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NCM- ABC Critical Care Nursing -specialized area of nursing that caters to critical clients and require specialized

care -life of patients are in threatening condition -deals with human responses to life threatening problems and critical conditions -specialty nursing -- CONAPI, AACN ROLES OF CRITICAL CARE NURSES A. DIRECT PATIENT CARE -detects and interprets indicators that signify varying conditions of the critically ill with the assistance of advanced technology and knowledge -plans and initiates nursing process to its full capacity in a need driven and proactive manner -acts promptly and judiciously to prevent or halt deterioration when conditions warrant -coordinates with other healthcare providers in the provision of optimal care to achieve the best possible outcomes B. INDIRECT PATIENT CARE - the family -indirects family needs and provide information to allay fears and anxieties -assists family to cope with the life threatening situation or patient's impending death EXTENDED ROLES AS CRITICAL CARE NURSES -sampling and analyzing arterial blood gases -weaning patients off ventilations -adjusting intravenous analgesia/sedations -performing and interpreting ECG's -titrating intravenous and central line medicated infusion and nutrition support -initiating defibrilation to patient with ventricular filbrilation or lethal ventricular tachycardia -Removal of pacer wire, femoral sheaths and chest tubes CPR should be performed on atrial ventricular fibrilation Pwaves-indicates ventricular functioning PATIENT ADVOCATE -Management and Leadership Role 1.) perform management and leadership skills in providing safe and quality care 2.) accountability for safe critical care nursing practice 3.) delivery of effective health programs and services to critically ill patients in the acute setting 4.) management of the critical care nursing unit/acute care setting 5.) take lead and supervision among nursing support staff 6.) utilize appropriate mechanism for collaboration, networking, linkage building and referrals

RESEARCHER ROLE a.) engage self in nursing or other health related research with or under supervision of an experienced researcher b.) utilize guidelines in the evaluation of research study/ report c.) apply the research process in improving patient care infusing concepts of quality improvement and in partnership with other team players ACUTE BIOLOGIC CRISIS HEART --- EFFECTS OF AGING> dec. Muscle elasticity --- CONSEQUENCES> dec. Cardiac output FORCES DETERMINING OXYGEN CONSUMPTION HEART RATE-the more the heart has to pump, the more oxygen it will require to do that PRELOAD-Amount of blood that is brought back to the heart to be pumped around AFTERLOAD-resistance against which the heart has to beat stretch of the ventricles, the more stretch, the more oxygen consumption there would be CARDIOVASCULAR SYSTEM subj and obj findings: complaints of fatigue with inc. Activity ; inc. HR recovery time; normal BP less than 140/90 mmHg Health promotion: exercise regularly pace activities avoid smoking eat a low fat and salt diet participate in stress reduction activities check BP regularly medication compliance weight control FACTORS THAT MAY AFFECT THE CARDIAC RATE AND RHYTHM build up of waste products(account for higher acidity) acidosis drugs decreased oxygen levels changes in the electrolytes in the area Potassium-responsible for cardiac function Assessment: health history a.presenting problem 1.) nonspecific symptoms may include

-fatigue -cough -syncope -shortness of breath -headache -difficulty sleeping -palpitations -weight loss/gain -dizziness 2.) specific signs and symptoms a) chest pain b.) dyspnea (shortness of breath) c.) orthopnea/ paroxysmal nocturnal dyspnea d.) palpitations e.) edema f,) cyanosis B.) Lifestyle: occupation, hobbies, financial status, stressors, exercise, smoking, living conditions C.) use of medications: OTC drugs, contraceptives, cardiac drugs D.) personality profile: type A, manic depressive, anxieties E.) nutrition: dietary habits, cholesterol, salt intake, alcohol consumption F.) past medical history G.) family history: heart disease (congenital, acute, chronic) risk factors (DM, hypertension, obesity) PHYSICAL EXAMINATION -skin and mucous membrane color/texture, temperature, hair distribution on extremities, atrophy/ edema, petechiae -peripheral pulses O=absent 1= palpable 2=normal 3=full 4= full and bounding schamroth technique -if you see white diamond on nails - normal -assess for arterial insufficiency and venous impairment -measure and record blood pressure -inspect and palpate the neck vessels a.) jugular veins: note location, characteristics, jugular venous pressure b.) carotid arteries: location and characteristics ausculate heart sounds -normal (s1, s2) -abnormal (s3, s4): murmurs, galloping heart sounds; best auscultated on external border 4th valve

1st: aortic 2nd: pulmonic 3rd: mitral 4th: tricuspid LABORATORY/DIAGNOSTIC TESTS A. BLOOD CHEMISTRY AND ELECTROLYTE ANALYSIS 1.cardiac enzymes: in MI a.) troponin T: detected 3-12 hours after chest pain (expensive) b.) troponin I: detected 3-12 hours c.) creatinine phosphokinase (CPK-MB): 6-12 hours (best specific confirmatory test for MI) d.) aspartate aminotransferase (AST)(SGOT): 24 hours after chest pain 2.) electrolytes a.) sodium (Na) 135-145 meq/L: major electrolyte outside the cell hyponatremia: fluid excess hypernatremia: fluid deficit b.) potassium (K): 3.5-5 meq/L: major electrolyte inside the cell -dec/inc levels can cause dysrythmias c.) magnesium (Mg): 1.3-2.1 meq/L -dec levels can cause dysrythmias d.) calcium (Ca): 4.5-5.3 meq/L -dec for blood clotting and neuromuscular activity -dec levels causes tetany -inc levels causes muscle atony -inc and dec levels causes dysrythmias 3.) serum lipids Hign density lipids (HDL) 30-85 mg/dL -low levels predispose to CVD Low density lipids (LDL) 50-140 mg/dL - inc levels predispose to atherosclerotic plaque formation Triglycerides 10-150 mg/dL -high levels increases risk of atherosclerotic liver functions with fat metabolism B. HEMATOLOGIC STUDIES -CBC -Coagulation time: 5-15 mins, inc levels indicate bleeding tendency, used to monitor heparin treatment -Prothrombin time (PT) 9.5-12 sec; used to monitor warfarin/heparin treatment

continuous backpain-indicates bleeding C.) urine studies (routine analysis) D.) ECG -non invasive ECG -portable recorder (holter monitor) E.) exercise ECG (stress test): the ECG is recorded during prescribed exercise, may show heart disease when resting, ECG does not NURSING DIAGNOSIS FOR THE CLIENT WITH CVD INCLUDE fluid volume excess decreased cardiac output altered peripheral tissue perfusion impairment of skin integrity risk for activity intolerance PLANNING AND IMPLEMENTATION GOALS: a A.) fluid imbalance will be resolved, edema minimized B.) cardiac output will be improved C.) cardiopulmonary and peripheral tissue perfusion will be improved D.) adequate skin integrity will be maintained INTERVENTIONS cardiac monitoring a.) ECG 1.) strip small square:O.O4 secs large square: 0.2 secs 2.) P wave: produced by atrial depolarization indicates SA node function, pacemaker of the heart 3.) P-R interval (O.12-0.20 secs) a.) indicates AV conduction time: junction between right atrium and right ventricle b.) measured from beginning of P wave to beginning of QRS complex 4.) QRS complex (0.06-0.10 secs) a.) indicates ventricular depolarization b.) measured from onset of Q wave to end of S wave 5.) ST segment

a.) indicates time interval between complete depolarization of ventricles and repolarization of ventricles b.) measured after QRS complex to beginning of T wave 6.) T wave a.) represents ventricular repolarization b.) follow ST segment ventricular fibrilation- state of cardiac arrest : amiodarone, epinephrine CRITICAL POINTS OF ECG P-R INTERVAL: reflects the normal delay of conduction at the AV node Q-T INTERVAL: reflects the critical timing of repolarization of the ventricles S-T segment: reflects important information about the repolarization of the ventricles 1.) a hormone with physiologic effects that decreases BP is: atrial natriuretic factor- release by the heart; has the largest chemoreceptor 2.) phase of the cardiac cycle-relax-diastole 3.) when a patient has potassium imbalance- auscultate heart sounds DISORDERS OF THE CARDIOVASCULAR SYSTEM HEART CORONARY ARTERY DISEASE 1.) a variety of pathology that cause narrowing or obstruction of the coronary arteries 2.) major causative factor- atherosclerosis ATHEROSCLEROSIS RISK FACTORS Sex-male Age- middle age ,elderly Diabetes Mellitus BP high : hypertension Elevated cholesterol Tobacco ANGINA PECTORIS A.) gen. Info. 1.) transient,paroxysmal chest pain produced by insufficient blood flow to the myocardium resulting in myocardial ischemia 2.) ischemia -CAD

-hypertension -DM -aortic insufficiency 3.) precipitating factors -physical exertion -strong emotions -consumption of a heavy meal -extremely cold weather -sexual activity -cigarette smoking B. Medical management: 1.) drug therapy: nitrates, beta adrenergics blocking agents and/or calcium blocking agents, lipid reducing drugs if cholesterol is elevated calcium-causes contraction 2.) lifestyle modification 3.) surgery: coronary bypass surgery C. ASSESSMENT FINDINGS 1. Pain: substernal with possible radiation to the neck, jaw and arms releived by REST 2. Palpitations, tachycardia, dyspnea, diaphoresis 3. Elevated serum lipid level increased temperature> increases acidity> too much acid kills cells MI- pain substernal up to back, progressive cannot be relieved by rest, morphine (ready naloxone,narcan) nitrates: maximum of 3 doses 4. Diagnostic tests -ECG may reveal ST segment depression and T wave inversion during chest pain -stress test may reveal an abnormal ECG during exercise D.NURSING INTERVENTION 1.) administer oxygen 2.) give prompt pain relief with nitrates or narcotic analgesics as ordered 3.) monitor VS , status of cardiopulmunary function, monitor ECG 4.) place patient in semi- high fowler's position 5.) provide emotional support, health teachings flat on bed- intratentorial, brain surgery MYOCARDIAL INFARCTION

1.) the death of myocardial cells from inadequate oxygenation often caused by a sudden complete blockage of a coronary artery ASSESSMENT: pain same as in angina, crushing, viselike with sudden onset, unrelieved by rest or nitrates nausea and vomiting, dyspnea skin: cool, clammy, ashen gray increased in temperature initial increase in BP and pulse with abrupt changes sequence of elevated enzymes after MI time to call 911 from first to appear to last troponin CK-MB AST LDH1 * liver releases in large volume liver enzymes upon cardiac cells death MI COMPLICATIONS Heart failure/ hypertension Arrythmia- present during attack SHOCK (1ST: cardiogenic 2ND: hypovolemic) Cardiac rupture Aneurysm MEDICAL MANAGEMENT antiplatelet agent clopidogrel in combination with low dose aspirin could be given for at least 4wks after MI clopidogrel alone can be used for patients with aspirin hypersensitivity (vomiting, abdominal discomfort, rashes) if patient is unable to take clopidogrel consider treatment with aspirin and warfarin combined THROMBOLYTIC THERAPY -low dose decrease adverse reaction coagulant- macro, cannot dissolve clots platelets- micro, prevent platelet aggregation thrombolytic-lyses thrombus (streptokinase, furokinase)take at least 4 hours from the onset of pain/attack; tissue plasminogen activator contraindications to thrombolytic therapy

Normal ECG/ ECG not available unconscious w/o known cause CVA within last 6 months known intracranial pathology active pulmonary disease MANAGEMENT OF PATIENTS AFTER MI PHYSICAL ACTIVITY Patients should be advised to be physically active for 20-30 minutes a day to the point of slight breathlessness Patients who are not achieving this should be advised to increase their activity in a gradual, step by step way, aiming to increase their exercise capacity -MI patients are anxious quit smoking Diet: patient should be advised to eat a mediterranean style diet ( more bread, fruit, vegetables and fish, less meat and replace butter and cheese with products based on vegetable and plant oils) -cardiac rehabilitation should be available for all patient after an MI if cardiac output falls- enlargement of ventricular myocardium CONGESTIVE HEART FAILURE TYPES OF HEART FAILURE Left sided heart failure Right sided heart failure High Output failure HF causes HEART MAY DIE Hypertension Embolism Anemia Rheumatic heart disease Thyrotoxicosis (including pregnancy) Myocardial Infarct Arrythmia Diet and Lifestyle Infection Endocarditis CLASSIFICATION OF HF can be classified using 2 approaches: disease staging (med hsx,risk factor, diagnostic tests, existing damage)

functional classification (functional capacity, manifestations, level of capacity) DISEASE STAGING centered on its risk, evolution and progression STAGE A: high risk for HF without structural heart changes or disorders STAGE B: with structural disorder but without any symptoms of the disease STAGE C: with current/ past history of HF with structural disorder STAGE D: end-stage FUNCTIONAL CLASSIFICATION relationship between symptoms and activity level CLASS I: with cardiac disease but without limitations of activity, ordinary level of physical activity does not cause undue fatigue, palpitation CLASS II: with cardiac disease resulting in slight limitation of physical activity; comfortable at rest; ordinary physical activity causes fatigue and palpitations CLASS III: clients with cardiac disease resulting to marked limitation of physicalactivities comfortable at rest Less than ordinary physical activity causes fatigue, palpitation, dyspnea or anginal pain CLASS IV: (orthopneic/tripod position) with inability to carry on any physical activity without discomfort Symptoms of cardiac insufficiency even at rest any physical activity increases discomfort KEY FEATURES OF LEFT SIDED HEART FAILURE pulmonary congestion -hacking cough,worse at night -dyspnea, breathlessness -crackles, wheezes in lungs -frothy, pink tinged sputum -tachypnea Right sided heart failure systemic congestion jugular vein distention enlarged liver and spleen anorexia and nausea dependent edema (legs and sacrum) distended abdomen (no need to palpate) MEDS: diuretic, ace inhibitors, antilipemic agents, antiarrythmics, digitalis DIURETICS: monitor potassium (do not administer if hypokalemic or hyperkalemic) I&O, weight (report more than 2lbs. A day weight gain)

BP (withhold if BP is less than 90/60) antilipemics (3 months only) increase fluid intake to prevent constipation, take at night to facilitate enzyme activity to metabolize cholesterol 1month: wash out period Nursing interventions: monitor hemodynamic parameters weigh daily and report more than 2lbs weight gain LSLF diet SICKLE CELL ANEMIA COMPLICATIONS: stroke, swelling of hands and feet, spleen problems, infection, infarctions, crises (painful, sequestrations, aplastic), cholelithiasis, chest syndrome, chronic hemolysis, cardiac problems, kidney disease, liver disease, lung problems, erection (priapism), eye problems (retinopathy) TREATMENT: basic treatment of sickle cell crises includes: bed rest oral and intravenous fluids oxygen-to reduce pain and prevent complications pain relief medications avoid the following: dehydration drop in oxygen or change in air pressure (sometimes occur during airplane travel) fever infection avoid overexertion and stress avoid temperature extremes daily folic acid supplements, to build new RBC provide plenty of water to prevent dehydration genetic counseling get plenty of rest ARTERIOSCLEROSIS OBLITERANS - a chronic occlusive arterial disease that may affect the abdominal aorta or the legs. The obstruction to blood flow with resultant inschemia usually affects the femoral, popliteal, aortic and iliac arteries -occurs most often in men ages 50-60 -caused by atherosclerosis risk factor: cigarette smoking

B.MEDICAL MANAGEMENT 1. DRUG THERAPY -VASODILATORS: papaverine, isoxsuprine HCl (vasodilan), nylidrin HCl (arlidin), to improve arterial circulation; effectiveness questionable -analgesics to relieve ischemic pain 2.) SURGERY: bypass grafting, balloon catheter dilation, lumbar sympathectomy ( to inc. Bloodflow), amputation maybe necessary C. ASSESSMENT FINDINGS 1.) Pain both intermittent claudication and rest pain, numbness or tingling of the toes 2.) pallor after 1-2 mins of elevating feet and dependent hyperemia/rubor; diminished or absent dorsalis pedis, posterior tibial and femoral pulses, shiny, taut skin with hair loss on lower legs 3.) diagnostic tests -oscillometry may reveal decrease pulse volume -doppler, V/S reveals decrease blood flow through affected vessels -angiography reveals location and extent of obstructive process 4.) elevated serum triglycerides, sodium * administer med as ordered * assist with BUERGER-ALLEN exercise qid a.) client lies with legs elevated above heart for 2-3 mins b.) client sits on edge of bed with legs and feet and exercises feet and toes upward, downward, inward and outward- 3 mins. c.) client lies flat with legs at heart level for 5 mins. * assess for sensory function, protect client from injury THROMBOANGITIS OBLITERANS (BUERGER'S DISEASE) -acute inflammatory disorder affecting medium/smaller arteries and veins of the legs. -occurs as focal, obstructive process, results in occlusion of a vessel with subsequent development of collateral circulation -idiopathic -RISK FACTORS: men 25-40 and smokers ASSESSMENT FINDINGS 1.) intermittent claudication, sensibility to cold 2.)decreased/absent peripheral pulses (post tibial and dorsalis pedis) ulceration and gangrene (advanced) DX: same as atherosclerosis -prepare for symptoms 2.) provide client teaching and discharge planning -drug regimen, avoidance of trauma to affected disease RAYNAUDS PHENOMENON

-intermittent episode of arterial spasms most frequently involving fingers, most often affects women from teenage-40 factors: collagen disease (SLE RA), trauma (typing, playing piano) vasodilators: catecholamine-depleting antihypertensive drugs THROMBOPHLEBITIS -inflammation of the vessel wall with formation of a clot (thrombus); may affect superficial or deep veins -most frequent veins affected are the saphenous, femoral and popliteal -can result in damage to the surrounding tissues, ischemia and necrosis -risk factors: obesity, CHF, prolonged immobility, MI, pregnancy, oral contraceptives, trauma, sepsis, cigarette smoking, dehydration, anemias, surgery MED: ANTICOAGULATION THERAPY Heparin: blocks conversion of prothrombin to thrombin and reduces formation of thrombus side effects: spontaneous bleeding, ecchymoses, tissue irritation hypersensitivity: dermatitis, urticaria, pruritus, fever -other: transient hair loss, burning sensation of feet, bleeding complications surgery: vein ligation and stripping venous thrombectomy: removal of a clot ASSESSMENT FINDINGS: pain in the affected extremities superficial vein: tenderness, redness deep vein: swelling, + homan's sign venous distention of limb tenderness over involved pain doppler ultrasonography: impairment of blood flow ahead of thrombus venous pressure measurements: high in affected limb until collateral circulation is developed NURSING INTERVENTION provide bed rest, elevating involved extremities, apply continuous warm, moist soaks to decrease lympathic congestion a.) HEPARIN -monitor PTT, use of infusion pump to administer IV heparin -assess for bleeding, tenderness (hematuria,hematemesis, bleeding gums, epistaxis, melena) -have antidote (protamine sulfate) available b.)WARFARIN

-assess PT daily, advise client to withhold dose * monitor chest pain (possible pulmonary embolism) * provide client teaching and discharge planning a.) need to avoid standing, sitting for long periods; constrictive clothing, crossing legs at the knees, smoking and oral contraceptives b.) importance of adequate hydration c.) use of elastic stockings when ambulatory d.) importance of planned rest with elevation of feet HEAD INJURY HEAD INJURY can occur when -head and neck thrown violently>brain rebounds to the skull>brain may bleed, swell> increased ICP * whiplash injury TYPES OF HEAD INJURIES CONCUSSION-jarring injury to the brain, may feel dazed and may loss vision or balance for awhile; a violent jarring and shaking CONTUSION-bruise of the brain, bleeding may occur and can lead to swelling SKULL FRACTURE- when the skull cracks and sometimes cause buts to the brain HEMATOMA-bleeding in the brain that collects and clots -tumor-increases volume of brain tissue *MONROE-KELLY HYPOTHESIS -if any of contents would increase in terms of volume would increase ICP pressure TRIAGE ER/clinical setting-deal with clients who need help first; most critical state Community- deal with clients with greater survival -head injury can be classified as either closed or penetrating CLOSED HEAD INJURY-the head sustains a blunt force by striking against an object PENETRATING HEAD INJURIES- a high velocity object breaks through the skull and enters the brain INDICATIONS OF HEAD INJURY scalp wound fracture swelling, bruising nasal discharge loss of consciousness stiff neck

-head injuries can range from a minor bump on the head to a devastating brain injury COMMON CAUSES: -traffic accidents -falls -physical assault -accidents at home, work, outdoors or while playing sports SUBDURAL HEMATOMA HEAD INJURY > BLOOD LEAKS FROM DAMAGED BLOOD VESSELS> INCREASED IN ICP> DAMAGE TO BRAIN TISSUE> BRAIN HERNIATION CSF LEAK HEAD TRAUMA>TEAR IN THE DURA> CSF LEAK ------EMERGENCY SITUATION!!! BRAIN HERNIATION INCREASED ICP (headache, decreased level of LOC, irritable, lethargy) > DISPLACEMENT OF BRAIN TISSUE > PROGRESSIVE BRAIN TISSUE DETERIORATION SYMPTOMS: -stiff neck/vomiting -inability to move one or more limbs -pupil changes -inability to hear, see, taste, smell -Loss of consciousness, confusion, drowsiness -low breathing rate/ drop in BP -convulsions, fracture in the skull or face -facial bruising, swelling at the site of the injury or scalp wound -fluid damage from nose, mouth or ears (maybe clear or bloody) -severe headache -initial improvement followed by worsening symptoms -irritability(especially in children) -personality changes or unusual behavior -restlessness, clumsiness, lack of coordination -slurred speech/ blurred vision If there is CSF leak- immobilized, dont move head and neck Get medical help immediately if the person: -becomes unusually drowsy -develops a severe headache or stiff neck -vomits more than once (projectile-change in CSF) -loses consciousness

-behaves abnormally For moderate-severe head injury ASSESSMENT -check patients airway, breathing and circulation; if necessary, begin rescue breathing and CPR -If persons breathing and HR are normal but person is unconscious, treat as if there is a spinal injury -stabilize the head and neck by placing hands on both sides of head, keeping the head in line with spine and preventing movement; wait for medical help -stop any bleeding by firmly pressing a clean cloth on the wound. If the injury is serious be careful not to move persons head. If blood soaks through cloth, do not remove. -if you suspect a skull fracture, do not apply direct pressure to the bleeding site and do not remove any debris from wound. Cover the wound with sterile gauze dressing -if the person is vomiting, roll the head, neck and body as one unit to prevent choking, this still protect the spine which you must always assume as injured MILD HEAD INJURY -no specific treatment -critical= 24 hours= closely watch the person for any concerning symptoms over the next 24 hours -symptoms of a serious injury can be developed -while person is sleeping wake every 2-3 hours DO NOT.. -wash a head wound that is deep/bleeding a lot -remove any object sticking out of a wound -move the person unless absolutely necessary -shake the person unless if he/she seems dazed -remove a helmet if you suspect a serious head injury -drink alcohol within 48 hours of a serious head injury SYMPTOMS Progressive loss of consciousness Coma Irregular breathing Respiratory arrest (no breathing) Irregular pulse -cardiac arrest (no pulse) Loss of all brainstem reflexes (blink gag, pupillary reaction to light) SIGNS AND TEST NEUROLOGIC EXAM- would show impaired LOC; patient would show inability to breathe consistently and heart rhythms would be irregular TREATMENT: -brain herniation is a medical emergency

-the goal of treatment is to save patients life -to help revise/ prevent a brain herniation, the medical team will treat increased swelling and pressure in the brain Can be accomplished by: CORTICOSTEROIDS: dexamethasone, especially when tumor is involved MANNITOL/OTHER DIURETICS -a drain placed into the brain to drain off fluid in the case of a mechanical obstruction causing herniation -removing the blood if a massive hemmorhage is present and causing herniation, although the outlook in these case is poor -placing a tube in the airway (endotracheal intubation) and mechanically ventilating (forced breathing) at a rapid rate to reduce the levels of carbon dioxide (CO2) in the blood. EXPECTATIONS (PROGNOSIS) -once a herniation in the brains temporal lobe/ cerebellum occurs, death is often inevitable -herniation of other areas of the brain has a more variable outlook COMPLICATIONS: -permanent and significant neurologic problems -brain death INCREASED ICP - Increased in normal brain pressure can be due to an increase in CSF pressure COMMON CAUSES: -severe head injury -hydrocephalus -brain tumor - encephalitis -subdural hematoma -hypertensive brain hemorrhage -intraventricular brain hemorrhage -meningitis -status epilepticus -stroke INFANTS: -bulging fontanelle -seperated sutures -lethargy -vomiting OLDER CHILDREN AND ADULTS: -vomiting

-headache -seizures -changes in behavior -decreased LOC -lethargy -neurologic deficits LATE SIGN: function of brainstem EARLY SIGN: changes in LOC SIGNS AND TESTS: MRI/CT SCAN is often used to determine the cause and confirm the diagnosis ICP may be measured during SPINAL TAP (LUMBAR PUNCTURE) ICP is measured in millimeters of mercury (mmHg) CVP- millimeter of water (mmH2O) (compression of vital brain and structures) COMPLICATIONS: -reversible neurologic problem -permanent neurologic problem -seizures -death GCS-neurological scale which aims to give a reliable, objective way of recording conscious state of a person (limited applicability to children-especially below the age of 36 months) RANCHO LOS AMIGOS SCALE-used to assess the recovery of brain injury of patient CVA It is a non traumatic brain injury caused by occlussion or rupture of cerebral blood vessel that results in sudden neurological deficit TYPES Ischemic- most common 80% Hemorrhagic- 20%

DEFINITION OF TERMS: TIA- TRANSIENT ISCHEMIC ATTACKS -neurologic deficits resolve within 24 hours RIND-REVERSIBLE ISCHEMIC NEUROLOGIC DEFICIT -not later than 72 hours STROKE IN EVOLUTION-progressive loss of neurologic functioning; poor prognosis

RISK FACTORS OF CVA: HYPERTENSION-most important risk factor HEART DISEASE- important risk factor ATRIAL FIBRILATION AND VALVULAR HEART DISEASE- increases risk of cerebral infarction because of presence of cerebral emboli DM- independent risk factor that doubles the risk of stroke- if increases the risk of ischemic stroke to 3-6 times. The prevalence of diabetes among stroke survivors is 20% HYPERLIPIDEMIA-poses only small additional risk for strokes mainly for individuals younger at age of 55 Increased in blood viscocity hematocrit and serum fibrinogen CEREBRAL BLOOD FLOW NORMAL: 50-60ml/100 g/min REVERSIBLE: 20 ml/100 g/min IRREVERSIBLE: 10 ml/100g/min STROKE PREVENTION ANTIPLATELET THERAPY- aspirin is the most frequently prescribe antiplatelet agent -Aspirin achieves a significant anti-platelet effect at fairly low serum concentrations ANTICOAGULATION-the use of warfarin anticoagulation for primary stroke prevention SIGNS AND SYMPTOMS - Decreased LOC, cognitive changes, weakness/ paralysis of any body area - Speech deficits - DYSPHONIA-impairment in ability to produce sound - DYSARTHRIA-disorder of speech, inability to produce spoken words - APHASIA-partial/total loss of ability to communicate verbally or written words - Urinary /bowel incontinence - Dysphagia - Partial hemianopsia SURGERY: CAROTID ENDARCTERCTOMY MANAGEMENT: -maintain peak physical health -structuring the environment -promoting socialization -promoting independent functioning -preserving the family unit SPINAL CORD INJURY damage to the spinal cord DIVISIONS:

COMPLETE: means that there is no function (no sensation or voluntary movement) below the level of the injury INCOMPLETE: there is some function below the level of injury. A person may be able to feel parts of the body that cannot be moved. CERVICAL NECK INJURIES-usually result in quadriplegia -injuries above the C-4 level may require a ventilation for the person to breath C-5 INJURIES- often result in shoulder and bicep control but no control at wrist or hand C-6 INJURIES-generally yield wrist control but no hand function -loss of sensation and motor functioning VERY HIGH INJURIES (C1-C2) can result in a loss of many involuntary function including the ability to breath; necessitating breathing aids such as mechanical ventilator SCALE OF MOTOR STRENGTH IN SPINAL CORD INJURY 0- No contraction/ no movement 1- Minimal movement 2- Active movement but not against gravity 3- Active movement against gravity 4- Active movement against resistance 5- Active movement against full resistance TYPES OF SPINAL CORD PARALYSIS PARESIS- weakness MONOPLEGIA-paralysis of 1 limb DIPLEGIA-paralysis of both upper or lower limbs PARAPLEGIA-paralysis of both lower limbs HEMIPLEGIA- paralysis of upper limb, torso and lower leg on one side of the body QUADRIPLEGIA-paralysis of all 4 limbs SPINAL CORD PARALYSIS LEVELS C1-C3- all daily function must be totally assisted; breathing is dependent on a ventilator, motorized wheelchair controlled by sip and puff or chin movements is required C4-same as C1-C3 except breathing can be done without a ventilator C5-good head, neck, shoulder movements, as well as elbow flexion; electric wheelchair or manual for short distances C6-wrist extension movements are good assistance needed for dressing and transitions from bed to chair and car may also need assistance C7-C8-all hand movements, ability to dress, eat, drive, do transfers and do upper body washes T1-T4-(paraplegia) normal communication skills; help may only be needed for heavy household work/loading wheelchair into car T5-T9- manual wheelchair for everyday living. Independent for personal care T10-L1-partial paralysis of lower body

L2-S5-some knee, hip and foot movements with assistance on aids. Only heavy home maintenance and hard cleaning will need assistance SEIZURES 1.) Normal brain function requires an orderly, organized, coordinated discharge of electrical impulses 2.) Electrical impulses enable Seizures: transient occurrence of clinical symptoms due to abnormal neuronal behavior Convulsions: seizures with prominent body movement Non-convulsive seizures: seizures with minimal or no body movement Epilepsy: brain disorder with an enduring predisposition to generate epileptic seizures Epilepsy syndromes: groups of epileptic patterns of varying cause but similar course and response to treatment EPILEPSY -second most common neurological disorder in USA Prevalence: - 1 % (2.5 million) Incidence: 125 000-180 000 new cases per year Total annual epilepsy associated costs: $ 125 billion Occurs at all ages GENERALIZED TONIC CLONIC SEIZURES EMERGENCY CASE!! (SHOULD BE PRIORITIZE THAN STATUS EPILEPTICUS) -loss of consciousness -fall, cry -muscular rigidity (tonic) -rhythmic jerking (clonic) -respiration inhibited -tongue bite/incontinence/ injury can occur -usually last 1-3 minutes STATUS EPIPLEPTICUS (also need immediate attention) -two or more seizure without recovery of consciousness in between -single seizure greater than 20-30 min (operationally greater than 5 mins)

Types: -generalized convulsive -non convulsive -simple partial A sudden involuntary, time-limited alteration in behavior, motor activity, autonomic function, consciousness or sensation, accompanied by an abnormal electrical discharge

EEG- recording of the brains electrical activity; 20 small adhesive electrodes TYPES OF SEIZURES PRIMARY GENERALIZED SEIZURE -begins with a widespread electrical discharge -involves both sides of the brain at once -hereditary factors are important PRIMARY GENERALIZED SEIZURE 1.) Absence seizure -brief episodes of staring -most common movement are eye blinks 2.) Atypical absent seizure - unusual or not typical -eye blinking/slight jerking 3.) Monoclonic seizures -very brief jerks, last only for 2-3 seconds -seizures usually cause abnormal movements on both sides of the body at the same time 4.) Atonic seizures -atonic means without tone -muscles suddenly lose strength -eyelids may drop, the head may nod 5.) Tonic seizures 6.) Clonic seizures SEIZURES HAVE BEGINNING, MIDDLE AND END BEGINNING -this stage can be said as warning or aura -sometimes individual is not aware o such aura -middle stage-aura followed by symptoms MIDDLE -aura may convert into convulsions -complex partial seizure END Transition from seizure back to normal state Post-ictal period Recovery period of brain Lasts from seconds to minutes to hours If a person has a convulsion, level of awareness gradually improves during the post-ictal period

EARLY SYMPTOMS *SENSORY/THOUGHTS -dejavu -jamais vu -smell -sound -taste -visual loss/blurring -racing thoughts -strange feelings -tingling feeling * EMOTIONAL -fear/panic -pleasant feeling *PHYSICAL -dizziness -headache -lightheadedness -nausea -numbness NO WARNINGS sometimes seizures come with no warnings MIDDLE SEIZURE SYMPTOMS -black out -confusion -deafness -electric shock feeling - loss of consciousness -smell -spacing out -foot stomping -out of body experience -visual loss/blurring -fear/panic -chewing movement -convulsion -eyes rolling up -falling down -hand waving -inability to move POST-ICTAL STATE THOUGHT -memory loss -writing difficulty -confusion

-depression and sadness -fear -frustration -pain -thirst -urge to urinate/defecate -shame/embarassment -bruising -difficulty talking -injuries -sleeping -exhaustion -headache -nausea -weakness DRUGS USED TO TREAT SEIZURE ACETAZOLAMIDE- absence seizures when other anticonvulsants are ineffective Side effect: kidney stones and chemical imbalance in blood CARABAMAZEPINE-generalized seizures, partial seizures Side effect: a low white blood cell count; granulocytopenia- production of too few blood cells (aplastic anemia w/c can be fatal disorder), a low platelet count (thrombocytopenia), digestive upset, inability to articulate words, lethargy, dizzines and visual disturbances CLONAZEPAM-atonic seizures atypical absence seizures, infantile spasms, myoclonic seizures Side effect: drowsiness, abnormal behavior, loss of coordination and loss of effectiveness of the drug after 1-6 months DIVALPROEX-absence seizures, febrile seizures, generalized tonic-clonic seizures, infantile spasms, juvenile myoclonic, epilepsy, myoclonic seizures Side effect: nausea, vomiting, abdominal pain, diarrhea, temporary drowsiness, dizziness, shaking (tremor), reversible hair loss, weight gain and liver damage HOME CARE/COMMUNITY SETTING -stay with person until recovery or you have professional medical help -monitor pulse, rate of breathing and BP -do not give the person anything by mouth until convulsions have stopped and the person is full awake and alert -do not move the person unless he/she is in danger or near something hazardous -do not place anything including your fingers between the persons teeth, you can break persons teeth, if you do so. DIAGNOSTIC TESTS: -blood tests -CT SCAN/MRI of brain -EEG -lumbar puncture PRECAUTIONS:

-people with uncontrolled seizures should not drive -drinking should be avoided -medicines should be taken regularly -avoid activities such as climbing to high places, biking and swimming -use of sharp instruments such as knife should be avoided * * * * Seizure is a life threatening disease No specific way to prevent seizures But it is curable if instructions are followed Good habits may help to control seizures

EPILEPSY has no cure -sleep deprivation and poor diet must be avoided -good sleep habits, stress reduction, proper exercise and sound nutrition may help -use of helmets to avoid head injury -have faith in yourself and seizure is curable -green leafy vegetables stabilizes neuronal activities ENDOCRINE DISORDERS SIADH: SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE -hypersecretion of ADH SIGNS AND SYMPTOMS: Signs of fluid overload, changes in LOC and mental status, weight gain, hypertension, tachycardia, hyponatremia -Monitor I&O and daily weight; monitor fluid and electrolytes -restrict fluids as prescribed; administer diuretics, monitor IV fluids carefully MEDS: DEMECLOCYCLINE (declomycin) inhibits ADH induced water reabsorption and produces water diuresis DIABETES INSIPIDUS -hyposecretion of ADH and deficiency of vasopressin SIGNS& SYMPTOMS: polyuria of 4-24L/day; polydipsia; dehydration, dec. skin turgor, dry mucus membranes, inability to concentrate urine, dec. specific urine gravity o 1.004 or less (main indicator of DI), fatigue, postural hypotension, headache INOTROPIC-facilitates power of muscles to contract CHROMOTHROPIC-heart rate, slow and fast beating of heart DROMOTHROPIC-combination of the 2 -provision of safe environment especially with decreased LOC, monitor I&O with specific gravity -wear medic alert bracelet

MEDS: vasopressin tannate (pitressin tannate), desmopressin acetate (DDAVP, stimate) Lypressin (diapid) -enhances reabsorption of water in the kidneys promoting antidiuretic effect and regulates fluid balance -weight monitoring needed! ADVERSE REACTION: hypertension, nasal congestion DO NOT WAIT FOR PULMONARY EDEMA AND CHANGES IN LOC! DISORDERS OF ADRENAL GLANDS -hyposecretion of the adrenal cortex hormones ASSESSMENT: SUBJ: muscle weakness, fatigue, lethargy, dizziness, fainting, nausea,abdominal pain and cramps OBJ: V/S dec. BP, orthostatic hypotension; PULSE: increase, collapsing, irregular SUBNORMAL TEMPERATURE: critical, signifies vascular collapse and may resolve to shock -weight loss, vomiting, diarrhea, tremors SKIN: poor turgor, excessive pigmentation (bronze tone) ,hyponatremia, hypoglycemia, hyperkalemia SIGNS AND SYMPTOMS: Bronze pigmentation of skin Changes in distribution of body hair GI disturbances Weakness Hypoglycemia Postural hypotension Weight loss ADRENAL CRISIS: profound fatigue, dehydration, vascular collapse, renal shutdown, dec. serum sodium, inc. serum potassium MANAGEMENT: 1.) Decrease stress: provide quiet environment and appropriate schedule 2.) Promote adequate nutrition Diet: acute phase: high sodium ; non acute phase: high carbohydrates and protein Fluids: force to balance fluid, monitor I&O, weigh daily Administer lifelong exogenous replacement therapy as ordered: glucocorticosteroids (prednisone, hydrocortisone) ; mineralocorticoids ADDISONIAN CRISIS -life threathening disorder caused by acute adrenal insufficieny precipitated by stress, infection, trauma, surgery -may cause hyponatremia, hypoglycemia, hyperkalemia and shock -given glucocorticoids IV

-severe generalized muscle weakness, severe hypotension, hypovolemia shock (vascular collapse) -check BP and electrolyte levels -strict bed rest in quiet environment and protect from infection CUSHINGS SYNDROME -hypersecretion of corticoids ASSESSMENT: SUBJ: -headache, backache, weakness, dec. work capacity OBJ: -hypertension, weight gain, pitting edema -characteristics fat deposits, truncal and cervical obesity (buffalo hump) -pendulous abdomen, purple striae, easy bruising -moon face, acne, hyperpigmentation, impotence -virilization in women, hirsutism, breast atrophy, amenorrhea -pathologic fractures, dec. height -slow wound healing -personality changes -inc. susceptibility to infection -hyperglycemia -CNS irritability -Na and fluid retention -thin extremities -GI distress: inc. acid MALES: gynecomastia, fat deposits on back, osteoporosis FEMALES: hirsutism, amenorrhea, thin skin, purple striae, bruises and petechiae NURSING MANAGEMENT: -promote comfort: protect from trauma -prevent complications: monitor fluid balance, glucose metabolism, hypertension, infection -health teachings: diet: inc protein, potassium, dec. calories and Na MEDS: Cytoxic agents: aminoglutenthimide (cytaden), trilostane (modrastane), mitotane (lysodren) dec. cortisol production Replacement hormones as needed Signs and symptoms of progression of disease hyperactivity of adrenal gland Prepare client for adrenalectomy

HYPERALDOSTERONISM (CONNS SYNDROME)

-hypersecretion of aldosterone from the adrenal cortex of adrenal gland commonly caused by adenoma SIGNS AND SYMPTOMS: hypertension, hypokalemia, headache, polydipsia, polyuria, hypernatremia, low urine specific gravity Monitor I&O and administer spirinolactone (aldactone) and Potassium supplements and maintain Sodium secretion -administer antihypertensives as prescribed -wear medic alert bracelet -usually will be undergoing adrenalectomy; administer glucocorticoids pre and post op PHEOCHROMOCYTOPENIA -cathecolamine producing tumor usually found in the adrenal gland -causes hypersecretion of epinephrine and norepinephrine by the adrenal medulla Complications: hypertensive, retinopathy, CVA and CHF Signs and symptoms: Hypertension, severe heart ailment, palpitations, pain in chest/abdomen, hyperglycemia and glycosuria, profuse sweating, nausea and vomiting, dilated pupils, tachycardia, cold extremities -monitor for hypertensive crisis and avoid stimuli which triggers it such as: Increase abdominal pressure, vigorous abdominal palpitation and micturation -instruct patient not to smoke, drink cola, coffee or tea -monitor blood glucose and urine for glucose and acetone DISORDERS OF THE THYROID GLAND MYXEDEMA COMA-rare but serious which result from persistently low thyroid hormone precipitated by acute illness, rapid withdrawal of thyroid meds, use of sedatives and narcotics Signs & symptoms: hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, respiratory failure, stupor, coma and death Patent airway Keep patient warm and check VS frequently Administer IV fluids and levothyroxine Na (synthroid) Give IV glucose and corticosteroids

THYROID STORM- acute and life threatening condition in uncontrolled hyperthyroidism RISK FACTORS: infection, surgery, beginning labor, to give birth, taking inadequate antithyroid medications before thyroidectomy Total thyroidectomy: grave cardiac complication SIGNS AND SYMPTOMS: feverm tachycardia, hypotension, irritability, respiratory distress, apprehension, irritability, agitation, restlessness, confusion, seizures

MEDS: PTU, sodium iodide IV, lugols solution, propanolol, aspirin, steroid, diuretics THYROIDECTOMY removal of thyroid gland and performed in persistent hyperthyroidism PRE-OPERATIVE CARE -asesss VS, weight, electrolyte and glucose level -take DBE and coughing as well as how to support neck in post-op period when coughing and moving POST-OP CARE -monitor for respiratory distress and have tracheostomy -set oxygen and suction machine -maintain semi fowlers position to dec. edema -immobilized head with pillows/sandbags; prevent flexion and hyperextension of neck -check surgical site for edema and bleeding -limit client from talking and assess for hoarseness -assess for laryngeal nerve damage, high pitched voice, stridor, dysphagia, dysphonia and restlessness -monitor for signs of hypocalcemia and tetany and have calcium -calcium gluconate THYROID HORMONES LEVOTHYROXINE -controls the metabolic rate of tissues and accelerates heat production and oxygen consumption -for hypothyroidism, myxedema and cretinism (cramps, diarrhea, nervousness, tremors, hypertension) HYPOPARATHYROID CRISIS-acute loss of PPH DANGER SIGNS OF HYPOCALCEMIA -positive chvosteks sign -positive trosseaus sign Administer: calcium supplements, calciferol, phosphate binders Avoid precipitating stimulus such as bright lights and noise-may lead to seizure Bedside: tracheostomy set due to laryngospasms Hormonal replacement therapy-lifetime DM II Type 1: no insulin production; secretion of autoimmune destruction of beta cells from pancreas Type 2: dec. insulin production; dec. insulin actions, inc. insulin resistance HYPEROSMOLAR HYPERGLYCEMIC NON KETOTIC SYNDROME Intercurrent illness inc. demand for insulin, polyuria, severe dehydration

DKA (DIABETIC KETOACIDOSIS)- post cardiac arrest caused by arrythmia -usually as type 1 disorder -due to deficieny of insulin -usually caused by non adherence to insulin regimen, concurrent illness or infection Main clinical features: hyperglycemia, dehydration and electrolyte imbalance Glucose entering cells is decreased/reduced, liver produces and releases glucose, kidneys try to compensate by excreting glucose, H2O, electrolytes, inc. urination leads to dehydration and electrolyte loss, breakdown of fat into free fatty acids and glycerol, liver converts free fatty acids into ketones, accumulation of ketones is DKA LAB VALUES: GLUCOSE varies between 300-800 Severity does not depend on glucose Low serum bicarb- 0-15meq/L Low PH- 6.8-7.3 Low PCO2- 10-30 mmHg Reflects respiratory compensation (kussmaul respiration) for the metabolic acidosis Ketones in blood and urine Na and K can be low, normal or high depending on H2O loss from dehydration Inc. creatinin or BUN MANAGEMENT: -rehydration -normal saline at rapid rate (1L/hr) -initially .45% normal saline can be used for hypertension, hypernatremia or risk of CHF -may switch to D5W with glucose 300mg/dL or less to prevent sudden decrease -frequent VS and I&O monitoring -restore electrolyte- potassium -shift from intracellular to extracellular -monitor potassium frequently -factors reducing serum K rehydration MANAGEMENT: -reverse acidosis -administer insulin (inhibit fat breakdown) at slow but continuous rate Insulin drip continued until serum bicarb at least 15-18 meq/L or until patient can eat INSULIN: slows down fat metabolism HHNS Hyperosmolarity and hyperglycemia predominate with change of mental status; ketosis minimal or absent due to insulin resistance Persistent hyperglycemia-osmotic diuresus, loss of H2O and potassium

H2O shift from intracellular to extracellular Usually occurs in type 2 Glycosuria and dehydration--- hypernatremia SIGNS AND SYMPTOMS: hypertension, profound dehydration, tachycardia, change of mental status, diagnostic findings: glucose between 600-1200 mg/dL, osmolality greater than 350 mOsm/kg MANAGEMENT: -fluid replacement -correction of electrolyte imbalances -insulin administration -CVP or hemodynamic pressure monitoring -glucose fluid replacement -potassim added to IV fluids when urinary output is adequate -continuous EKG monitoring -frequent lab determination of potassium start with 0.9% or 0.45% NS HYPOGLYCEMIA -occurs in more than 90% of type 1 DM -also called insulin shock SYMPTOMS -cold sweats -blood glucose 45-60 mg/dL -palor -tremors -anxiety -tachycardia -palpitations -hunger -diaporesis -headache -deep sleep -confusion -visual disturbances -seizures -coma TREATMENT AND PREVENTION: Provide immediate replacement of glucose Glucagon 1mg IM D50 Milk and sandwich for those who are able to eat Prevention achieved with individual treatment

Blood glucose monitoring and education ACUTE RENAL FAILURE OLIGURIC PHASE: hypernatremia, hypocalcemia, hyperkalemia, hyperphosphatemia, hypermagnesemia, metabolic acidosis (any elevation in electrolytes causes acidosis) DIURETIC PHASE: hyponatremia, hypokalemia, hypovolemia, tremendous increased in CREA CONVALESCENT PHASE: normal urine volume, increase in LOC, BUN stable and normal NURSING CARE: -monitor fluid and electrolyte balance -monitor alteration in fluid volume -promote optimal nutritional status -prevent complications from impaired mobility -prevent fever and infection -support client /significant other and reduce/relieve anxiety DIALYSIS TYPES: PERITONEAL DIALYSIS: 1.) CAPD 2.) APD 2.1) CCPD HEMODIALYSIS: shunting of blood from the clients vascular system through an artificial dialysing dialyzate solution ARTERIOVENOUS SHUNT: both vessels are connected (arterial line-venous line) with use of graph ARTERIOVENOUS FISTULA (anastomosis of artery and vein shunting arterial blood into vein) NURSING CARE: BEFORE AND DURING HEMODIALYSIS -have client void -chart clients weight -assess vital signs before and 30 minutes during procedure -withhold antihypertensives, sedations and vasodilators prevent hypotensive episode(unless ordered otherwise) -ensure bed rest with frequent position changes for comfort CRRT: CONTINUOUS RENAL REPAIRMENT THERAPY -inform client that headache and nausea may occur -monitor closely for signs of bleeding -assess for complications -chart clients weight