provide pain relief, preventing blood clots, and physical therapy.Complications:difficulty breathing, residual numbness, heart and blood pressure problems, pain, bowel and bladder issues, blood clots, pressure sores, relapse

Myasthenia Gravis

Myasthenia GravisThe immune system produces antibodies that attack receptor sites and ultimately block nerve signals from communicating with the body.Causes:altered immune functionPredisposing Factors:use of beta blockersrecent infectionstress from hospitalizationrecent antibiotic useSymptoms:get worse over time and include impairment of eye, face, throat, neck, and limb muscles.The main symptoms of MG are double vision, difficulty chewing, swallowing, speaking, and making expressions, and weakness in extremities.Diagnostics:neuro exam, blood tests for the antibody, repetitive nerve stimulation, CT or MRI to rule out other diagnoses.Treatment:Medications:Cholinesterase inhibitors: enhance the nerve signal transmissionCorticosteroids: limit antibody production, but prolonged use is harmfulImmunosuppressants: to limit the production of harmful antibodiesIV Therapies:plasmapheresis: filters the blood to remove antibodies that may disrupt nerve signal transmissionmonoclonal antibodiesImmunoglobulin: assists the body in creating normal antibodiesSurgery: for thymus gland removalCholinergic Crisis (over medication): is the over-stimulation of a nerve receptor from too much acetylcholine, resulting in weakness and or paralysis of the muscle.Myasthenic Crisis (under medication): is particularly focused on the lack of muscle control in the muscles that assist with breathing.

Abdominal Aortic Aneurysm

An enlargement of the aorta, the main blood vessel that delivers blood to the body, at the level of the abdomen.An abdominal aortic aneurysm (AAA) can be life-threatening if it bursts. Abdominal aortic aneurysms are most common in older men and smokers.An abdominal aortic aneurysm often grows slowly, without symptoms. As it grows, some people may notice a pulsating feeling near the navel. Pain in the back, belly, or side may be signs of impending rupture.Stopping smoking may slow their growth. Small ones may only need monitoring. Aneurysms that are too large or growing too quickly should be repaired with surgery.Clinical manifestations:Pain in the abdomen, back, or chest can radiate to other areas, a pulse in the stomach, cool lower extremities, fever, and or weight loss can also occur if the cause is inflammatory or infectious.Diagnostics:abdominal ultrasound, CT scan, and MRI.Treatment:Surgical repair

Multiple Sclerosis: MS

A chronic, intermittent, progressive disease of the CNSMore common, the further one lives from the equatorA disease of the young, diagnosed between 20-50 y/o2-3x greater in womenCommon in caucasionLife expectancy is 30 years or more from the onset of treatmentThe suicide rate is high in people with MSMyths of MS:Fertility: is not affectedHaving children: does not always pass along to offspringSymptoms of MS tend to relapse in the first trimester and postpartumInherited disease: not directly inherited, but offspring have a higher incidence of acquiring MSWheelchair: not all people with MS are in a wheelchair80% of people will have a walking issueDying Young: must be compliant with treatment to live a long life⅔ of death from MS are from complications

Etiology of MS

An immune-related response where the body has an abnormal response to CNST cells, see myelin as a foreign body, and it starts to attack it and cause inflammationCause is unknownTriggersA genetically susceptible person with one or more environmental factorsGeographyVitamin D from the sunSmokingIncreases the progression of the disease fasterInfectionMeasles, varicella, herpes simplex, Epstein-Barr, CandidaGeneticsNot hereditary, first, second and third generations are more susceptible

Precipitating Factors of MS

Poor diet, lack of vitamin D and CaInjuriesEmotional stressPregnancyPoor Health

Types of MS:

Clinically Isolated Syndrome (CIS)The first episode of neurological symptoms is caused by inflammation and demyelination. Can last for a minimum of 24 hours and then disappear.Primary-Progressive MSThere are no exacerbations and remissions. A constant steady decline. Experience neurological disorders because of increased spinal cord lesions. Can be weeks, months, or years, with no return to baselineRelapse-Remitting MSMost common type. Diagnosed between 20-30 y/o. Relapses vary. Increased brain lesions (plaque), and an increase in inflammatory lesions.Blurred vision, numbness, fatigue, spasticity or stiffness in extremities, bowel/bladder issues, neurological disorders.Can be sudden or gradual. The fewer relapses the better the outcome. May have mild symptoms for 1-2 days, which can lead to secondary progressive after 10 years of having it.Secondary-Progressive MSNo relapses or readmissions. Slow continual decline.Worsen in neuro symptoms, walking abilities.

Pathophysiology of MS

Neurons: allow to think, speak, feel, see and hearAxons: allows nerve impulses to travel from one place to anotherMyelin is the protective coating of the axonCNS v PNSMyelin is only affected in the CNS with MSOligodendrocytes: specific cells that produce myelin for CNSInflammation ProcessA trigger causes an inflammatory response in the CNS, damages the myelin and oligodendrocytes, and starts to make the nerve fibers more open because there is no protective coating therefore the nerves become damaged and they lessen over time. Inflammation causes plaque, the more plaque forms in the brain the less the cognitive function is.Myelin can regenerate, that is called remissionEarly-stageThe myelin sheath is damaged but the nerve fiber is okayLate StageThe myelin becomes more damaged the axon gets involved. Myelin gets replaced by scar tissue, therefore there are no impulses and permanent loss of function.

Clinical Manifestations of MS

Weakness, pain syndrome (chronic), gait, fatigue, lack of coordination, spasticity, cognitive, visual, numbness/ tingling of the arms and the legs, dizziness/ vertigo, bowel (constipation) and bladder dysfunction, sexual dysfunction, emotional, fatigueMG Hug: feels like chest compressionLhermitte Sign: electrical shocks going down the spinal cordLess Common Signs:Speech and swallowing issues, seizures, hearing loss, loss of taste, tremors, and breathing issuesSecondary Assessments:Frequent UTIsAcid diet, self-catheterizationInactivityPressure injuries, decubiti, constipation, loss of muscle toneTertiary Assessments:Vocational, loss of income, support systems

Diagnostic Studies for MS

Criteria: how many episodes have been had, each episode must be at least one month apart. Need a minimum of two separate episodes. They are looking at the brain, spinal cord, SNSMRI shows plaque and demyelinationCSF studies, spinal taplooking for IgG bands and oligoclonal bands and protein that break down the myelinEvoked potential studiesLooks at the electrical activity in the brain and how the brain respondsOther diseases that need to be ruled out?Syphilis, Lyme's disease, HIV, vasculitis, lupus, sarcoidosis, vitamin d deficiency, herniated disc

Medications for MS

ImmunosuppressivesNovantrone (mitoxantrone)- monitor for leukemia, Copaxone- monitor for SOBSpasticityClonazepam (Klonapin), diazepam (Valium), dantrolene (Dantrium), baclofen (Lioresal)Dizziness/VertigoMeclizine (Antivert)Interferon-beta 1b: slow the rate of the symptomsBetaseron, extaviaInterferon-beta 1a: reduce the number of the relapses and the severity of the relapseTysabrin (natalizumab), avonex refib, plegridyIncrease liver enzymes, neutrophilsanxiety, depressionAntispasmodicsOxybutynin (Ditropan), propantheline (propantheline), botoxUrinary OutflowTamsulosin (Flomax), terazosin (Hytrin)InfectionsSulfamethoxazole (Bactrim, Septra), ciprofloxacin (Cipro), phenazopyridine (Pyridium), nitrofurantoin (Macrodantin)Bowel DysfunctionDocusate (Colace), bisacodyl (Dulcolax), mineral oil, sodium phosphate (Fleets Enema), Milk of MagFatigueModafinil (Provigil), fluoxetine (Prozac), Adderall, Ritalin, synthetic cannabisDepressionCelexa, Cymbalta, Effexor, Prozac, ZoloftSexualCialis, ViagraTremors/ AntiseizureKlonapinWalking/GaitAmpyraItchingHydroxyzine (Atarax)

Plasmapheresis

Plasma exchange to remove T-lymphocytesArteriovenous shuntA blood cell separator removes the antibodiesCellular blood components transfused with 5% fresh plasma or albumin2-5 hour treatmentSome meds may need to be heldCheck vitals every 15-20 mins, weights, H+H, full CBC, clotting types, type and cross them

Nursing Care for MS

Be aware of the patients' triggersSlow the progressionDecrease the relapses, with longer periods of remissionManage the s/s, increase their functionHigh risk for injury r/t sensory deficits and demyelinationForce fluids to 3000 mL/dayAcid-ash dietUrinary retention = cholinergicUrinary incontinence = anticholinergics

Muscular Dystrophy: MD (Duchenne's)

Discovered in the 1800s by Guillaume DuchenneX-linked recessive geneLack dystrophin, progressive muscle wastingIn the early stages, cognitively orientedDystrophin is what helps strengthen their muscles and give muscles their shape, without dystrophin the muscles are weak and contractures are present9 types of MD, we will only talk about Duchenne'sMost common in malesGenetic, mutation of gene DMD-2 (largest gene encoded for dystrophin)Onset is usually 2-6 y/oBy age 10 using a walkerBy age 12 usually in a wheelchairDeath usually comes in the late teens to late 20sMost do not live past 30 y/o b/c of cardiovascular issuesSteroids slow the progression of MD for the first 3 yearsNo cure

Signs and Symptoms of MD

Muscles are weakening, myotoniaPoor coordinationLegs contracted, starts in legs moves upwardFrequent fallsPneumonia, because of weakened lung musclesPermanent Trach b/c of weak respiratory musclesPEG tube for tube feeding to prevent aspirationLimited movement in armsSP tube for urinary eliminationA heart murmur is expected as the disease progresses, as well as cardiomyopathyEjection fracture is normally 25-45 percentTachycardic, low blood pressuresVery skinnyPressure UlcersIncontinenceThe central line for long-term antibioticsSignificant mental declineRegression in mental status

Diagnostics for MD

1) Muscle biopsy, looking for degeneration in the protein of dystrophinNo dystrophin indicates MD2) Genetic testing of the DMD-2 gene, if large changes indicative of Duchenne'sMuscle serum for CPK-3 levels, therefore if present positive for MGMuscle conduction testsEKG changesProgressive weakness

Medications for MD

Steroids, prednisoneTegretol, if seizures or painCyclosporinesPneumonia vaccineBaclofen for spasticity with bladder issuesNorepinephrine, vasopressin for low BP or MAP

Parkinson's Disease

The progressive degeneration of nerve cells in the basal gangliaDegeneration of dopamine-producing neurons in substantia nigra in midbrain/cerebellumLack of dopamineGenetic and environmental factors contributeCause: unknown

Risk Factors for Parkinson's

HereditaryEnvironment: pesticides, agent-orange, smoking, caffeine, head injuries, occupations

Disease Progression of Parkinson's

movements slow down, an increase of muscle tone, tremors, impaired posture, spasticity, symptoms usually start over 60Changes are gradualCognitive and behavioral changesDevelop dementiaEarly stages: little to no facial expression, imbalance gait, soft or slurred speechNo cure

Parkinson's Assessments

Resting tremors, rigidity, bradykinesia, fatigue, muscle weakness, stooped posture, difficulty rising, inability to move in bed, mask- face, decreased eye blinking, speech, depression, increased salivation, handwriting, autonomic symptoms

Parkinson's Diagnostics

No definitive DxMust have 2 of the 4 main symptomsTremorBradykinesiaStiffnessBalance disturbancePET/MRIDetailed medical historyComplete neurological and physical exam

Parkinson's Medications

DopaminergicLevodopa/ L-dopaRelives tremors, stiffness, and muscle weaknessCarbidopa-levodopa/ SinemetPrevents the breakdown of dopamineDopamine agonistsStimulates the release of dopamine, use once levodopa loses its effectivenessPramipexole (Mirapex)Ropinirole (Requip)Rotigotine (Neupro Patch)ApomorphineHydrochloride injectionAmantadineGocovri extended releaseDyskinesiaAnticholinergicsCogentinTremors and works better with younger peopleMAO inhibitors: blocks the breakdown of dopamineHelps with depressive symptomsEldeprylRasagiline (Azilect)SafinamideAdenosine A2a antagonist: reduces the time that the medications are not working, therefore meds last longerX2 the dose of this medication if their person smokes a P/DIstradefylline (Nourianz)Cannabis

CAM Treatments for Parkinson's

CalciumVitamin DFolateGingerGingko BilobaVitamin B12Coenzyme Q10Mediterranean Diet, increase in monosaturated fatsYoga, Thai-chi, meditation

Acute Myocardial Infarction

A blockage in the coronary arteries that is blocking the muscle, causing cardiac deathMust restore blood flow within 20-40 minutes to prevent irreversible muscle damageAtherosclerosis is the main cause of an MI

Risk Factors for MI

Smoking, HTN, diabetes, elevated cholesterol, family history of CAD or MI, people who are non-compliant with their medication, women b/c smaller hearts and smaller blood vessels and atypical symptoms, obesity

S/S of Anteroseptal Wall MI

Left ventricle location, at risk for Vtach and Vfib, heart failure, crackles in the lungs, full-blown pulmonary edema, increased PCWP, decrease in L ventricular function, decreased CO, SOB/DOE, decreased pulses, decreased cap refill, don't give too much fluid

S/S Inferior MI

ST depression, Right side location, ar risk for heart blocks and bradycardia, decreased CO, Increased CVP pressure, right-sided heart failure, edema, JVD, nauseous, vomiting, hiccups b/c diaphragm irritation, give fluids

Diagnostics for MI

12 lead EKG done x 3 days, within 10 minutes of the onset of chest painEvery 6 hours for the first dayST segmentsSTEMI vs NSTEMISTEMI: 1 mm or more than the baseline in more than 1 leadNSTEMI: no ST elevation, but the cardiac enzymes are elevatedQ waves = transmural MIIf Q waves are present injury has occurred through every layer of the heart muscleCPKTroponinCK-MB, elevate within 4-6 hours, peak within 12-14 hoursCBCs for baselineCoagulationsCMP for electrolytesCBIGK: to help protect the heartCalcium gluconateBicarbInsulinGlucoseKayaxylate

MI Treatments

The goal is to preserve cardiac muscle and functionStenting to open the occlusionA cardiac cath is the best way to diagnose the percentage of the occlusionCABG if the occlusion is too advanced for a stentFrom the onset of pain, there should be 60 minutes to get pt to the cath labThrombolyticsDo they meet the criteriaIf not integrilin instead with heparin, Plavix, aspirin,Effian especially for stentingA low dose of Lovenox: only works if pt is under 300lbs100cc vial reconstituted based on the pt.s weightBolus dose, then the rest is given over the next hourBeta-blockers, help to prevent the MI from going through all of the layers of the heartACE inhibitors, enhance the effect of beta-blockersMonitor renal function b/c of the ACE inhibitorVasopressors if not maintaining a MAP of 65 or greaterNorepi, epi, dopaminePain medsMorphine, DilaudidCa-channel blockers help the heart not work as hardAnti-arrhythmicsAmio, lidocaineTemporary Pacemaker

Nursing Interventions for MI

12 lead EKG within 10 minsLabs within 10 minutesTroponin (0-0.04), BNP (<100), d-dimer (<0.5), PT(11-13.5)/PTT(25-35)/INR (<1.1), CBC, CMP, lipid profile (LDL <100, HDL >60, triglycerides <150, total cholesterol < 200)Administer medicationsBegin O2 at 2L/minPCI within 90 minutesFibrinolytic Therapy within 30 mins if PCI is unavailableAssessment within 10 minsCardiac, pulmonary, neuroContinuous EKG monitoringKeep HOB flat after PCIProvide educationCoronary angiogram

MI Complicaitons

Heart failure, cardiogenic shock, pericarditis, extended MI up to 6 days long, ventricular wall rupture: papillary muscle rupture, therefore the heart cannot contract and you die

Acute Coronary Syndrome

O2 supply and demand is not meeting the myocardial needsLow supply therefore chest pain, SOB, diaphoretic

Left Anterior Descending: LAD

Occlusion results in an anterior wall infarctionEKG changes in V3 and V4The left side of the heart is the powerhouse of the heartThe widow-maker, b/c people do not always live with an anterior MITend to have arrhythmias, Vtach and VfibMonitor lab work to ensure the electrolytes are okay

Left Circumflex Artery

Comes down and around the heart on the left sidePosterior or lateral wall infractionsLateral wall of the left ventricleEKG changes in I, V5, V6, and aVL

Right Coronary Artery: RCA

Occlusion results in inferior wall infarction and or posterior wall infarction of the right sideAV node is affected: junctional rhythms and periods of bradycardia or heart blocksEKG changes II, III, AVF

Ischemia

ST depressionTemporaryCan fix with nitrates

Injury

ST-elevationIschemia leads to injury, and injury is the death of cardiac muscle

Congestive Heart Failure

A syndrome that occurs when the client cannot tolerate exercise and has fluid retention due to structural heart diseaseLow cardiac output then arterial underfilling, and an elevation in left ventricular diastolic pressuresLeft-sided heart failure:SOB, DOE, crackles, orthopnea, increase wedge pressureRight-sided heart failure:Systemic, JVD, increased peripheral edema, increased weight, increased CVP pressuresDiagnosed byAssessmentBiomarker b-type natriuretic peptide (BNP)Normal is <100Anything 100> is heart failure

Medications for CHF

ACE inhibitorsLisinopril, captopril, enaliprilDry cough is a side effectARBSWhen they cannot tolerate ace inhibitorslosartanBeta-blockersDo affect HR and BPMetoprolol, carvedilolNo wheezing, no vtach or vfibSpironolactone, K sparing diureticIV loop diureticsDrop LV filling pressuresAssessments to consider:Increased urine outputWeightEdemaElectrolyte levels, BUN, creatinineHydralazineNitrates (Nitro, Isordil)Pulls fluid away from the heartAffect BPPatients with hypoperfusion+ inotropesDecrease preload and afterload, and increase contractility and COPrimacore, digoxin, dobutamineVasopressorsNorepi, epi, dopamine

Treatments for CHF

LVADLeft ventricular assist deviceUsed for people with end-stage heart failure, but not ready to give up, but do not qualify for a transplantIf they qualify for a transplant and are waiting for their transplantCannot get a BP, must use a doppler to listen for a systolic BPCannot do CPRHuman B-type natriuretic peptide (NATRECOR)Used for people with acute decompensated heart failure or end-stage heart failureDo not use if MAP is less than 60Causes hypotensionContinuous drip for 3 daysOnset is 15 minutes and peaks within 1 hourICU for first-time administrationBiventricular PacemakerHeart Transplant

Normal Sinus Rhythm

Rhythm: RegularRate: Normal (60-100 bpm)P Wave: Normal (positive and precedes each QRS)PR Interval: Normal (0.12-0.20 sec)QRS: Normal (0.06-0.10 sec)

Atrial Flutter

an atrial tachydysrhythmia identified by recurring, regular, saw tooth-shaped flutter waves that originate from a single ectopic foci.-Causes: CAD, HTN, mitral valve disorders, PE, chronic lung disease, cardiomyopathy, hyperthyroidismRhythm: Regular or irregularRate: Fast (250-300 BPM atrial), by the ventricular rate is slowerP Wave: non observable, but saw-tooth flutter waves are presentPR interval: not measurableQRS: normal (0.06-0.10 sec)-Clinical Significance; decreased CO → HF and clot formation-Treatment:Slow the ventricular rateCa Channel Blockers and Beta BlockersElectrical CardioversionAntidysrhythmics: convert NSR and maintain NSRIbutilide (Covert)amiodarone , flecainide, dronedarone (Multaq)Radiofrequency catheter ablationMedications:Ca Channel Blockers- decrease automaticity of the SA node, delay AV conduction, reduces myocardial contractility.Beta- Blockers- decrease automaticity of the SA node, slow impulse conduction to AV node, reduce atrial & ventricular contractility.Potassium Channel Blockers- delay repolarization, resulting in prolonged duration of action potential and refractory periodibutilide(Corvert) & amiodarone (Cordarone)Antidysrhythmic Drugsdigoxin (Lanoxin)- decrease conduction through AV node reduce automaticity of SA nodedronedarone (Multaq)- decrease conduction through AV nodes, reduce automaticity if SA node.

AFIB

characterized by a total disorganization of arterial electrical activity, resulting in loss of effective atrial contraction-can be paroxysmal or persistent-Causes: A-fib can occur in patients with underlying heart disease such as CAD, HF, cardiomyopathy. Also seen with ETOH intoxication, caffeine use, stress, electrolyte disturbances.Rhythm: irregularRate : very fast (> 350 bpm) for martial, but ventricular rate may be slow, normal or fastP Wave: absent - erratic waves are presentPR interval: absentQRS: normal but may be widened if there are conduction delays-Clinical Significance: decreased CO → HF and clot formation-Treatment:Slow the ventricular rateCa Channel Blockers and Beta BlockersElectrical CardioversionAntidysrhythmics: convert NSR and maintain NSRIbutilide (Covert)amiodarone , flecainide, dronedarone (Multaq)Radiofrequency catheter ablationAnticoagulation for patients in Afib>48hours-Synchronized Cardioversion:Non-emergent; patient is awake but sedatedA synchronized circuit in the defibrillator delivers a shock that is programmed to occur on the R wave of the QRS complex.Synchronized switch MUST be turned on.-Radiofrequency Catheter Ablation:Considered to be a non-pharmacologic treatment option to atrial dysrhythmias with RVR refractory to drug therapy.Uses electrical energy to ablate accessory pathways or ectopic sites in the atria, AV node, and ventricles.

1st Degree Heart Blocks

every impulse is conducted to the ventricles but the time of the AV conduction is prolonged. Impulse moves through the AV node slowly, but the ventricles usually respond normally.-Causes: MI, CAD, rheumatic fever, hyperthyroidism, electrolyte imbalances (hypokalemia), medications (digoxin, beta-blockers, Ca Channel Blockers.Rhythm: regularRate: the underlying rateP Wave: normalQRS: normal (0.06-0.10 sec)NOTE: a first degree AV block occurs when electrical impulses moving through the AV node are delayed (but not blocked). First degree indicated slowed conduction, without missed beats.-Clinical Significance: patients are usually asymptomatic, generally not serious-Treatment: no treatment. Monitor patients for any new changes, heart blocks can progress. Determine causative factors and make changes.

2nd Degree, type 1 heart block

a gradual lengthening of the pR interval. Prolonged AV conduction time until an artail impulse is not conduction and a QRS complex is blocked.-Mobitz or Wenckebach-Causes: medications (digoxin and beta blockers) or CADRhythm: irregular but with a progressively longer PR interval lengtheningRate: the underlying rateP Wave: normalPR interval: progressively longer until a QRS complex is missed, then the cycle repeatsORS: normal (0.06-0.10 sec)-Clinical Significance: usually a result of a MI. Generally transient. May be a warning sign for more serious events and progress.-Treatment:-Asymptomatic: monitor patient and rhythm. Have a transcutaneous pacemaker near.-Symptomatic: atropine or temporary pacemaker.-Atropine: increases HR, improves AV conduction

2nd degree type 2 heart block

a P wave is non-conducted without progressive PR lengthening-On conducted eats, the PR interval is constant-More serious because of the impulses from the SA node not conducted to the ventricles- 2:1 or 3:1-Mobitz IIRhythm: regular (atrail) and irregular (ventricular)Rate: Characterized by atrial rate usually faster than the ventricular rate, which is usually slowerP wave: normal form, but more p waves than QRS complexesPR interval: normal or prolongedQRS: normal or wide-Clinical Significance: poor prognosis - reduced HR → decreased CO. often progresses to 3rd degree or complete heart block-Treatment: transcutaneous pacing or insertion of a temporary pacemaker-ATROPINE IS NOT EFFECTIVE FOR 2ND DEGREE, TYPE 2

3rd Degree Heart Block

a form of AV dissociation in which no impulses from the atria are conducted to the ventricles-atria are simulated and contract independently to ventricles-ventricular rhythm is escape rhythm-Causes: severe heart disease; CAD, MI, myocarditis (digoxin, beta-blockers, and Ca Channel BlockersRhythm: Regular, but atrial and ventricular rhythms are independentRate: characterized by atrial rate usually normal but faster than ventricular rateP Wave: normal shape and size, may appear within the QRS complexPR interval: absentQRS: normal, but wide if junctional escape focus-Clinical Significance: significantly reduced CO with subsequent ischemia, HF, and shock. Syncope may occur, resulting from bradycardia or periods of asystole.-Treatment: transcutaneous pacemaker or medications (dopamine or epinephrine)-ATROPINE IS NOT EFFECTIVE

ABG Compensation

Uncompensated: pH is out of range, PaCO2 or HCO3 are out of range, never both.PaCO2 not in normal range: respiratoryHCO3 not in normal range: metabolicPartially Compensated: pH, PaCO2, & HCO3 are all out of rangePaCO2 and HCO3 will be opposite each otherCompensated: pH is always within normal range. CO2 & HCO3 are both out of range.PaCO2 and HCO3 will be opposite each other

ABG Ranges

pH: 7.35← Acid 7.4 Alkalotic →7.45PaCO2 (respiratory):45← Acid 40 Alkalotic →35HCO3 (metabolic):22← Acid 24 Alkalotic →26

Methicillin-resistant Staphylococcus Aureus: MRSA

Staph infection that is an antibiotic resistant organismStaph is usually found on the skin or in the nasal liningOccurs in hospital or community settingsMay become life-threateningContact PrecautionsTreatmentAntibioticsClindamycin PO or IV depending on the severityVancomycinDoxycycline

Vancomycin-resistant Enterococcus: VRE

Enterococci are usually found in the intestinesAntibiotic resistant organismMuch more virulent than MRSATypically infects the bloodstream, intestines, urinary tract, and woundsContact precautionsTreatmentAntibiotics that organism is sensitive toPenicillin

Clostridium Difficile: CDiff

Spore-forming, Gram positive anaerobic bacillusSpores can live of surfaces for 3 daysUsually from recent antibiotic use (fluoroquinolones, third/fourth generation cephalosporins, clindamycin, carbapenems)Leads to watery diarrhea, fever, loss of appetite, nausea, abdominal tenderness/painEnteric Contact PrecautionsHand-washing with soap and waterTreatmentOral Vancomycin, because it needs to be treated in the GI tractNo imodium, then toxic megacolon, leading to a colon burstHigh fiber diet to bulk the stoolRectal tubes are implemented sometimes

Human Immunodeficiency Virus: HIV

Retrovirus that causes immunosuppressionAdvances in preventing, testing and treatment have resulted in longer lif-spans and lower death ratesIn the United States1.2 million people have HIV and 13% of them don't know itRate of new diagnosis has been declining (about 35,000)Transmission:Fragile virus transmitted only through contact with body fluids under specific conditionsBlood, semen, rectal fluid, vaginal secretions, breast milkSexual contact with an infected partner is the most common mode of transmissionCan also be transmitted through injections with an infected needlePerinatal transmissionThe infected person can transmit HIV within a few days after becoming infectedTransmission subject to the same requirements as other microorganisms:Large enough amountFrequency and duration of contactVirulence and concentration of organismHost immune system

Pathophysiology of HIV

Cells with CD4 receptors are targetedBinds to receptor site on the cell membrane allowing access to cell nucleusRNA is transcribed into a single strand of viral DNAStrand copies itself becoming double strand DNAOnce virus is in the cell nucleus it becomes a permanent part of the cell genome

HIV Life Cycle

Binding (attachment): HIV binds to receptors on the surface of a CD4 cellCCRS antagonistPost-attachment inhibitorsFusion: the HIV envelope and the CD4 membrane fuse, which allows the HIV to enter the CD4 cellFusion inhibitorsReverse Transcription: inside the CD4 cell, HIV releases and uses reverse transcriptase (an HIV enzyme) to convert its genetic material HIV-RNA into HIV-DNA. The conversion of HIV-RNA to HIV-DNA allows HIV to enter the CD4 cell nucleus and combine with the cell's DNA.Non-nucleoside reverse transcriptase inhibitorsNucleoside reverse transcriptase inhibitorsIntegration: Inside the CD4 cell nucleus, HIV releases integrase (an HIV enzyme). HIV uses integrase to integrate its viral DNA into the DNA of the CD4 cell.Integrase inhibitorsReplication: once integrated into the CD4 cell DNA, HIV begins to use the machinery of the CD4 cell to make long chains of HIV proteins. The protein chains are the building blocks for more HIVAssembly: New HIV proteins and HIV-RNA move to the surface of the cell and assemble into immature (noninfectious) HIV.Budding: Newly formed immature HIV pushes itself out of the host CD4 cell. The new HIV releases protease (an HIV enzyme). Protease breaks up the long protein chains in the immature virus, creating the mature (infectious) virus.Protease inhibitors

Clinical Manifestations of HIV

Stage 1: Acute HIVFlu-like symptoms-accompany seroconversionFever, swollen lymph nodes, sore throat, headache, malaise, nausea, muscle, joint pain, diarrhea, diffuse rashOccurs 2-4 weeks after infectionLasts for 1-2 weeksHigh viral loadEasily transmit the HIVStage 2: Chronic HIV (latency)Likely not aware of infection due to low level symptomsFatigue, headache, low-grade fever, night sweatsHIV transmission can occurDuring the latent stage may start demonstrating signs that HIV is advancing to a more active state:CD4+ T cells drop to 200-500 cells/mm3Increasing viral loadSymptoms from the early phase return and become worseNew problems develop such as:ShinglesPersistant candida infectionsHerpesBacterial infectionsStage 3: AIDSImmune system severely compromisedGreat risk for opportunistic diseasePossible malignancies,, wasting, and dementiaDiagnosis of AIDS subject ot CDC guidelines:CD4+ count <200 cells/mm3 or...Presence of opportunistic infections/opportunistic cancerCryptococcal meningitis, cytomegalovirus retinitis, mycobacterium avium complex, kaposi sarcoma, pneumocystis jiroveci pneumonia, tuberculosis, wasting syndrome, candida

HIV Diagnostics

Nucleic acid test (NAT)Identifies virus through presence of RNAHighly specific and sensitiveAntigen/antibody testDetects HIV antigens and antibodiesAntibody testsTests for antibodies, not useful in the first few weeks after infectionsRapid HIV antibody test useful if there is doubt if patient will:Return for resultsFollow restrictions on at risk behaviors until test results return.Viral load: viremia (Large viral levels in blood) for the first 2 to 3 weeks of infectionTransmission is more likely when viral load is highFollowed by prolonged period (years) of low viral loadCD4 countsCBCCMPResistance tests: help determine new drug combinations for patients not responding to ART

Antiretroviral Therapy: ART

Given dependent of the stage the person is in of HIVNucleoside reverse transcriptase inhibitors (NRTIs)Non Nucleoside reverse transcriptase inhibitors (NNTRIs)Integrase inhibitorsProtease inhibitors (PI)Fusion inhibitorsCCR5 AntagonistPost-attachment inhibitorsFixed-dose combination products

HIV Prophylaxis

PrEp: Pre-Exposure ProphylaxisUsed to prevent HIV for people who are at risk for HIV due to sex or drug injectionsCombo of 2 HIV meds in 1 pill:Truvada (for all)Descovy (Men and Transgender Women)Injection every 2 months by HCP:ApretudePEP: Post Exposure ProphylaxisUsed in emergent situationsMust start within 72 hours of exposure (sooner the better)HCP will determine which medications to prescribeTake medications every day for 28 days

Systemic Lupus Erythematosus

Chronic, multisystem inflammatory autoimmune diseaseComplex interactions amongst many factorsCharacterized by unpredictable exacerbations and remissionsExact etiology is unknownHormonal, genetic, and environmental pieces to the diseaseEtiology/pathophysiologyOveraggressive autoimmune reactions directed against constituents of:Cell nucleusSingle and double-stranded DNAImmune complexes are deposited in capillaries basement membranes triggering inflammation and destructionTrigger that damages the cells they go through cell death and release the contents, then there is a buildup of nuclear antigens, then B cells produce antinuclear antibodies, then the formation of antibody antigen complex, then antibody antigen enters the bloodstream, then complexes are deposited into the bodies tissues.

Clinical Manifestations of Lupus

SLE is extremely variable in severityRanges from a relatively mild disorder to rapidly progressive disease affecting many organ systemsMost commonly affects the skin, muscles, lining of the lungs, heart, nervous tissue, and the kidneysSkin: rashes, blisters, butterfly rash, and color changesJoints: inflammation of the joint lining (most commonly in the hands and wrists), joint painHair lossFatigue caused by anxiety, sleep disturbances, vitamin D deficiency, and low exerciseNervous system: seizures, peripheral neuropathy, cognitive dysfunctionHematologic: blood clots, anemia, leukopenia, thrombocytopenia (avoid live vaccines)Infection: increased susceptibility to infections, deficiencies in antibody production, immunosuppressive effect of many anti-inflammatory drugs, increased risk or death from infection.Cardiopulmonary: tachypnea, cough, pleurisy, dysrhythmias, pericarditisRenal

Lupus nephritis

Manifests in about 40% or patients75% will present with renal damage within 2 years of dxRanges from mild proteinuria in glomerulonephritisGoal of treatment is to slow the progression of renal damageScaring can result in permanent damage leading to ESRDRenal failure is the leading cause of death in SLE patients

Diagnostics for Lupus

No specific testSLE is diagnosed primarily on criteria relating to patient history, physical, and lab findingsANA is present in 97% of persons with SLEESR, CRPCBC, BMPUA

Medications for Lupus

NSAIDsIbuprofen, NaproxenRenal impairment, GI issuesAntimalarial drugsHydroxalinechloraphinLong-term use, but effects are not immediateRetina damageImmunosuppressive aka Steroid-sparing drugsMethotrexateLowers the use of steroidsIncreases risk for infections and cancersCorticosteroidsPrednisone, methylprednisoloneShouldn't be for long-term use

Biologic and Targeted Therapy for Lupus

Decreases antibody attacksInfusions or injectionsTakes up to 6 months to see resultsAffects mental health, depression and suicidal thoughtsInterfere with the immune responseCombat osteoporosisImprove cutaneous casesSafe use, proper administration and possible side effects should be taughtAbrupt cessation may cause exacerbation

Pregnancy and Lupus

Symptoms should be under control for 6 months prior to getting pregnantWomen with SLE are considered high-risk pregnanciesRisk for preeclampsia, miscarrigae and stillbirth for current flare upPostpartum period is common for a flare-up

Maslow's Hierarchy of Physiological Needs

1) physiological needsBreathing, food, water, shelter, clothing, sleep2) safety and securityHealth, employment, family and social stability3) love and belongingFriendship, family, intimacy, sense of connection4) self-esteemConfidence, achievement, respect from others, the need to be a unique individual5) self-actualizationMorality, creativity, spontaneity, acceptance, experience purpose