Myocardial Infarction a.k.a.

Heart attack  Partial or complete occlusion of one or more of the coronary artery Pathophysiology:  Coronary artery occlusion deprives the myocardium (muscle of the heart) of O2 and blood. Subsequently, death of myocardial tissue occurs Etiology:  Thrombus (clot) occludes an artery in 90% of cases  Coronary artery spasm, hypoxia, inflammation from disease, severe exertions or stress in the presence of significant coronary artery disease, hemorrhage Manifestations:  Severe and persistent pain (pain does not subside with rest and nitrates)  Crushing or squeezing sensation in center of chest behind sternum  Pain may radiate or be localized to the:  Shoulder  Neck  Arm  Back  Teeth  Jaw  4th and 5th fingers of the left hand  Pain more than 20 min.  Nausea and vomiting  Sweating  Cold clammy skin  SOB  Pale or ashen color Note:  15-20% of MI are painless

ECG  To see the view and electrical impulses  Dysrhythmias  T-wave inversion  ST segment elevation  Pathologic, deep Q wave Diagnosing a MI:  To diagnose a MI, you need to go beyond looking at a rhythm strip and obtain a 12 lead ECG  Look for ST segment elevation The 12 lead ECG:  Sees the heart from 12 different views  Helps you see what is happening in different portion of the heart  The rhythm strip is only 1 of the 12 views

The 12 leads include:  3 Limb Leads  Lead I, II, III  3 Augmented Leads  aVR, aVL, aVF  6 Precordial Leads  V1-V6 Views of the heart:  Anterior= V1-V4  Inferior= Lead II, III, aVF  Lateral= Lead I, V5-V6, aVL

Normal ST segment

Normal T wave

ST Depression

Tall T wave

Concave ST Elevation

Inverted T wave

Convex ST Elevation

Flattened T wave

Age of MI:  Immediately before an MI starts

 Acute MI w/in hours after the MI starts

 Acute MI hours later

 Old MI weeks, months, years later

ECG changes:  Can also help in assessing the extent of damage Myocardial Ischemia  ST segment elevation and inverted T wave Myocardial Injury  ST segment elevation or depressed and peaked(tall) T wave Myocardial Infarction  ST segment elevation and inverted T wave  Q wave develops w/in 1-3 days after MI Sequence of ECG changes:  ST segment T wave Q wave  The same sequence in normalization Laboratory Test:  Acute MI  Elevated troponin I and troponin T w/in 1 hour of myocardial damage  Createnine Kinase MB CKMB increase 3-6 hours after the onset of MI  Chronic MI  Increase LDH  Increase WBC Zone of infarction  When necrosis is present in all 3 layers Penumbra  Is the hypoxic area of the injury around the infarction site that can return to normal if blood flow returns (reversible damage) Medical Treatment: Medical care should be instituted w/o delay  Hemodynamic and ECG monitoring  Morphine-DOC  Thrombolytic therapy w/in 3-12 hours (after Mi has occur)  Streptokinase- dissolves the clot - be careful in administering - slow IV push w/ the span of 30 min.  Administer O2  Antiarrhytmias- intravenous  Lidocaine- has mixed with epinephrine or adrenaline -only 2 % plain  Cardioversion  Correcting irregular rhythm of the heart by the use of Defibrilator at Lower Joules  ECG tracing- baseline  Antihypertensive drugs  Hydralazine- DOC - IV preparation

 

 

- monitor regulation Calcium Channel Blockers  To prevent reinfarction and ischemia but only in non Q wave infarctions  Also an antihypertensive drugs  Verapamil  Diltiazems Beta Adrenergic Blocker  Reduce the duration of ischemic pain and incidences of ventricular fibrillation  Decrease mortality  Metoproplol, Nadolol, Propranolol Analgesics  Reduce pulmonary congestion  Reduce myocardial O2 consumption  Morhine- check the V/S especially RR Nitroglycerin  Nitrates reduce ischemic pain by dilation of blood vessels and helps to lower BP Heparin  Anticoagulant (prevents a clot from forming)  Client is prone to hemorrhage/bleeding tendencies  WOF s/s of bleeding tendencies Warfarin  Oral anticoagulant  Prevents synthesis of clooting factors Antiplatelets  Aspirin  Dipyridamole Argatroban  Direct thrombin inhibitor  Helps prevent formation of clots  Given IV Alteplase  Thrombolytic drugs  Streptokinase, Urokinase, Tenecteplase  Administer as early as possible Diet Modification  Low Fa- Ca- Cho- N (low fat, calcium, cholesterol, sodium) Place on CBR w/o bathroom prriveledges  Provide a commode or bed pan

Nursing diagnosis:       Alteration in tissue perfusion (cardiac) Pain Potential alteration in cardiac output (decreased) Activity intolerance Knowledge deficit Anxiety

Nursing Interventions: Monitor  Cardiovascular  Look for changes or stability of pulse  Heart sounds

 Respirations  Changes in respiration  Fluid in lung fields (*pulmonary congestion- fluid stay in the lungs)  SOB  V/S  Check for changes in BP (narrowing of pulse pressure)  Pulse quality or strength (apical and radical pulse)  Peripheral pulses  Pulse oximetry  95-100 O2 saturation of tissues  ABG  O2 saturation in the blood Health Teachings:      Diet Medications Limit activities Stress reduction BST s  Avoid FUSHIAE  Fatigue  Unfamiliar partners  Stress  Heavy meals  Intake of  Alcohol  Extreme temperature Must be able to climb 2 flight of stairs before resuming sexual activities Do not take Viagra (Sildenafdil), it dilates blood vessel Assume less fatiguing position Comfortable environment Best in the morning

    

Prognosis:  Mortality rate is 30-40% with over half of the deaths occurring w/in the 1st hour after onset of symptoms and prior to the arrival at an acute care facility Angina pectoris  Transient chest pain or feeling of constriction Pathophysiology:  Deficiency of O2 to the heart muscle results in pain Etiology:         Coronary artery disease- #1 cause of death HTN CHF Spasm usually precipitated by exercise Stress Exposure to cold (12am-8am) Large meal- meat Symptoms usually last 1-4 minutes less than 20 minutes

Manifestations:          Types:  Stable angina  Predictable severity  Relieved by rest or nitrates  Unstable angina/ crescendo  Occurs at rest, minimal exertion w/ increasing severity of pain  Rest and nitroglycerine do not relieve the attacks  Similar manifestations to MI but NO ECG changes  Intractable or Refractory  Severe incapacitating pain  Prinzmental angina  Not caused by atherosclerotic plaque but by coronary spasm  Occurs during rest and usually at night and early morning  May show ST segment elevation  Silent ischemia  No symptoms  Sign of ischemia on the ECG during a stress test  stress test- test use to try to reveal cardiac problem that usually occurs when doing activity  Nocturnal  Possibly associated w/ rapid eye movement (REM) during sleep  Angina Decubitus  Occurs when client reclines and is relieved when client sits or stands up  Post Infarction angina  Occurs after MI  Residual ischemia may cause episode of angina Medical Treatment:          O2 Vasodilators (nitrates) Beta adrenergic blockers Calcium channel blockers Rest Reduction of stress Coronary Anteriography/Angiography- see the area of occlusion Coronary Artery Stent- balloon Coronary Artery bypass Graph (CABG)-replace artery of the heart coming from leg or arm Pain last 3-5 minutes or less than 20 minutes Feeling of constriction or tightness or heath burn Typically radiates to the left shoulder and down the left arm, back or jaw or rarely to abdomen Mimics MI but does not cause cellular death Anxiety Occurs after exertion, excitement or exposure to cold due to increase O2 demands Sweating Tachycardia DOB and SOB

Nursing Diagnosis:  Decrease (cardiac) tissue perfusion  Pain  Activity intolerance

 Knowledge deficit  Anxiety Nursing Care:  Assess and record details of attack  Provide immediate rest and quiet environment during attack  Monitor effects of medical treatment  Bleeding  Eliminate precipitating factors  Provide education  Instruct the patient to seek immediate medical attention of 3 doses of nitroglycerine at 5 minutes intervals Prognosis:  Varies with proper rest and care, recovery is possible, but prognosis may be grave

Congestive Heart Failure  Failure of the cardiac muscle to maintain sufficient CO and tissue perfusion Pathophysiology:  The left ventricle loses its ability to eject blood into the systemic circulation, resulting in a large volume of blood remaining in the left ventricle after systole. Backup of blood may progress to the left atrium then to the pulmonary system (left sided heart failure), then to the right ventricle and right atrium and finally into the systemic circulation (right sided heart failure) Etiology:  Congenital defects, HTN, cardiac valvular/peripheral vascular disease  Damage to cardiac tissue/MI, rheumatic fever, fluid overload, severe anemia, obstructive lung disease  Endocrine disorders, sepsis or electrolyte imbalances Manifestations:  Dependent upon the degree of left vs. right heart failure and the compensatory mechanism Left sided heart failure  Left ventricular hypertrophy  Tachycardia <100 bpm-CO is not sufficient  Dysrhytmias-ECG  Tachypnea  Orthopnea  Anxiety  Cyanosis- assess by checking finger nails (bluish), lips, tongue  Decrease BP and peripheral pulses  Crackles, wheezes  Decrease CO and index- check BP  Narrow pulse pressure- decrease CO  Assess Central venous Pressure  S3/S4 gallop, apical murmurs  S3- heard on the apex of the left ventricle, 4th ICS best heard when lying on the left side  Soft sound caused by vibration of the ventricular wall during rapid filling  S4- heard at the same location as S3 Right sided heart failure  Cardiomegaly (x-ray)  Dependent edema  Bounding pulse  Distended jugular vein  Oliguria  Dysrhytmias  Hepatomegaly  Splenomegaly  Increase central venous pressure  Catheter insert at arm  Normal CVP- 8-12mmphg  Altered liver function test 

 Caused by vibration of the valves and ventricular walls during the 2nd phase of ventricular filling when atria contracts  Murmers- turbulence caused by blood flow heard anywhere in the heart

Test Results:     B- type natriuretic peptides- elevated levels in CHF, produced when ventricles are stretched RCG may show ischemia T wave inversion CBC low hgb and hct Renalproblems CXR (LSHF)  Pulmonary congestion  Pleural effusion  cardiomegaly

CXR (RSHF)  Fluid in the lungs  Enlarged left ventricle (left ventricle hypertrophy)

Treatment:  Diuretics- oral or IV  Furosemide, metolazone, spironolactone  ACE inhibitors- decrease after load  Captopril  Betablockers- help to raise ejection fraction and decrease ventricular size  Inotrope- to strengthen myocardial contractility  Digoxin  Vasodilators- to reduce the preload, relieve dyspnea  Nitroprusside, nitroglycerin ointment  High fowlers  O2  Low Na diet Nursing Diagnosis:          Decrease CO Impaired gas exchange Fluid volume excess Potential deficit r/t diuretic use Activity intolerance Knowledge deficit Anxiety Potential for infection Impaired skin integrity r/t edema and poor tissue perfusion

Nursing care:        Monitor V/S Peripheral pulses Heat or lung sounds I and O Elevate HOB Assist with ADL Promote calm environment

 Calculate safety of digitalis dose  Monitor HR before administering digitalis  Monitor response to medications and therapy  Count pulse for a full minute prior to administration of digitalis- decisions to withhold digitalis are based on knowledge of age-appropriate pulse rate  Turn q 1-2 hours  Educate and provide emotional support Prognosis:  Varies greatly with etiology, severity, compliance and complicating factors  Many people live productive lives for decades following diagnosis  CHF in children usually resolves after correction of the underlying cause

Hypertension

For adults:  Pre HTN- 120-139 systolic; 80-99 diastolic  Stage 1 HTN- 140-159 systolic; 50-99 diastolic  Stage 2 HTN- 160 systolic; 100 diastolic Whichever reading is higher (systolic or diastolic) is used to classify BP Etiology:     Obesity Hereditary Lifestyle- diet Kidney problem

Pathophysiology:  Usually unknown (essential, primary/idiopathic HTN). Excess rennin may increase the production of angiotensin II, which raises BP. HTN may be caused by insulin resistance, structural cardiac/vascular defects/disease, pregnancy, obesity, cocaine (most common cause of young adult HTN, presentation to ER), sleep, apnea, thyroid/parathyroid disease, kidney disease, pheochromocytoma. Manifestations:  Initially essential HTN is usually asymptomatic except for elevation of BP  Occasionally headache  Late complication of uncontrolled HTN include manifestations of damage to eyes (retinopathy), kidneys, heart or brain Medical Treatment:  Lifestyle changes  Treatment and prevention of obesity and hyperlipidemia by increasing exercise and decreasing dietary calories, fat and sodium  Smoking cessation and moderation of alcohol consumption  Antihypertensive meds- usually more than 1 medication is needed 4 Steps plan:  Step 1  Lifestyle changes

      Step 2   

Reduce weight Low Na diet No smoking Reduce alcohol intake Reduce caffeine intake

Administer diuretics- to reduce circulating blood volume Beta Blockers- to lower HR Calcium channel blockers- to cause peripheral vasodilation Ex. Verapamil, diltiazem, nicardipine  Administer ACE inhibitors- to inhibit angiotensin aldosterone system, in DM ACE inhibitors also delay progression of renal disease Ex. Catopril, enalaprril, benazepril, quinapril  Step 3  Increase dosage of medications  Step 4  Multi drug is needed

Nursing Diagnosis:      Risk for decrease CO (vasoconstriction) Risk for sexual dysfunction (atherosclerosis/side effect of meds) Pain (headache) Knowledge deficit Impaired adjustment

Nursing Care:      Check BP @ q office visit or @ least once per shift when hospitalized Teach regarding healthy weight Exercise, diet Smoking cessation- interfere the effectivity of hypertensive drugs Alcohol moderation

Prognosis:     Excellent with BP controlled below 140/90 or 130/80 for those with DM or kidney failure Uncontrolled HTN may result in damage to eyes, kidneys, heart, brain These complications are called END IORGAN DAMAGE Heart failure and death are possible

Cerebro Vascular Accident  Occurrence of an ischemic or hemorrhagic lesions within the intracranial vasculature  Often called STROKE or APOPLEXY Pathophysiology:  Obstruction of the supply of O2 and nutrients to the brain, which results in varying degrees of cellular injury and neurologic dysfunction Etiology:  Thrombus  Embolism  Bleeding into a intracranial vessel

 Predisposing or causative factors includes atherosclerosis, HTN, and AV malformation Manifestation:      S/S of increase ICP- headache, altered LOC Papillary changes Seizures Sensori motor dysfunction Altered in speech, cognition or cranial nerve functions

Medical Treatment:         Airway maintenance ICP management Anticoagulation and thrombolytic therapy Vasodilators, diuretics, (mannitol,- osmotic diuretics) Dexamethasone Anticonvulasants possible surgery- craniotomy Early institution of rehabilitation therapy

Nursing Diagnosis:       Alteration in tissue perfusion (cerebral) Impaired physical mobility Impaired swallowing- prone to aspiration Impaired verbal communication Alteration in thought process Numerous psychosocial diagnosis

Nursing Care:        Maintain airway Monitor V/S and neurologic status frequently Evaluate effects of medical regimen Monitor I and O and nutritional status Turn q 1-2 hours Coordinate and support rehabilitative regimen Provide emotional support and patient & family education

Prognosis:  Varies from full recovery to persistent vegetative state or death depending on type, location and severity of the event as well as complicating factors

Neurologic Care Assessing the pupil Pupil size  Bilaterally equal and reactive  Unilateral, dilated (4mm), fixed and non reactive Findings  Normal  Occulomotor nerve damage  Brain stem compression  Increase ICP  Head trauma and subsequent subdural or epidural hematoma  Normal in some people  Severe midbrain damage

 Bilateral, dilated (4mm), fixed and non reactive

 Bilateral, midsized (2mm), fixed and non reactive  Unilateral, small (1.5 mm), non reactive  Bilateral, pinpoint (<1 mm), usually non reactive

    

Hypoxia Midbrain involvement Edema Hemorrhage Disruption of sympathetic nerve supply to the head (eg, trauma)  Hemorrhage  Blocked sympathetic impulses

Assessing DTR (deep Tendon Reflexes) General considerations:      Upper Limb: biceps, triceps, fingers Lower Limb: knees, ankles, plantar Always compare one side to the other Let hammer fall by gravity in most cases Don t keep hammering a patient if cant elicit it

Meningeal Irritation  Kernigs sign  Brudzinskis sigh Stages of Altered Arousal Stage  Confusion  Disorientation Manifestations  Loss of ability to think rapidly  Impaired judgment and decision making  Beginning loss of consciousness  Disorientation to time and place  Impaired memory  Lack of recognition of self (last to go)  Limited spontaneous movement or speech  Possible disorientation to time, place, person  Mild to moderate reduction in arousal  Limited responsiveness to environment  Ability to fall asleep easily in the absence of verbal or tactile stimulation from others  Minimum response to questions  Deep sleep  Arousable with difficulty (motor/verbal)  Withdrawing or grabbing response to stimulation  Lack of motor/verbal response to any stimulus  No response to deep pain

 Lethargy  Obtundation

 Stupor

 Coma

Glasgow Coma Scale Eye Opening  Spontaneous  To speech  To pain  None Motor  Obeys  Localizes  Withdraws

4 3 2 1 6 5 4

Open eyes spontaneously Open eyes to verbal command Open eyes to painful stimulus Doesn t open eyes Reacts to verbal command Identifies localize pain Flexes and withdraws from painful stimulus

   Verbal   

Abn. Flexion Abn. Extension None Oriented Confused Inappropriate words

3 2 1 5 4 3 2 1

Assumes a decorticate posture Assumes a decerebrate posture No response: flaccid Oriented and converses Oriented and confuse Replies randomly with incorrect words Moans and screams No response

 Incompensable  None

Decorticate:     Results from damage to one or both corticospinal tracts Arms are abducted and flexed Wrist and fingers flexed on the chest Legs are stiffly extended and internally rotated with plantar flexion of feet

Decerebrate:      Results from damage to the upper brain system Arms are adducted and extended Wrists pronated Fingers flexed Legs are stiffly extended with plantar flexion of the feet

Cerebral lesions Upper Motor Neuron Defects     Spastic weakness No significant muscle atrophy Hyperflexia Positive babinski reflex

Lower Motor Neuron Defects     Flaccid weakness Significant atrophy Hyperflexia Babinski reflex

Cerebral Angiography             Uses intra arterial contrast medium Femoral, carotid, brachial, vertebral arteries Consent Allergies- iodine Fast for 8-10 hours Local anesthesia Warmth and burning is felt during injection Void Test takes 2-4 hours Bed rest Apply firm pressure to site Hydrate

 Resume usual diet as ordered  Femoral site  Keep the legs straight @ the hip and check pulses, temperature, color, sensation  Carotid  WOF dysphagia, and neurovascular compromise and TIA (transient ischemic attack)  Brachial site  Keep arm straight @ the elbow and assess distal pulses Computed Tomography, Intracranial          Provides a series of tomograms, translated by computer Consent Caution on crackling sound Test lasts 15-30 minutes No to pregnant client Allergies to seafood Instruct not to move and stay still Children- enlargement of 3rd ventricle suggest hydrocephalus Provide psychological support

Electroencephalograpgy (EEG)          Reading portions of the brains electrical activity Consent Wash and dry hair No tranquilizers, barbiturates and other sedatives for 24-48 hours before the test Limit sleep to 4-5 hours prior No food restriction, no caffeinated drinks, chocolates, smoking 8 hours prior Last for about 1 hour Maintain safe environment Seizures precaution

Electromyography      Records electrical activity of skeletal muscle 2 rest Consent Check for meds that may alter result No NPO; 2-3 hours prior may stop smoking No coffee, cola, tea

Lumbar Puncture         Cerebrospinal fluid drawn from between 2 vertebrae Sampling of CSF No NPO Keep flat on bed 4-6 hours after Nay turn from sides Fluids Analgesics as ordered In increase ICP, CSF should be remove cautiously  Cerebral herniation  Medullary compression  Normal:  Pressure: 50-80 mmH2o  Appearance: clear, odorless  CHON: 15-45 mg/dl  Gamma Globulin: 3-12%

     Renal Failure

Glucose: 50-80 mg/dl Cell count: 0-5 WBC VDRL: non reactive Chloride: 118-130 mEq/l Gram stain: no organism

Evaluation Normal Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis

pH 7.35-7.45 <7.35 >7.45 <7.35 >7.45

paCO2 35-45 >45 <35 WNL WNL

HCO3 22-28 WNL WNL <22 >28

Respiratory Acidosis pH down CO2 up Respiratory alkalosis pH up CO2 down Metabolic acidosis pH down HCO3 down Metabolic Alkalosis pH up HCO3 up Causes: PRE RENAL Sudden and severe drop in BP (shock) Interruption of blood flow to the kidneys from severe injury INTRA RENAL Direct damage to the kidneys by inflammation, toxins, drugs, infections or reduced blood supply POST RENAL Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor or injuries

PRE RENAL Before the kidneys Occurs when impaired blood flow that leads to hypoperfusion of kidneys and decrease GFR

Causes: Hypovolemic stages (hemorrhage, dehydration) Impaired cardiac performance (cardiogenic shock, heart failure, decrease CO) Vasodilation (sepsis, anaphylaxis) Hypotension Bilateral obstruction in the renal arteries INTRA RENAL In the kidneys Occurs when there is parenchymal damage to the glomeruli and or kidney tubules Causes: Prolonged renal ischemia (myoglobulinuria, hemoglubinuria) Nephritic agents (NSAIS s, aminoglycoside, ATB, heavy meals, ACE inhibitors) Burns Crushing injuries Infection (acute pyelonephritis and acute glomerulonephritis) POST RENAL After the kidneys Occurs when there is obstruction in the distal part of the kidneys (urether, urinary bladder, and urethra) that often leads to rise in pressure in the kidney tubules and decrease GFR Causes: Calculi (stones) Tumor Benign prostatic hyperplasia Blood clots due to trauma, crushing injuries Phases of Acute Renal Failure Oliguria Polyuria Recovery period

Chronic Renal Failure Slow, usually insidious, loss of function, occurring over a period of months or year, becomes irreversible at some point Exact cause: unknown Risk Factors: Chronic glomerulonephritis DM Chronic illness or abuse of drugs Autoimmune d/o Genetic d/o Prolonged urinary obstruction Recurrent obstructive urinary calculi Multiple injuries CRF is an ARF which is left untreated or mismanaged Development of CRF: 1. Decrease Renal Reserve GFR- 40-50% BUN and Createnine is normal Symptomatic 2. Renal Insufficiency GFR 20-40% BUN and Createnine begins to rise Mild anemia and azotemia (urea in blood), itchy skin 3. Renal Failure GFR 10-20% BUN and Createnine rise Polyuria and nocturia 4. End Stage Renal Disease/ Uremia GFR <10% BUN and Createnine further increase Olioguria Signs of CHF Low Ca, high PO4, high K, low Na Fractures, joint pain Signs of renal failure Uremia Infertility, amenorrhea in women Manifestations: Neurologic d/o Fatigue, lethargy, sleep disturbances

Headache, seizures, encephalopathy, peripheral neuropathy including restlessness, leg syndrome, paresthesia Motor weakness, paralysis Hematologic d/o Anemia, bleeding tendency due to platelet dysfunction Cardiovascular d/o Pericarditis, HTN, CHF, CAD, myocardiopathy Pulmonary d/o Pleuritis, uremic lung (fector) Gastrointestinal d/o Anorexia, N/V, gastroenteritis, GI bleeding, peptic ulcer Metabolic Endocrine d/o Glucose intolerance, hyperlipidemia, hyperuricemia Malnutrition, sexual dysfunction and infertility Bone calcium Phosphorus d/o Hyperphosphatemia, hypocalcemia, tetani metastatic calcification Secondary to hyperthyroidism, 1.5 dehydroxy vitamin D deficiencies Osteomalecia, osteoporosis, osteosclerosis Skin d/o Pruritus, pigmentation, easy bruising, uremic frost Psychological d/o Depression, anxiety, denial, psychosis F & E d/o Hyponatremia, hyperkalemia, hypermagnesemia Metabolic acidosis, volume expansion or depletion Clinical Findings: .Decrease GFR Anuria (urine output < 50ml/day) Oliguria (urine output <400 ml/day) .Metabolic Acidosis Azotemia (retention of other metabolic waste products) Increase serum createnine, increase BUN .Anemia .Loss of urine diluting and concentrating abilities

.Uric acid retention occurs with GFR <40 ml/min .Hypocalcemia, hyperphosphatemia, hyperkalemia Management: Goals: Remove or reverse the causes Prevent or postpone progression Support or augment renal function Non pharmacologic: Control Na and fluids Nutritional support Fluid replacement or BT Limiting protein intake 44-56 g ATB for existing infections (pharmacologic) Special procedures: Catheterize Dialysis Peritoneal Dialysis Intermittent 8-12 H x 3-5x/week Ambulatory 3-5 passes/day Continuous cycling 3-7x during sleep Hemodialysis

Peritoneal dialysis Consider: Explaining procedure Monitor V/S plus weight Monitor or note for signs of infection Assess skin integrity Check tubing Positive pink tinged effluent or presence of small strings is normal Blood is normal for several days W/ ascites from other sites substitute a lower concentration of dialysate

Hemodialysis .AV fistulas Internal AVF Internal graft AVF Internal AV graft w/ external access device Complications: Thrombosis Local infections Aneurysms Steal syndrome Advantages: Hemodialysis Rapid removal of solutes and water Takes less time Personnel form procedure in a dialysis center Contact with health professionals at dialysis center maybe reassuring Can be used even if you have abdominal problem, no risk for peritonitis Contact with other people having dialysis may help Peritoneal dialysis Simple to perform Easier access No anticoagulation Fewer problem with hypotension or disequilibrium Less rigid dietary and fluid restrictions More flexibility in lifestyle and activity

Disadvantages: Hemodialysis Bulge from fistula or graft is obvious Risk for vascular complication, infection, distal ischemia, carpal tunnel syndrome, HTN, disequilibrium Strict fluid and diet Lifestyle cycle around dialysis appointments

Home hemodialysis requires space for the machine and training to use it Needs to be done at hospital or dialysis center Causes you to feel tired on the day of treatment Maybe complicated by blood clot formation in the dialysis access Peritoneal dialysis More time consuming Weight gain from glucose in dialysate Peritonitis is a potential complication Requires training and motivation Must be done everyday of the week May not be able to manage the technical aspects of the procedure or have someone who can help you

Complications: Hemodialysis Muscle cramps hemorrhage Air embolus Hemodynamic change Hypotension Cardiac dysrhythmia Anemia Peritoneal dialysis Protein loss Peritonitis Hyperglycemia Respiratory distress Bowel perforation

Contraindications: Hemodialysis Hemodyanamics Instability Peritoneal dialysis Extensive peritoneal adhesions

Peritoneal fibrosis Recent abdominal surgery

Assess: Hemodialys Vascular access route Peritoneal dialysis Intra abdominal catheter

Procedure: Hemodialysis Complex Specially trained RN required Peritoneal dialysis Simple Training is less complex than hemodialysis

Nursing implication: Hemodialysis Restrict diet Vascular access care Peritoneal dialysis Abdominal catheter care More flexible diet

Renal transplantation Procedure: ABO compatibility Histocompatibility WBC cross match Mixed lymphocyte culture and reaction Complications: HTN

Hyperkalemia w/ dysrhythmias CHF Pulmonary edema Pericarditis Pneumonia Accelerated atherosclerosis Bleeding Peptic ulcers Seizures, stupor, trauma *they make the patient to be immunocompromised in order to the transplanted kidney will not react Nsg. Process: Altered nutrition less than body requirement Altered skin integrity Fluid volume excess Altered cardiovascular tissue perfusion Altered tissue perfusion Home health teaching: Changes in lifestyle Adherence to medication Diet Follow up visits Effects to immunosupressants WOF: s/s of rejections