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Pericarditis and cardiac tamponade HIGH RISK ADULT HEART FAILURE The CARDIOVASCULAR SYSTEM Classification (New York Heart Association) Class 1 Ordinary physical activity does NOT cause chest pain and fatigue No pulmonary congestion Asymptomatic NO limitation of ADLs New York Heart Association Class 2 SLIGHT limitation of ADLs NO symptom at rest Symptom with INCREASED activity Basilar crackles and S3 New York Heart Association Class 3 Markedly limitation on ADLs Comfortable at rest BUT symptoms present in LESS than ordinary activity New York Heart Association Class 4 SYMPTOMS are present at rest Congestive heart Failure PATHOPHYSIOLOGY LEFT Ventricular pump failure back up of blood into the pulmonary veinsincreased pulmonary capillary pressurepulmonary congestion (edema)Pulmonary manifestations RIGHT ventricular failure blood pooling in the venous circulation increased hydrostatic pressure Peripheral edema RIGHT ventricular failureVenous blood poolingvenous congestion in the kidney, liver and GIT LEFT SIDED CHF Left sided ASSESSMENT FINDINGS 1. Dyspnea on exertion 2. PND 3. Orthopnea 4. Pulmonary crackles/rales 5. Cough with Pinkish, frothy sputum 6. Tachycardia 7. Cool extremities 8. Cyanosis 9. Decreased peripheral pulses 10. Fatigue 11. Oliguria 12. Signs of cerebral anoxia RIGHT SIDED CHF ASSESSMENT FINDINGS

The main functions of this system are: to transport oxygen, hormones and nutrients to the tissues and to transport waste products to the lungs and kidneys for excretion. Congestive Heart Failure Inability of the heart to pump sufficiently The heart is unable to maintain adequate circulation to meet the metabolic needs of the body This can happen acutely or chronically Acute in Myocardial infarction Chronic cardiomyopathies Classified according to the major ventricular dysfunctionLeft Ventricular failure Right ventricular failure The Heart: Physiology The PRELOAD is the degree of stretching of the heart muscle when it is filled-up with blood The AFTERLOAD is the resistance to which the heart must pump to eject the blood STROKE VOLUME Preload degree of stretch at the end of diastole Inc volume inc stretch inc preload greater contraction and inc stroke volume Increased by inc blood volume and exercise, dec by diuretics 2. Afterload amount of resistance to ejection of blood from ventricle Also called systemic vascular resistance Inverse relationship with stroke volume Etiology of CHF 1. CAD 2. Valvular heart diseases 3. Hypertension 4. MI 5. Cardiomyopathy 6. Lung diseases 7. Post-partum 1

1. Peripheral dependent, pitting edema 2. Weight gain 3. Distended neck vein 4. hepatomegaly 5. Ascites 6. Body weakness 7. Anorexia, nausea LABORATORY FINDINGS 1. CXR may reveal cardiomegaly 2. ECG may identify Cardiac hypertrophy 3. Echocardiogram may show hypokinetic heart 4. ABG and Pulse oximetry may show decreased O2 saturation 5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF Medical Management 1. Determination & elimination/control of underlying cause. 2. Drug therapy: digitalis, diuretics, vasodilators 3. Sodium restricted diet to decrease fluid retention NURSING INTERVENTIONS Digoxin Health teaching Oral tablet usually once a day Increases force of contraction DECREASES heart rate Assess: Apical pulse, ECG, hypokalemia Digoxin Health teaching Withhold the drug if apical pulse is less than 60 Note for early signs of toxicity: Provide potassium supplements Nursing intervention: 1. Monitor respiratory status and provide adequate ventilation 2. Provide physical & emotional rest 3. Increase cardiac output 4. Reduce/eliminate edema 5. Provide client teaching discharge Monitor respiratory status and provide adequate ventilation 1. Administer o2 therapy 2. Maintain client in semi-high fowlers position 3. Monitor ABGs 2

4. Assess breath sound, noting any changes 5. Provide physical & emotional rest Constantly assess level of anxiety 1. Maintain bed rest with limited activity 2. Maintain quiet, relaxed environment 3. Organized nursing care around rest period Increase cardiac output 1. Administer digitalis as ordered and monitor effect 2. Monitor ECG 3. administer vasodilators as ordered 4. Monitor vital sign Reduce/eliminate edema 1. Administer diuretics 2. Maintain accurate I&O 3. Assess for peripheral edema 4. Measure abdominal girth daily 5. Monitor electrolyte level 6. Monitor CVP 7. Provide sodium restricted diet as ordered 8. Provide meticulous skin care Nursing intervention: 1. Provide client teaching discharge 2. Need to monitor self daily for signs and symptoms of HF 3. Medication regimen 4. Prescribed dietary plan 5. Need to avoid fatigue and plan for rest period CARDIAC DYSRHYTHMIAS DYSRHYTHMIAS Disturbance in rhythms Abnormal conduction of electrical impulses that result in malfunction of heart muscle. The Cardiovascular System The CONDUCTING SYSTEM OF THE HEART Consists of the 1. SA node- the pacemaker 2. AV node- slowest conduction 3. Bundle of His branches into the Right and the Left bundle branch 4. Purkinje fibers- fastest conduction The Heart: Physiology The intrinsic conduction system causes the heart muscle to depolarize in one direction

The rate of depolarization is around 75 beats per minute The SA node sets the pace of the conduction This electrical activity is recorded by the Electrocardiogram (ECG) Sinus tachycardia Heart rate >100 bpm originating in the SA node Cause: Fever, apprehension, physical activity anemia, hyperthyroidism Drugs ( epinephrine, theophylline) Myocardial Ischemia , caffeine TX: correction of underlying cause, elimination of stimulant, sedatives, propranolol Sinus Bradycardia Slowed heart rate initiated by SA node HR <60 bpm Cause: Excessive vagal or decreased sympathetic tone MI , meningitis , myxedema, welltrained athletes Treatment may be necessary if the client is symptomatic Administer O2 as prescribed Cardiac output inadequate : Atropine, isoproterenol Drugs not effective : Pacemaker Atrial dysrhythmias Atrial flutter Atrial rate 250-400 bpm, ventricular rate 75-150 bpm saw-toothed pattern/shape ( F waves ) usually indicates the presence of organic heart disease Cause: Valvular disease, hypertension, cardiomyopathy, hyperthyroidism , moderate to heavy alcohol consumption. TX: correction of underlying problem, betablockers, calcium channel blocker, amniodarone,digitalis Atrial fibrillation Rapid disorganized and uncoordinated twitching of atrial musculature HR: 350-600 bpm Atria quiver lead to formation of thrombi No definitive P wave can be observed Different rates radial & apical 3

Rhythm: atrial & ventricular regularly irregular Cause: Rheumatic mitral stenosis Thyrotoxicosis, cardiomyopathy Hypertensive heart disease , CHD INTERVENTION: 1. Administer Oxygen 2. Administer anticoagulants as prescribed because of risk of thrombi 3. Administer cardiac medications as prescribed to control the ventricular rhythm and assist in the maintenance of cardiac output TX: digitalis, propranolol, Prepare client for cardioversion as prescribed Atrial fibrillation Atrial fibrillation, the P waves may be absent. There is no PR interval, and the QRS duration usually is normal and constant. In NSR, a P wave precedes each QRS complex, the rhythm is essentially regular, the PR interval is 0.12 to 0.20 second in duration, and the QRS interval is 0.06 to 0.10 second in duration. Bradycardia is a slowed heart rate, and tachycardia is a fast heart rate. Ventricular dysrhythmias Premature ventricular Complex ( PVC) Firing of an irritable pacemaker in the ventricles before the next normal sinus impulse reaches the AV node. PVCs occurs in repetitive patterns 1. Bigeminy- every other heartbeat 2. Trigeminy- every third beat 3. Quadrigeminy- every 4th heartbeat 4. Couplet 2 sequenstial PVCs Cause: Hypoxemia Hypokalemia PVCs are abnormal ectopic beats originating in the ventricles. They are characterized by an absence of P waves, presence of wide and bizarre QRS complexes, and a compensatory pause that follows the ectopy. PVCs are considered dangerous when they are frequent (more than 6/min),

occur in pairs or couplets, are multifocal (multiform), or fall on the T wave. In each of these instances, the clients cardiac rhythm is likely to degenerate into ventricular tachycardia or ventricular fibrillation, both of which are potentially deadly arrhythmias. Ventricular dysrhythmias INTERVENTION: 1. Notify physician if PVCs occur 2. Treatment of underlying cause 3. Evaluate O2 saturation- to assess hypoxemia 4. Administer O2 as prescribed 5. Evaluate electrolytes: K+ 6. Lidocaine may be prescribed 7. Notify the physician if the client complains of chest pain Ventricular Tachycardia ( V-Tach) Occurs due to repititive firing of an irritable ventricular ectopic focus. Atrial: 60-100bpm / ventricular 110250 bpm Can lead to CARDIAC ARREST Cause: Acute MI, CAD , digitalis intoxication, hypokalemia TYPES Stable client with sustained VT- with pulse (-) s/sx decrease cardiac output Unstable client with pulse (+) s/sx of decrease cardiac output DYSRHYTHMIAS INTERVENTION STABLE Administer O2 as prescribed Administer antidysrhythmics drugs Amniodarone Lidocaine Procainamide UNSTABLE Administer O2 as prescribed Administer antidysrhythmics drugs as prescribed Prepare synchronized cardioversion if unstable Attempt COUGH CPR ask client to cough hard every 1-3 seconds PULSELESS CLIENT with V-tach DEFIBRILLATION and CPR With ventricular tachycardia in a stable client, the nurse assesses airway, breathing, and circulation; administers oxygen; and confirms the 4

rhythm via a 12-lead ECG. The physician is contacted and antiarrhythmics may be prescribed. With pulseless ventricular tachycardia, the physician or a specially trained nurse must immediately defibrillate the client or initiate CPR followed by defibrillation as soon as possible. VT, it usually is not possible to determine the atrial rhythm. The ventricular rhythm usually is regular or nearly regular. The P waves usually are not visible and are obscured in the QRS complexes. VT occurs with repetitive firing of an irritable ventricular ectopic focus, usually at a rate of 140 to 180 beats/min or more. SYNCHRONIZED CARDIOVERSION Consider sedation Turn on defibrillator Attached monitor leads to the patient Engage the synchronization mode by pressing the sync control button Look for marker on R waves indicating sync mode Select appropriate energy level Position conductor pads / paddle Annouce to team member: Charging cardiovertor- STAND CLEAR! Press charge button on apex paddle ( right hand) Iam going to shock on three.One, Im clear , two , you are clear, three everybodys clear. ( check yourself one more time before pressing the SHOCK BUTTONS) Ventricular Fibrillation Life threatening Disorganize ventricular rhythm Ventricle quiver and there is no cardiac output Client lack of BP,RR and HR FATAL if not successfully terminated within 3-5 minutes Cause: Idiopathic sudden death, electrical shock INTERVENTION DEFIBRILLATE the client immediately3x @ 200,300, 360 Joules Initiate CPR Administer O2 as prescribed

Administer epinephrine or vasopressin and antidysrhythmic therapy with amiodarone or lidocaine. RESPIRATORY FAILURE RESPIRATORY FAILURE Sudden and life threatening deterioration of the gas exchange function of the lungs Insufficient O2 is transported to the blood Inadequate carbon dioxide is removed from the lungs & client compensatory mechanism fail

5. Status asthmaticus 6. Lobar atelectasis 7. Pulmonary edema Chronic RESPIRATORY FAILURE (CRF) Causes 1. COPD 2. NEUROMUSCULAR DISEASE RESPIRATORY FAILURE s/sx Early sign : restlessness, fatigue, headache, dyspnea, air hunger, tachycardia & inc. BP Late sign: confusion, lethargy, tachycardia, tacypnea, central cyanosis, diaphoresis & respiratory arrest PE : Decrease Breath sound Medical Mgt: Correct underlying cause Restore adequate gas exchange in the lung Mechanical ventilation (MV) & oxygenation Nursing Mgt: 1. Assist with intubation 2. Maintain MV 3. Care @ ICU ( turning sched, mouth care, skin care, range of motion exercise) 4. Assess respiratory status 5. Monitor level of responsiveness , ABG pulse oximeter & VS 6. Assess patient understanding of the Mgt strategies that are used 7. Initiate form of communication to enable patient to express concern & needs health care team 8. Provides teaching as appropriate to address disorder. ACUTE RESPIRATORY DISTRESS SYNDROME ( ARDS) ARDS Severe form of acute lung injury Severe ventilation-perfusion mismatching Assessment: s/sx : sudden & progressive pulmonary edema Rapid onset severe dyspnea ( 1248H) Arterial hypoxemia

2 types : 1. Acute respiratory failure ( ARF) 2. Chronic respiratory failure ( CRF) RESPIRATORY FAILURE Acute Respiratory Failure(ARF) decrease in arterial 02 tension <50 mmHg (hypoxemia) Increase PaC02 > 50 mm Hg ( hypercapnia) pH < 7.35 Chronic Respiratory Failure Deterioration in the gas exchange function of the lung that has developed insidiously after episode of ARF RESPIRATORY FAILURE ARF Ventilation Or Perfusion Mechanism In The Lung Are Impaired. CAUSES: 1. Decrease Respiratory drive 2. Dysfunction of the chest wall 3. Dysfunction of the lung parenchyma 4. RESPIRATORY FAILURE-ARF Decrease Respiratory drive 1. Severe hypothyroidism 2. Sedative medication 3. Severe brain injury Dysfunction of the chest wall 1. Musculoskeletal disorder 2. Muscular dystrophy 3. Polymyositis 4. Myastenia gravis 5. Spinal cord disorder Dysfunction of the lung parenchyma 1. Pleural effusion 2. Hemothorax 3. Pneumothorax 4. Pneumonia 5

CXR: increase bilateral infiltrates Causes: 1. sepsis 2. Smoke inhalation- direct 3. Pneumonia 4. Drug overdoses 5. Shock indirect 6. Fluid volume overload Assessment: Dyspnea, cough, tachypnea with ICS/suprasternal retraction Changes in orientation, tachycardia, cyanosis Increased pC02 and decreased p02 hypoxemia Cause of death : Multiple-system organ failure + sepsis Mortality rate: 50-60% Management 1. Identify and treat the cause of the ARDS 2. Administer O2 as prescribed 3. Place client in high fowlers position 4. Restrict fluid intake as prescribed 5. Provide respiratory treatment as prescribed 6. Administer diuretics, anticoagulant or corticosteroid as prescribed 7. Prepare client for intubation and mechanical ventilation using positive end expiratory pressure (PEEP) RENAL FAILURE Acute renal failure Sudden inability of the kidneys to regulate fluid and electrolyte balance and remove toxic products from the body. Rapid loss of kidney function from renal cell damage Causes: Prerenal Interfers with perfusion decrease blood flow & GFR Ex: CHF, cardiogenic shock, hemorrhage, burns, sepsis, hypotension. Intrarenal Cause that damage the nephrons Ex. Acute tubular necrosis, DM,AGN, tumor, blood transfusion reaction Postrenal 6

Mechanical obstruction ( tubules to urethra) Ex: Calculi , BPH , stricture, blood clots, trauma, anatomic malformation Assessment: 1.Oliguric Phase Urine output <400 ml/24H duration : 1-2 wks s/SX : hypernatremia, Hyperkalemia, hyperphospatemia,hypermagnesemia, hypocalcemia, metabolic acidosis DX: BUN/CREA increase 2.Diuretic Phase 3.Recovery or convalescent phase Assessment: Diuretic Phase Diuresis may occur ( output 3-5 L/day) 2-3 wks S/SX: hyponatremia,hypokalemia and hypovolemia DX: BUN/Crea elevated Recovery or convalescent phase Renal function stabilizes with gradual improvement over next 3-12 months Nursing intervention 1. Monitor & maintain fluid & electrolyte balance 2. Baseline appearance and amount of clients urine 3. Measure I&O q hourly 4. Administer IV fluids and electrolytes supplement as ordered 5. Weigh daily and report gains 6. Monitor alteration in fluid volume 7. Monitor ECG and auscultate heart as needed Promote optimal nutritional status 1. Weigh daily 2. Maintain strict I&O 3. Administer TPN as ordered 4. With enteral feeding check for residual 5. Restrict protein intake Prevent complication from impaired mobility 1. Pulmonary embolism , skin breakdown , atelectasis Prevent fever/ infection 2. Antipyretic as needed 3. Assess for sign of infection 4. Use strict aseptic technique for wound and catheter care

Support client/ relieve anxiety Provide client teaching & discharge concerning Adhere to prescribed dietary regime Sign and symptoms of recurrent renal disease Importance of planned rest period Use of prescribed drugs only Sign and symptoms of UTI or respiratory infection, need to report to physician immediately Chronic Renal failure Slow Progressive, irreversible destruction of the kidneys that continues until nephrons are replaced by scar tissue Loss of renal function gradually Affects all major body systems & requires dialysis or kidney transplantation to maintain life. RENAL FAILURE-CRF Assessment: N/V, diarrhea or constipation, decreased Urine output, dyspnea Early hypotension ; late : hypertension Lethargy, convulsions , Heart failure Diagnostics: Urinalysis Specific gravity, platelets and calcium decreased RENAL FAILURE-CRF STAGES OF CRF Stage I diminished renal reserve Renal function reduced No accumulation of metabolic waste Decrease ability to concentrate urine Nocturia and polyuria Healthier kidney compensates Stage II renal insufficiency Metabolic waste begin to accumulate Decreased responsiveness to diuretics Decreased ability of the healthier kidney to compensate Oliguria and edema STAGES OF CRF Stage III End stage Excessive accumulation of metabolic wastes Kidneys unable to maintain homeostasis Dialysis or other renal replacement therapy required

Nursing Management: 1.Prevent neurologic complication 1. Assess every hour for signs of uremia 2. ( fatigue,loss of appetite, decreased urine output , confusion, elevated BP, seizure, edema of face , itchy skin) 3. Assess for changes in mental functioning 4. Orient confused client to time , place , date and person 5. Monitor serum electrolytes 2.Promote G.I function 1. Assess/provide care for stomatitis 2. Monitor N/V, anorexia, administer antiemetics as ordered 3. Assess for hyperphosphatemia 4. Paresthesias, muscle cramps,seizures , abnormal reflexes 5. Administer amphojel,alternaGel as ordered 3.Promote maintenance of skin integrity 4.Monitor bleeding complication, prevent injury to client 5.Promote/ maintain maximal cardiovascular function 6.Provide care for client receiving dialysis Provide care for the client receiving dialysis BEFORE & DURING DIALYSIS 1. Have client void 2. Chart weight 3. Assess VS before and every 30 minutes during procedure 4. Withhold antihypertensive, sedatives and vasodilators to prevent hypotensive episodes 5. Ensure bed rest with frequent position changes for comfort 6. Inform client that headache and nausea may occur 7. Monitor closely for signs of bleeding since blood has been heparinized for procedure SPECIAL PROBLEM IN RENAL FAILURE 1. Activity intolerance and insomnia 2. Anemia 3. Gastrointestinal bleeding 4. Hyperkalemia/ hypermagnesemia/hyperphosph atemia 5. Hypertension 6. Hypervolemia

7. Hypocalcemia 8. Hypovolemia 9. Infection 10.Metabolic acidosis HEPATIC Encephalopathy HEPATIC Encephalopathy -Known as portal systemic encephalopathy or hepatic coma - Reversible condition -Terminal complication in liver disease Cause: Cirrhosis GI hemorrhage Uremia Hepatoxic meds consipation Protein absorbed in the GUT/intestine Pathophysiology -Liver unable to perform its detoxifying function toxin accumulate -Impaired metabolism of ammonia & other products of protein digestion. -Elevated ammonia toxic to nerve tissue & causes constellation of symptoms Assessment: Early course : changes in mental functioning, insomnia, slow slurred speech, slight tremor, hyperactive reflexes. Progressive :asterixis, disorientation,apraxia,tremor Late: coma, absent reflexes Diagnostics: Increased serum ammonia level PT prolonged Decreased Hgb & Hct Nursing intervention: 1. Neurologic assessment and report deterioration 2. Restrict protein in diet, provide high carbohydrate intake and vitamin K supplements. 3. Administer enemas, cathartics, intestinal antibiotics and lactulose as ordered to reduce ammonia levels. 4. Protect client from injury 5. Avoid administration of drugs detoxified in liver 6. Maintain client on bed rest to decrease metabolic demands on liver DIABETIC KETOACIDOSIS (DKA) 8

Diabetes Mellitus- DKA Acute complication of DM characterized by hyperglycemia and accumulation of ketones in the body. Occurs in insulin-dependent diabetic clients WHAT HAPPEN??? Decrease glucose utilization Insulin required for the entrance & utilization of glucose by cell. Increased fat mobilization Glucose not available fat stores are consumed leading to KETONE FORMATION Increased protein utilization Lack of insulin protein wasting & higher glucose level Inadequacy of prescribed therapy for DM Precipitating factor: 1. Undiagnosed diabetes 2. Neglect of treatment 3. Infection 4. Cardiovascular disorder Sign and symptoms 1. Blood glucose level - >350 mg/dl 2. Elevated ketone levels 3. fruity breath odor 4. Metabolic acidosis 5. HCO3 level less than 10 mEq/L ; CO2 level less than 10 mEq/L 6. Hyperventilation with possible Kussmauls respiration pattern 7. Flushed appearance 8. Dry skin , thirst , anorexia, vomiting ( hypovolemia) 9. Drowsiness 10.Shock & coma 11.Mild hyponatremia , extreme hypokalemia Diagnostics: Serum glucose and ketones elevated BUN/crea , Hct elevated sNa decreased , K normal or elevated at first ABG : metabolic acidosis DKA- Nursing intervention 1. Maintain a patent airway 2. Administer IV therapy as ordered 3. NSS (0.9% NaCl)

4. When blood sugar drops to 250mg/dl may add 5% dextrose to IV 5. K+ will be added when urine output is adequate DKA- Nursing intervention 1. Administer insulin as ordered a. Regular insulin IV drip ( drip or push) or subcutaneously b. Monitor blood glucose level frequently 2. Check urine output every hour 3. Monitor VS 4. Assist client with self care 5. Provide care for the unconscious client if in a coma 6. Discuss with client the reason for ketosis & provide additional diabetic teaching HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNK) Complication of diabetes characterized by hyperglycemia and a hyperosmolar state without ketosis. Occurs in non-insulin-dependent diabetics or nondiabetic persons HHNK sign & symptoms 1. Serum glucose 600 to 2,400 mg/dL 2. Slight drowsiness, insidious stupor, or frequent coma 3. Polyuria for 2 days to 2 weeks before clinical presentation 4. Absence of hyperventilation, no breath odor 5. Extreme volume depletion (dehydration, hypovolemia) 6. Occasional gastrointestinal symptoms 7. Failure of thirst mechanism, leading to inadequate water ingestion 8. CNS symptoms (disorientation, focal seizures) 9. HCO3 level greater than 16 mEq/L ; CO2 level normal 10.Usually normal serum potassium 11.Hypernatremia 12.Ketonemia absent 13.Lack of acidosis High mortality rate Nursing intervention: Same as DKA except treatment for ketosis & metabolic acidosis 9

THYROID Thyroid hormones influence all major body systems THYROID Storm Acute life threatening condition occus in a client with uncontrollable hyperthyroidism Thyrotoxicosis is a term used for the acceleration of metabolism with toxic manifestation that occur when thyroid hormone are extremely elevated. Thyroid crisis or thyroid storm serious form of thyrotoxicosis which is life threatening. Precipitating factors: Stress, infection, unprepared thyroid surgery, pregnancy , emotional trauma Caused by manipulation of the thyroid gland during surgery and the release of thyroid hormone into the blood stream Assessment finding: Elevated temperature Tachycardia Systolic hypertension Nausea, vomiting ., diarrhea Agitation, tremors,anxiety Irritability, agitation, restlessness, confusion, seizure Delirium and coma Intervention 1. ICU 2. Maintain patent airway and adequate ventilation 3. Administer 02 as ordered 4. IV- correct volume & electrolyte depletion 5. Administer medication as ordered a. Antithyroid drugs b. Corticosteroids c. Sedatives d. Cardiac drugs TREATMENT AND NURSING INTERVENTION

1. Reduce body temperature (Hypothermia Blanket,ice packs,cool environment) 2. Reduce heart rate (Carotid massage,Propanolol and digitalis) 3. Humidified O2 @ 2-3LPM/N.C. To improve tissue oxygenation and meet the high metabolic demands 4. Intravenous fluids with dextrose are administered to replace Liver Glycogen stores that have been decreased 5. PTU and Methimazole as ordered by Physician to impede the formation of thyroid hormone 6. Hydrocortisone to treat shock or adrenal insufficiency 7. Iodine in the form of Lugols Solution to decrease release from the thyroid gland 8. Symphatolytic agents to treat atrial fibrillation,dysrhythmias ( Propanolol in combination with digitalis (Verapamil, Digoxin/Lanoxin) ADRENAL CRISIS ADRENAL Glands Play a major role in the bodys response to stress. Adrenal medulla catecholamines (epinephrine,norepinephrine & dopamine) Adrenal Cortex secretes steroid hormones (glucocorticoid (cortisol), mineralocorticoid & androgen) Cortisol major glucocorticoid regulation of blood glucose levels Anti-inflammatory ADRENAL CRISIS A life threatening disorder caused by acute adrenal insufficiency Precipitating factors: Strenuous activity, infection, trauma, stress Failure to take medication Iatrogenic: surgery on adrenal gland, rapid withdrawal of exogenous steroids in a client on long term steroid therapy ADRENAL CRISIS- ADDISONIAN CRISIS Assessment : Severe headache 10

Severe abdominal, leg and lower back pain Generalized weakness Irritability and confusion Severe hypotension shock Life threatening if untreated COMPLICATION: Hyponatremia, hyperkalemia,hypoglycemia and shock ADRENAL CRISIS- ADDISONIAN CRISIS CBR Avoid stimuli High dose of hydrocortisone Treat shock Restore fluid balance ECG monitoring assess the cardiac effect of hyperkalemia & hypercalcemia ADRENAL CRISIS Nursing intervention: 1. Administer IV fluids ( D5NSS) as ordered 2. Administered IV glucocorticoid (hydrocortisone-solu-cortef) and vasopressor 3. If crisis precipitated by infection, administer antibiotic as ordered 4. Maintain strict bed rest and eliminate all forms of stressful stimuli 5. Monitor vs, I&O, daily weights 6. Protect client from infection 7. Provide client teaching and discharge planning a. Life long replacement therapy- never omit medication b. Need to avoid stress & trauma & strenuous exercise c. Diet modification- high in protein, carbohydrates and sodium) d. Use of salt tablet or ingestion of salty foodincrease sweating e. Alternate regular exercise with rest period MULTI-SYSTEM ORGAN FAILURE Multiple organ dysfunction syndrome is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention.

It usually involves two or more organ systems. Multiple Organ Dysfunction Syndrome (MODS) Progressive failure of two or more organ systems after a very severe illness or injury END

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