Abc RGT

ACUTE BIOLOGIC CRISIS
ROWELL G. TRINIDAD, RN
OBJECTIVES
OBJECTIVES
On completion of this concept, the students will be able to: 1. Compare and contrast a termed neonate from a preterm neonate. 2. Use the nursing process as a framework for the care of a preterm neonate.
OBJECTIVES
3. Explain cardiac physiology in relation to cardiac anatomy and the conduction system of the heart. 4. Identify the clinical significance and related nursing implications of the various tests and procedure used for diagnostic assessment of patients with Myocardial Infarction and arrythmias.
OBJECTIVES
5. Describe diagnostic tests used for assessment of suspected neurologic disorders and related nursing implications. 6. Use the nursing process as a framework for care of the patient with endocrine disorders.
CONCEPT OUTLINE
CONCEPT OUTLINE
I Prematurity a. Review of the characteristics of a termed neonate b. Termed versus Premature neonate c. Physiologic handicaps of premature d. Sudden Infant Death Syndrome (SIDS) II Cardiac Disorders
CONCEPT OUTLINE
a. Review of the structure and function of the heart. b. Myocardial Infarction - Types - Diagnostic examination - Management c. Cardiogenic Shock
CONCEPT OUTLINE
d. Arrhythmia - Types - Symptoms - Management III Endocrine Disorders a. Review of the different glands b. Addison s disease
CONCEPT OUTLINE
c. Cushing s syndrome d. Diabetes mellitus e. Liver cirrhosis f. Hyperthyroidism -Acute hyperthyroidism -Chronic hyperthyroidism IV Neurologic Disorders
CONCEPT OUTLINE
a. Myasthenia Gravis b. Increased Intracranial Pressure c. Spinal Cord Injury d. Adult Respiratory Distress Syndrome
PREMATURITY
PREMATURITY
Termed Neonate birth between the thirtythirty-eighth and forty-second week of fortygestation. Preterm (Premature) birth at less than 36 week s gestation, regardless of weight.
PREMATURITY
Characteristics of a TERM infant: 1. Appropriate for gestational age (AGA) weight falls between 10th and 19th percentile for age. 2. Body is normally pink with slight cyanosis of hands and feet (acrocyanosis) 3. Heart rate is rapid and regular (120 to 180 beats per minute)
PREMATURITY
4. Respirations are abdominal and irregular with a rate of 30 to 56 breaths per minute. 5. Head and chest circumference nearly equal with chest slightly smaller than head. 6. Fine, downy hair growth over the entire body.
PREMATURITY
7. Temperature maintained at 36.2 degrees Celsius or 36.6 degrees Celcius, environmental factors may affect temperature. 8. Digest simple carbohydrates ,fats and proteins readily.
PREMATURITY
9. Enlargement of breasts in males (gynecomastia) and females is normal as a result of hormones transmitted to infant by mother 10. Initial weight loss of 5% to 10% of birth weight is normal and usually regained by tenth day of life.
PREMATURITY
Characteristics of a PRETERM infant: 1. Less subcutaneous fat (wrinkled skin, blood vessels and bony structures are visible), lanugo present on face, eyebrows are absent, ears are poorly supported by cartilage, breast buds size is small with underdeveloped nipples. 2. Circumference of the head is large in comparison with the chest, the fontanels are small and bones are soft.
PREMATURITY
3. Skin color changes when infant is moved, HARLEQUIN sign is present. 4. Posture is one of complete relaxation with marked extension of the legs and abduction of the hips, random movements are common with slightest stimulus.
PREMATURITY
5. Heat regulation poorly developed because of immaturity of CNS. - heat loss caused by large skin surface area and lack of subcutaneous and brown fat. - poorly developed respiratory center with diminished oxygen consumption causing asphyxia. - weak heart action.
PREMATURITY
- insufficient heat production caused by inadequate metabolism. 6. Respirations are not efficient because of muscle weakness of lungs and rib cage and limited surfactant production, retraction at xiphoid process is evidence of air hunger.
PREMATURITY
7. Atelectasis can occur, manifested by: cyanosis that decreases with crying, rapid & irregular respirations, flaring of nostrils, intercostal or suprasternal retractions, grunting on expiration. 8. Greater tendency toward capillary fragility; red and white blood cell counts are low with resulting anemia during first few months of life.
PREMATURITY
9. Higher incidence of intracranial hemorrhage; manifested by muscle twitching, convulsions, cyanosis, abnormal respirations, and a short, shrill cry. 10. Weak sucking and swallowing reflexes, small capacity of stomach, low gastric acidity, slow emptying time of the stomach.
PREMATURITY
11. Reduced glomerular filtration rate results in decreased ability to concentrate urine and conserve fluid. Nursing Care of Preterm infants: 1. Respiratory rate and effort; heart rate, temperature, blood pressure. 2. Oxygen concentrations by pulse oximeter
PREMATURITY
3. Skin color and integrity 4. Daily weight, fluid and electrolyte status 5. Ability of infant to suck, nutritional status 6. Parents ability to cope with preterm birth
PREMATURITY
Nursing Diagnosis: 1. Risk for aspiration 2. Impaired gas exchange 3. Inability to sustain spontaneous ventilation 4. Hypothermia 5. Risk for infection 6. Altered nutrition: less than body requirements
PREMATURITY
Nursing Management: 1. Maintain airway; check respirator function if used, position to promote ventilation, suction when necessary; maintain temperature of environment. 2. Observe for changes in respiration, color and vital signs.
PREMATURITY
3. Check efficacy of Isolette: maintain heat, humidity and oxygen concentrations, administer oxygen if necessary, monitor oxygen carefully to prevent retinopathy of the newborn. 4. Maintain aseptic technique to prevent infection
PREMATURITY
5. Adhere to the techniques of gavage feeding for safety of infant. 6. Observe weight-gain patterns. weight7. Determine blood gases frequently to prevent acidosis. 8. Institute phototherapy should hyperbilirubinemia occur.
PREMATURITY
9. Support parents by letting them verbalize and ask questions to relieve anxiety. 10. Provide liberal visiting hours for parents, allow them to participate in care. 11. Arrange follow-up before and after followdischarge by a visiting nurse.
PREMATURITY
Nursing Evaluation/Outcomes: 1. Maintains respiratory functioning 2. Maintains body temperature within acceptable limits 3. Remains free from infection 4. Gains weight
SUDDEN INFANT DISTRESS SYNDROME (SIDS)
SUDDEN INFANT DISTRESS SYNDROME The sudden death of any infant or young child, and in which a thorough postmortem examination fails to demonstrate an adequate cause of death. It is the cessation of breathing for more than 20 seconds or a shorter episode associated with bradycardia, cyanosis or pallor.
SUDDEN INFANT DISTRESS SYNDROME The number one cause of death in infants between 1 month and 1 year of age, incidence of 1.4 in every 1000 live births. Peak age of occurrence: healthy infants 2 to 4 months of age - 95% occur by 6 months Pulmonary edema and intrathoracic hemorrhages found on autopsy.
SUDDEN INFANT DISTRESS SYNDROME Etiology: 1. Unknown may result from many different pathologic processes. 2. Apnea related to organic disorders: a. Seizure disorders b. Gastroesophageal reflux c. Significant anemia d. Sepsis, severe infection
SUDDEN INFANT DISTRESS SYNDROME e. Hypoglycemia f. Impaired regulation of breathing g. Maternal cocaine abuse 3. High risk factors: a. Prematurity b. History of SIDS in the family
SUDDEN INFANT DISTRESS SYNDROME c. Males d. Low-birth weight: newborns with Lowlow APGAR score e. Infants with CNS disturbance f. Infants sleeping on abdomen or on softer bedding, pillows, comforters, quilts, and sheepskin g. Infants with respiratory disorders such as bronchopulmonary dysplasia
SUDDEN INFANT DISTRESS SYNDROME h. Maternal factors such as youth, smoking during pregnancy, substance abuse. Clinical Manifestations: 1. Sudden, unexplained death of an infant under 1 year of age 2. Frothy, blood-tinged fluid fills mouth bloodand nose
SUDDEN INFANT DISTRESS SYNDROME Therapeutic Interventions: 1. Avoid implying wrongdoing, abuse, or neglect 2. Support parents 3. Be nonjudgmental about parents attempts at resuscitation.
SUDDEN INFANT DISTRESS SYNDROME

Nursing Assessment: 1. Parental knowledge of SIDS 2. Parental support system Nursing Diagnosis: 1. Family coping: potential for growth 2. Ineffective family coping: disabling 3. Altered family processes 4. Dysfunctional grieving
SUDDEN INFANT DISTRESS SYNDROME Nursing Intervention: 1. Know signs of SIDS to distinguish it from child neglect or abuse, do or say nothing that instill guilt in the parents 2. Reassure the parents that they could not have prevented the death or predicted its occurrence 3. Reinforce that an autopsy should be done on every child to confirm diagnosis
SUDDEN INFANT DISTRESS SYNDROME 4. Visit the parents at home to discuss the cause of death and help them with their guilt and grief. 5. refer the parents to a national SIDS parent group
SUDDEN INFANT DISTRESS SYNDROME Nursing Evaluation: 1. Family exhibits positive coping behavior 2. Family uses support services 3. Family exhibits appropriate bereavement behavior 4. Parents maintain supportive relationship with other children
STRUCTURE & FUNCTION of the HEART
STRUCTURE & FUNCTION of the HEART Structure and function of the cardiovascular system: Heart is a hollow, muscular organ lies in the mediastinum and rests on the diaphragm.
STRUCTURE & FUNCTION of the HEART 1. Pericardium a thin, membranous sac that encase the heart that has a visceral layer in contact with the heart and an layer, outer parietal layer, contains 20 to 30 ml. of serous fluid which protects the heart from trauma and friction. 2. Heart wall is a specialized muscle tissue consisting of three tissue layers:
STRUCTURE & FUNCTION of the HEART a. Epicardium the thin, serous outer layer b. Myocardium the thick, muscular middle layer c. Endocardium the smooth inner layer that comes in contact with blood 3. Heart Chambers a membranous muscular septum divides the heart into two distinct sides.
STRUCTURE & FUNCTION of the HEART a. Right Atrium b. Right Ventricle c. Left Atrium d. Left Ventricle 4. Heart valves connect the chambers and outflow tracts of the heart. Two types of heart valves are atrioventricular and semilunar valves
STRUCTURE & FUNCTION of the HEART a. Atrioventricular (AV) valves separates the atria from the ventricles 1. Tricuspid valve contains three leaflets, located between the right atrium and ventricle. 2. Mitral valve (bicuspid valve) with two leaflets, located between the left atrium and ventricle.
STRUCTURE & FUNCTION of the HEART b. Semilunar valves - each containing three cusp, located between each ventricle and its corresponding artery. 1. Pulmonic valve located between the right ventricle and pulmonary artery. 2. Aortic valve located between the left ventricle and aorta.
STRUCTURE & FUNCTION of the HEART c. Papillary muscle is a muscle bundles on the ventricular walls, Chordae tendinae fibrous bands extending from the papillary muscles to the valve cusps. - keep the valves closed during systole, this maintains unidirectional blood flow through the AV valves and prevents backflow of blood.
STRUCTURE & FUNCTION of the HEART 5. Cardiac Conduction System consist of specialized cardiac cells that initiate or propagate electrical impulses throughout the myocardium as a precursor to cardiac muscle contraction. a. Electrical Impulses 1. Sinoatrial (SA) node located at the junction of the right atrium and superior vena cava, functions as the pacemaker of the myocardium, initiating rhythmic electrical impulses at 60 to 100 impulses per minute.
STRUCTURE & FUNCTION of the HEART 2. AV node located in the septal wall of right atrium ,receives impulses from SA node and relays them to the ventricles. 3. Bundle of His bundle of specialized muscle fibers in the myocardial septum, conducts impulses from AV node. a. Right bundle branch (RBB) conducts impulses down the right side of the septum
STRUCTURE & FUNCTION of the HEART b. Left bundle branch conducts impulses into right and left fascicles that fan out into the left ventricular muscle Purkinje fibers where RBB and LBB terminate which propagate electrical impulses into the endocardium and on to the myocardium.
STRUCTURE & FUNCTION of the HEART b. Electrical impulse activity electrical impulses traveling through the cardiac conduction system can be measured and recorded by ECG. 1. Phases of electrocardiogram (ECG) P, Q, R, S and T P wave represents atrial depolarization PR interval represents the time from the beginning of atrial depolarization to the beginning of ventricular depolarization.
STRUCTURE & FUNCTION of the HEART QRS complex represents ventricular depolarization T wave represents ventricular repolarization 2. Normal sinus rhythm - Heart rate: 60 to 100 beats/min. - P waves precede each QRS complex
STRUCTURE & FUNCTION of the HEART - PR interval is 0.12 to 0.20 sec. - QRS complex is 0.04 to 0.1 sec. - Conduction is forward and cyclical through the conduction system - Rhythm is regular with no abnormal delay 6. Coronary arteries - supply the heart with blood from branches that originate in the right or left sinus of valsalva of the aortic valve cusps.
STRUCTURE & FUNCTION of the HEART a. Right coronary artery supplies blood to the right heart wall. b. Left main coronary artery which divides into the left anterior descending coronary artery and the circumflex artery, supplies most of the blood to the left heart wall.
STRUCTURE & FUNCTION of the HEART Functions of the Heart: 1. Cardiac output (CO) is defined as the volume of blood ejected by each ventricle in a minute. Cardiac output (CO) = Stroke volume (SV) X Heart rate (HR)
STRUCTURE & FUNCTION of the HEART a. Stroke volume is the amount of blood ejected by the left ventricle with each heart beat. Factors affecting Stroke volume: 1. Preload the end-diastolic filling endvolume of the ventricle, increases by increased returning volume to ventricle. 2. Afterload resistance to left ventricular ejection, increases by increased systemic arterial pressure.
STRUCTURE & FUNCTION of the HEART b. Heart rate is the number of hearbeats per minute, normal: 60 to 100 beats per minute. 2. Cardiac cycle each complete heartbeat or cardiac cycle consists of two phases in response to electrical stimulation. a. Systole is the contraction phase b. Diastole is the relaxation (filling) phase

3. Heart sounds result from vibrations caused by valve closure and ventricular filling. a. S1 is associated with tricuspid and mitral valve closure b. S2 is associated with aortic and pulmonic valve closure c. S3 known as ventricular gallop, is often normal in persons younger that age 30 but pathologic in older persons and occurs during the rapid ventricular filling stage of diastole.

d. S4 known as atrial gallop, is linked to resistance to ventricular filling as in hypertrophy or injury of the ventricular wall. 4. Neurologic factors regulating heart function a. Sympathetic nervous system stimulation release of norepinephrine, results in arteriolar vasoconstriction, increased heart rate and a positive inotropic effect.
STRUCTURE & FUNCTION of the HEART b. Parasympathetic nervous system stimulation with release of acetylcholine, results in decreased heart rate and slowed AV conduction. c. Chemoreceptors located in the carotid and aortic bodies, to decreased O2 and increased CO2 concentrations is to increase the heart rate.
STRUCTURE & FUNCTION of the HEART d. Baroreceptors located in the aortic arch, carotid sinus, vena cava, pulmonary arteries and atria is to decrease or increase heart rate, resulting in blood pressure changes.
NURSING PROCESS OVERVIEW for the CARDIOVASCULAR SYSTEM
NURSING PROCESS
Assessment 1. Health history: history: - Elicit a description of present illness and chief complaint (onset, course, duration, location and precipitating & alleviating factors) Cardinal signs & symptoms of altered cardiovascular function:
NURSING PROCESS
1. Pain over the lower sternal region & the upper abdomen characterized by heavy vicelike, beltbelt-squeezing pain that may radiate to shoulders, neck, and down arms. 2. Palpitations characterized by rapid irregular or pounding heartbeat. 3. Intermittent claudication characterized by extremity pain with exercise.
NURSING PROCESS
4. Dyspnea characterized by difficult breathing or shortness of breath with activity (ie. Dyspnea on exertion), in the supine position (ie. (ie. Orthopnea), or sudden onset at night (ie. Paroxysmal nocturnal dyspnea) 5. Fatigue with or without activity. 6. Syncope with or without dizziness 7. Diaphoresis with associated clamminess and cyanosis 8. Edema or weight (>3 lbs. in 24hrs)
NURSING PROCESS
2. Explore the client s health history for risk factors associated with cardiovascular disease (atherosclerosis) a. Positive family history for cardiovascular disease. b. Age (high risk >40 y.o.) c. Gender (greater in men than women, decrease after menopause) d. Race: mortality is greater for nonwhites than whites
NURSING PROCESS
e. Hypertension f. Hyperlipidemia (HDL & LDL ratio) g. Obesity h. Sedentary lifestyle i. Diabetes j. Stress k. Use of oral contraceptives 2. Physical Assessment
NURSING PROCESS
a. Assess the vital signs b. Inspection - observe general appearance for signs of distress, anxiety and altered LOC - inspect the lips and buccal mucosa for central cyanosis - inspect peripheral extremities for cyanosis & a capillary refill time of less 3 seconds - assess jugular venous pressure & observe for venous distention c. Palpation
NURSING PROCESS
- palpate the precordium to locate the point of maximal impulse (PMI) or the apical pulse - palpate all peripheral pulses including carotid, brachial, radial, femoral, popliteal, dorsalis pedis & anterior tibial Grade 0 no pulse 1+ - weak 2+ - normal 3+ - normal 4+ - bounding
NURSING PROCESS
d. Auscultation systematically auscultate the heart for normal & abnormal heart sounds, murmurs, & friction rub, covering four main areas: aortic area, pulmonary area, mitral area & tricuspid area e. Perform respiratory assessment - Cough (pulmonary congestion) - Crackles or Wheezing ( airway narrowing, atelectasis or left ventricular failure) - Hemoptysis (acute pulmonary edema) - Cheyne-Stokes respiration (severe left Cheyneventricular failure)
NURSING PROCESS
f. Perform abdominal assessment - Liver enlargement & ascites (decreased venous return secondary to right ventricular failure) - Bladder distention (decreased cardiac output) - Bruits above umbilicus (abdominal aortic obstruction or aneurysm)
NURSING PROCESS
3. Laboratory and Diagnostic studies: a. WBC detect signs of infection normal level: 5,000 to 10,000/cu. mm. b. Lipid profile examine cholesterol (HDL & LDL) and triglycerides cholesterol normal level: 150-200 mg./dl. or 1503.93.9-5.2 mmol/L LDL: 80-190 mg./dl. or 2.07-4.92 mmol/L 802.07HDL: 30-65 mg./dl. or 0.78-1.68 mmol/L 300.78(males), 40-85 mg./dl. or 1.04-2.2 mmol/L 401.04(females)
NURSING PROCESS
c. Cardiac enzymes: Creatinine phosphokinase (CPK) males: 5050325, females: 50-250 U/L 50isoenzymes: CPK-MB, Troponin & Lactate CPKdehydrogenase d. Blood coagulation studies: Prothrombin time 9.5-12 seconds 9.5Partial thromboplastin time 20-45 sec. 20-
NURSING PROCESS
e. Chest radiography determine heart size and silhouette & visualize the pulmonary system f. Electrocardiography evaluates the heart s electrical activity g. Holter monitoring (ambulatory ECG) allows for 2424-hour continuous measurement of the heart s electrical activity h. Exercise ECG (grade exercise test) evaluates electrical activity during physical stress, chemical induced ECG stress test is used if the client is unable to walk or bike for a long period of time.
NURSING PROCESS
i. Vectorcardiography provides a graphic representation of the direction and magnitude of the heart s electrical function. j. Echocardiography yields information about cardiac structures (especially valvular) & function k. Radionuclide testing evaluates ventricular function & myocardial blood flow & detects areas of myocardial damage. Types: Positron emission tomography (PET), MultipleMultiple-gated acquisition (MUGA) & Thallium scanning
NURSING PROCESS
l. Cardiac catheterization enables measurement of chamber pressures & oxygen saturation m. Arteriography visualizes coronary arteries with injections of radiopaque contrast media n. Ventriculography visualizes ventricles with injection of radiopaque contrast media o. Central venous pressure (CVP) reflects filling pressure of the right ventricle & help assess cardiac function & intravascular volume status
NURSING PROCESS
p. Pulmonary artery wedge pressure (PAWP) & Pulmonary artery pressure (PAP) measure left heart pressures q. Arterial line allows continuous monitoring of peripheral arterial pressures Nursing Diagnosis: 1. Decreased cardiac output 2. Impaired gas exchange
NURSING PROCESS
3. 4. 5. 6. 7. 8. 9. Activity intolerance Pain Risk for Infection Sleep pattern disturbance Anxiety Knowledge Altered family processes
NURSING PROCESS
Planning & Outcome Identification Major goals: - Enhancement of cardiopulmonary status - Increased gas exchange & activity tolerance - Prevention of pain & infection - Improved sleep pattern - Reduction of anxiety - Adherence to a self-care program with selfunderstanding of disease process & management - Improved family functioning
NURSING PROCESS
D. Implementation 1. Assess cardiopulmonary status - assess LOC, HR & rhythm, heart sounds, BP, peripheral pulses, peripheral edema, skin color & temperature, RR & lungs - Monitor ABG & pulse oximetry - Monitor ECG & telemetry - Monitor I&O & maintain 30 ml./hr. output, use urometer to ensure accurate output
NURSING PROCESS
2. Enhance cardiac output establish a patent intravenous line to administer fluids. 3. Promote gas exchange - encourage to maintain high fowler s position while resting in bed, keep client on bed or chair rest. - collaborate with respiratory therapist & administer O2 to maintain O2 saturation level of 95% to 100% if no other disease process is present - instruct to cough, breath deeply & turn frequently
NURSING PROCESS
4. Increase activity tolerance - balance period of rest & exercises - assist as needed with activities of daily living and self care 5. Promote comfort - assess client s description of chest discomfort, including location, radiation, duration & what precipitated pain
NURSING PROCESS
6. Prevent infection - Monitor skin integrity of lower extremities & incisions from cardiac surgery - Assess insertion sites from invasive procedures for signs of redness, warmth, edema & pain - Monitor V/S especially for fever - Assess breath sounds for changes associated with pneumonia in clients after surgery and those requiring bed rest
NURSING PROCESS
7. Promote adequate sleep - attempt to cluster nursing interventions to provide the client with several hours of uninterrupted sleep 8. Minimize anxiety - offer client opportunities to ventillate feelings, answer client s question truthfully & caring relationship with client & client s family
NURSING PROCESS
9. Provide client & family teaching - Teach family members or significant others about pathophysiology of the underlying disease process - Teach client the importance of low-fat, lowlowlowcholesterol, low sodium diet, smoking cessation & adequate amount of exercise - Teach energy conservation measures - Discuss medications, including possible adverse effects & interactions.
NURSING PROCESS
- discuss danger S/S requiring prompt medical attention including chest pain, increased shortness of breath, sudden onset of fever, irregular heartbeats & weight gain of more than 2 lbs. in less than 24 hours - discuss with client the necessity of advance directives & durable Power of Attorney for health care
NURSING PROCESS
10. Enhance family functioning - assist with adaptation to role changes caused disease related limitations & activity restrictions E. Outcome evaluation 1. The client demonstrate stable cardiac rhythm, vital signs, hemodynamic parameters and urinary output
NURSING PROCESS
2. The client responds to cardio pulmonary resuscitation. 3. The client verbalizes factors and events that precipitate pain. 4. The client limits activities to a level that permits the heart to rest. 5. The client is free of systemic & local infection. 6. The client demonstrate stabilization of the inflammatory process.
NURSING PROCESS
7. The client sleeps at least 6 hours each night uninterrupted. 8. The client can verbalize a understanding, preventive measures, and treatment of the disease process and the signs or symptoms that should be reported to the health care provider. 9. Family members or significant others verbalize an understanding of cardiopulmonary resuscitation (CPR) & the pathophysiology of underlying disease.
CARDIOVASCULAR DISORDERS
MYOCARDIAL INFARCTION
Myocardial infarction (MI) is destruction of myocardial tissue in regions of the heart abruptly deprived of adequate blood supply because of reduced coronary blood flow Etiology 1. Coronary artery narrowing due to atherosclerosis, coronary artery spasm, or complete arterial occlusion by embolism or thrombus 2. Decreased coronary blood flow due to hemorrhage or shock, causing a profound imbalance between myocardial oxygen supply & demand.
Pathophysiology of Myocardial Infarction
Etiology (atheroslcerosis, embolism, thrombus, hemorrhage, coronary artery spasm) Inadequate coronary blood flow Myocardial ischemia Depresses cardiac function Triggers autonomic nervous system response Exacerbate imbalance between myocardial supply & demand Persistent ischemia results tissue necrosis & scar tissue formation Permanent loss of myocardial contractility in the affected area Decreased myocardial contractility Inadequate CO
Cardiogenic shock death
Clinical Manifestations a. Chest pain b. Diaphoresis & cool, clammy, pale skin c. Nausea & Vomiting d. Dyspnea with or without crackles e. Palpitations or Syncope f. Restlessness & anxiety or feeling of impending doom g. Tachycardia or Bradycardia h. Decreased blood pressure i. Altered S3 heart sound, which indicates left ventricular failure
Laboratory & Diagnostic study findings a. ECG T-wave to be larger & inverted, ST elevation in epicardial myocardial ischemia, ST depressed in endocardial myocardial ischemia. b. Serum enzymes - elevated CPK & CPKCPKMB, LDH & Troponin levels c. WBC count is elevated
Nursing Management 1. Administer drug therapy - Administer morphine, nitrates, antilipidemics, thrombolytics & anticoagulants in acute situation or stool softeners during rehabilitation - Immediate treatment of MI; Morphine, oxygen, nitroglycerin & aspirin (MONA)
2. Provide ongoing assessment - Monitor cardiac enzymes - Monitor hemodynamic parameters as necessary through the multilumen pulmonary artery catheter 3. Minimize anxiety - Reassure the client & explain procedures as the situation warrants
4. Minimize metabolic demands - institute a liquid diet. - advance to a low-sodium, low-fat, lowlowlowlow-cholesterol, solid diet as tolerated 5. Prepare client for treatment - PTCA (Percutaneous Transluminal Coronary Angioplasty) - CABG (Coronary Artery Bypass Graft)
6. Provide client & family teaching - encourage family members & significant others to take CPR course 7. Provide referrals - American Heart Association - Coronary club - Mended Hearts Cardiac Rehabilitation
BODY S REACTION TO SHOCK

Impaired organ function Vasoconstriction of peripheral veins and arteries Hyperventilation Tachycardia * Fluid shifts
CARDIOGENIC SHOCK
Cardiogenic shock is the insufficient tissue perfusion due to the heart s inability to pump enough blood. Etiology: 1. Myocardial infarction 2. Congestive heart failure 3. Cardiomyopathy 4. Pulmonary edema 5. Cardiac tamponade
Pathophysiology of CARDIOGENIC SHOCK Inability of the heart to pump adequate blood Inadequate tissue perfusion on the body s organs Result in systemic symptoms cerebral perfusion - restlessness - lethargy - confusion - altered LOC respiratory system - Cough & Crackles - RR - Low PAO2 - PACO2 cardiovascular - Rapid weak pulse - Hypotension - CVP & PCWP
decrease periphery perfusion - cool & pale skin
Reduced renal perfusion - oliguria
CARDIOGENIC SHOCK
Nursing Management: 1. Administer medications to improve CO (inotropic drugs, preload & afterload reducers, diuretics & sedatives) 2. Monitor PCWP to determine left ventricular function 3. Prepare the patient for insertion of an intraaortic balloon pump. 4. Monitor oxygenation status including respiratory rate, lung sounds, pulse oximetry & ABG s.
CARDIOGENIC SHOCK
5. Institute ventilator support. 6. Monitor vital signs closely 7. Maintain strict intake & output measurements, measure urine output hourly 8. Promote rest & provide comfort measures
ARRHYTHMIAS
ARRHYTHMIAS
Arrhythmia or dysrhythmia refers to any sinus rhythm deviating from normal. Etiology: Arrhythmias results from altered impulse formation, altered impulse conduction, or both.
Pathophysiology of Arrhythmia
Etiology (altered impulse formation, altered impulse conduction) Injured myocardial cells/replaced scar tissue Decreased ability to respond to SA node impulses Other cells assume the pacemaker properties Initiates the heart beat Interrupts SA node impulses Arrhythmia occurs
NORMAL SINUS RHYTHM
I. SINUS TACHYCARDIA
Sinus tachycardia is a heart rate greater than 100 beats per minute, originating in the sinus node. Characteristics: 1. Rate is 100 to 180 bpm 2. P waves precede each QRS complex 3. PR interval is normal 4. QRS complex is normal 5. Conduction is normal 6. Rhythm is regular
SINUS TACHYCARDIA
Etiology: 1. Exercise 2. Anxiety 3. Fever 4. Drugs 5. Anemia 6. Heart failure 7. Hypovolemia 8. Shock
SINUS TACHYCARDIA
Clinical Manifestations: 1. Occasional palpitations 2. Hypotension 3. Angina with cardiovascular disease Nursing Management: 1. Administer prescribed treatment is directed at the primary cause.
SINUS TACHYCARDIA
- carotid sinus pressure - Beta blockers (Atenolol, Metoprolol, Nadolol, Propanolol) this is to reduce the heart rate quickly
SINUS TACHYCARDIA
II. SINUS BRADYCARDIA

Sinus bradycardia is a heart rate less than 60 beats per minute originating in the sinus node. This arrhythmia may be normal in athletes Characteristics: 1. Rate is less than 60 beats per minute 2. P waves precede each QRS complex 3. PR interval is normal 4. QRS complex is normal 5. Conduction is normal 6. Rhythm is regular
SINUS BRADYCARDIA
Etiology: 1. Drugs 2. Vagal stimulation 3. Hypoendocrine states 4. Anorexia 5. Hypothermia 6. Sinus node involvement in MI
SINUS BRADYCARDIA
Clinical Manifestations: 1. Fatigue 2. Lightheadedness 3. Syncope Nursing Management: 1. Maintain adequate CO through treating the underlying cause. 2. Administer Atropine SO4 (anticholinergic)
SINUS BRADYCARDIA
III. PAROXYSMAL ATRIAL TACHYCARDIA and SUPRAVENTRICULAR TACHYCARDIA
Paroxysmal atrial tachycardia (PAT) & Supraventricular tachycardia (SVT) is an abrupt onset & rapid heartbeat (palpitations) originating in the atria. Characteristics: 1. Rate is 150 to 250 bpm 2. P waves are ectopic & maybe found preceding T waves 3. PR interval is shortened (0.12 seconds) 4. QRS complex is normal 5. Conduction is normal 6. Rhythm is regular
PAT & SVT

Etiology: 1. Extreme anger & fear 2. Drugs 3. Alcohol, smoking & caffeine Clinical Manifestations: 1. Palpitations 2. Lightheadedness 3. Dyspnea 4. Anginal pain
PAT & SVT

Nursing Management: 1.Assist with carotid sinus pressure or vagal maneuver 2. Administer prescribed medication - Antiarrhythmics (Quinidine, Lidocaine, Flecainide, Propranolol & bretylium) - Cardiac glycosides (digoxin) - Adenosine is drug of choice for SVT 3. Assist with cardioversion
PAT & SVT
SUPRAVENTRICULAR TACHYCARDIA
IV. ATRIAL FIBRILLATION

Atrial Fibrillation is a disorganized & uncoordinated twitching of atrial musculature caused by overly rapid production of atrial impulses. Characteristics: 1. Rate: Atrial is 350 to 600 bpm & Ventricular 120 to 200 bpm 2. P wave is not discernible, with an irregular baseline 3. PR interval is not measurable 4. QRS is normal 5. Conduction is normal 6. Rhythm is irregular & usually rapid unless controlled
ATRIAL FIBRILLATION
Etiology: 1. Atherosclerosis 2. Rheumatic mitral valve stenosis 3. Congestive heart failure 4. Congenital heart disease 5. COPD 6. Hypothyroidism & thyrotoxicosis
ATRIAL FIBRILLATION
Clinical Manifestation: 1. Palpitations 2. Dyspnea 3. Pulmonary edema 4. Signs of cerebrovascular insufficiency Nursing Management: 1. Administer prescribed medication (cardiac glycosides & Ca channel blocker) 2. Assist with cardioversion 3. Implement anticoagulant therapy
V. ATRIOVENTRICULAR BLOCKS
AV block - is a conduction defect within the AV junction that impairs conduction of atrial impulses to ventricular pathways. Types: 1. First degree 2. Second degree 3. Third degree
ATRIOVENTRICULAR BLOCK
Characteristics: 1. Rate 1st degree 60 to 100 bpm or the inherent ventricular rate. 2nd degree rate is slowed, atrial rate is 2 to 4 times faster than the ventricular rate 3rd degree rate is slowed, usually 40 to 60 beats per minute or the inherent ventricular rate
2. P wave is normal & present in each type of block 3. PR intervals: 1st degree PR intervals are prolonged at 0.20 second 2nd degree PR intervals may be progressively lengthening 3rd degree no relationship between P waves & QRS complexes exist, PR intervals cannot be measured
4. QRS complex 1st & 2nd degree normal 3rd degree QRS is widened 5. Conduction 1st degree is delayed in the AV junction 2nd degree impulses are not regularly conducted through the AV junction 3rd degree - all sinus impulses are blocked, conduction through the ventricles is abnormal 6. Rhythm is regular in each type of block
Etiology: 1. Congenital 2. Atherosclerotic heart disease 3. Hypokalemia 4. Certain drugs: digitalis, vagotonic agents, symphatholytic agents, BetaBetaadrenergic blockers
Clinical Manifestations: 1st degree asymptomatic 2nd degree vertigo, weakness & irregular pulse 3rd degree hypotension, angina & heart failure Nursing Management: 1st degree no treatment, discontinue causative drug if indicated 2nd degree administer Atropine SO4 3rd degree Atropine SO4, pacemaker
st 1
degree AV Block
nd 2
degree AV Block
rd 3
degree AV Block
VI. PREMATURE VENTRICULAR CONTRACTIONS
PVC is caused by increased automaticity of ventricular muscle cells. Characteristics: 1. Rate 60 to 100 bpm 2. P wave underlying rhythm is normal, premature beat has no P wave 3. PR interval underlying rhythm is normal, premature beat has no PR interval
PREMATURE VENTRICULAR CONTRACTION 4. QRS complex premature beat is bizarre and is multifocal resulting to different configurations 5. Conduction is retrograde through conduction system 6. Rhythm is usually irregular when premature beat occurs, it may be in a regular pattern
PREMATURE VENTRICULAR CONTRACTION Etiology: 1. Myocardial damage 2. Hypoxia 3. Digitalis toxicity 4. Electrolyte imbalance 5. Increased catecholamines 6. Exercise
PREMATURE VENTRICULAR CONTRACTION Clinical Manifestations: 1. Palpitations 2. Weakness 3. Lightheadedness Nursing Management: 1. Asses the cause 2. Assess fro life threatening PVC s of more than six per minute
PREMATURE VENTRICULAR CONTRACTION 3.Assess PVC that are bigeminy, trigeminy, quadrigeminy 4. Assess PVC s that occur in a vulnerable phase of conduction cycle (R & T wave) 5. Administer lidocaine immediately (drug of choice) 6. Administer an antiarrhythmic as ordered 7. Administer procainamide & quinidine for long term therapy
PREMATURE VENTRICULAR CONTRACTION
VII. VENTRICULAR TACHYCARDIA

VT is three or more consecutive PVCs. It is considered a medical emergency because CO cannot be maintained because of decreased diastolic filling. Characteristics: 1. Rate 100 to 250 bpm 2. P wave is blurred in the QRS but the QRS complex has no association with the P wave 3. PR interval is not present
VENTRICULAR TACHYCARDIA
4. QRS complex is wide & bizarre, T wave is in the opposite direction. 5. Conduction is abnormal through ventricular tissue 6. Rhythm is usually regular Etiology: 1. Irritability of ventricular muscle
Clinical Manifestation: 1. Lightheadedness 2. Weakness 3. Dyspnea 4. Unconsciousness Nursing Management: 1. Administer antiarrhythmic drugs as prescribed (lidocaine, procainamide or bretylium)
2. If the client is conscious or if lidocaine is unsuccessful assist with cardioversion. 3. If rhythm deteriorates to ventricular or if the client is pulseless assist with defibrillation & use Advance Cardiac Life Support (ACLS) guide for resuscitation.
Important points for assisting with defibrillation or Cardioversion: 1. Always shout all clear & make sure that no one is touching the bed or client before discharging paddles. 2. Always have saline pads between the paddles & the client s skin 3. Make sure that paddles are correctly placed ( e.g. sternum & apex) & apply 20 to 30 lbs of pressure to ensure good skin contact 4. Make sure that the correct is applied before defibrilating or cardioverting the client.
5. Cardioversion is an elective procedure, the client is alert & requires informed consent, the client will be sedated.
VIII. VENTRICULAR FIBRILLATION

VF is rapid, ineffective quivering of ventricles that may be rapidly fatal. Characteristics: 1. Rate is rapid & uncoordinated, with ineffective motions 2. P wave is not seen 3. PR interval is not seen 4. QRS complex is seen as undulation with no specific pattern
VENTRICULAR FIBRILLATION
Etiology: 1. Myocardial infraction (most common) 2. Electrolyte imbalance (hypokalemia & hypercalcemia) 3. Digitalis or quinidine toxicity 4. Hypothermia Clinical Manifestation: 1. Loss of consciousness 2. Pulselessness 3. Loss of blood pressure 4. Cessation of respirations 5. Possible seizures 6. Sudden death
VENTRICULAR FIBRILLATION
Nursing Management: 1. Assist with defibrillation & CPR 2. Administer prescribed antiarrhythmic medications
IX. VENTRICULAR ASYSTOLE

Ventricular asystole is described as a lack of QRS complexes, heartbeat, palpable pulse & respiration, without immediate intervention, ventricular asystole is fatal. Characteristics: 1. Rate is not present 2. P wave may be visible but does not conduct through the AV node & ventricles 3. QRS complex is not present 4. Conduction is possible through the atria only 5. Rhythm is not present
VENTRICULAR ASYSTOLE
Etiology: 1. Causes of ventricular asystole may include any of the reasons for the previously described arrhythmias if medical treatment was not successful Clinical Manifestations: 1. Loss of consciousness 2. No respirations 3. Pulselessness 4. Sudden death
VENTRICULAR ASYSTOLE
Nursing Management: 1. Assist with CPR 2. Administer drugs such as Atropine SO4 & Epinephrine
ENDOCRINE DISORDERS
ENDOCRINE SYSTEM
In conjunction with the nervous system, controls and integrates body function Endocrine system sends it messages in the form of hormones in the bloodstream
ENDOCRINE SYSTEM
GlandsGlands- any structure of animals, plants, or insects that produces chemicals 2 TYPES ExocrineExocrine- releases secretion into ducts - external secretion Liver, mammary gland, lacrimal gland
ENDOCRINE SYSTEM
EndocrineEndocrine- discharge their secretions (Hormones) directly into the bloodstream Islet of langerhans Gonads( ovaries and testes ) Adrenal, pituitary, thyroid, parathyroid
ENDOCRINE SYSTEM
ENDOCRINE SYSTEM
Structure & Function of the endocrine system A. Hormones are chemical substances secreted by endocrine glands directly into the blood stream to act on specific target cells. Hormones regulate growth & development, fluid & electrolyte balance, reproduction, adaptation to stress & metabolism
ENDOCRINE SYSTEM
Types of hormones: 1. Protein or peptide act on cell membranes by binding to receptors (e.g. insulin, vasopressin, GH also called somatotropin, ACTH) 2. Amine hormones or amino acids act on cell membranes (e.g. epinephrine, norepinephrine) 3. Steroids act intracellularly to modify protein synthesis (cortisol, estrogen & testosterone) Hormone regulation hormone secretion is regulated through feedback mechanisms.
ENDOCRINE SYSTEM
I. Pituitary gland a. anterior lobe: 1. GH affects growth of bones and muscles 2. Prolactin affects mammary glands to stimulate milk production Thyroid3. Thyroid-stimulating hormone (TSH) stimulates thyroid hormone production 4. ACTH stimulates adrenal cortex to produce steroids (cortisol) 5. Follicle-stimulating hormone (FSH) Folliclestimulates ovaries to develop follicles & secrete estrogen or stimulates testes to develop seminiferous tubules & perform spermatogenesis
ENDOCRINE SYSTEM
6. Luteinizing hormone (LH) stimulates ovaries to form a corpus luteum, initiate ovulation & produce progesterone or stimulates testes to secrete testosterone. b. posterior lobe: 1. Oxytocin stimulates uterine & mammary gland contractions 2. Antidiuretic hormone (ADH, vasopressin) acts on distal renal tubule to increase water reabsorption
ENDOCRINE SYSTEM
II. Thyroid gland a butterfly-shaped gland butterflylocated in the neck behind the trachea. 1. Thyroxine (T4) & Triiodothyronine (T3) regulate cellular metabolic activity 2. Thyrocalcitonin secreted in response to high blood calcium levels, it lowers blood calcium levels by inhibiting bone resorption. III. Parathyroid glands - surround posterior thyroid tissue, difficult to locate & may be removed accidentally during thyroid or other neck surgery. 1. Parathyroid hormone (PTH) raises blood calcium levels by increasing calcium resorption from kidneys, intestines & bones
ENDOCRINE SYSTEM
IV. Adrenal glands a. adrenal medulla in the center of the gland, reacts to autonomic nervous system signals to release catecholamines. 1. Epinephrine accounts 90% of gland secretions, prepares the body for the fight-orfight-orflight response by converting glycogen, stored in the liver, to glucose & increasing cardiac output 2. Norepinephrine exerts effects similar to epinephrine & produces extensive vasoconstriction.
ENDOCRINE SYSTEM
b. adrenal cortex outer portion of the glands, is stimulated by ACTH to produce corticosteroids. 1. Mineralocorticoids (aldosterone) released in response to angiotensin II & ACTH, increase Na reabsorption & potassium loss primarily through the renal tubules 2. Glucocorticoids (cortisol) released in response to ACTH, increase blood glucose by stimulating gluconeogenesis & lipolysis, & decrease protein synthesis, suppress the inflammatory response & promote sodium retention & potassium loss. 3. Adrenal sex hormones (androgens & estrogen) govern development of certain secondary sex characteristics, secretion of adrenal androgens is controlled by ACTH.
ENDOCRINE SYSTEM
V. Pancreas a slender, elongated organ lying horizontally in the posterior abdomen behind the stomach. Functions: 1. Exocrine functions involve secretion of pancreatic digestive enzymes by specialized cells 2. Endocrine functions are controlled by the alpha, beta & delta cells of the islets genesis a. Alpha cells secrete glucagon, which increases blood glucose through gluconeogenesis b. Beta cells secrete insulin c. Delta cells secrete somatostatin (inhibitory hormone) & gastrin
ENDOCRINE DISORDERS
MANIFESTATIONS THAT DEVELOP IN SOME ENDOCRINE DISORDERS

Mental status changes- increase nervousness,changes in mood,mental confusion, changesdepression Changes in vital signs- increase body tempdue to hypothyroidism,insuffficient ADH signscan cause dehydration whereas oversecretion cause excessive water retention PalpitationsPalpitations- increase heart rate can occur in hypothyroidism TremorsTremors- possible indication for hyperthyroidism FatigueFatigue- may signify emotional stress WeaknessWeakness- indicates neurologic problems Appetite changes- watch for polyphagia or anorexia changesWeight loss- eating more and loosing wt may indicate DM or hyperthyroidism while losspeople with hypothyroidism may gain wt Polydipsia and polyuria- abnormal thirst plus passage of large amount of urine may polyuriaindicate DM Changes in bowel status- frequent loose stools are a sign of hyperthyroidism, while statusconstipation can indicate hypothyroidism Abnormalities involving the sex organs and libido- loss of menstrual cycle, loss of libidolibido, impotence
NURSING ASSESSMENT
Untoward changes in appearance- acromegaly produces enlargement of hands and appearancefeet while cushing s syndrome is manifested by moon face, thin extremities and truncal obesity Growth abnormalities- growth maybe delayed, stunted(dwarfism), abnormalitiesexcessive(gigantism) or inappropriate(acromegaly) Skin and tissue changes- hyperpigmentation occurs in chronic adrenocortical changesinsufficiency(addison s disease), poor tissue healing and susceptibility to infection are associated with DM HairHair- excessive hair in women may indicate ovarian or adrenocortical disorders, axillary and pubic hair loss may indicate a pituitary disorder, hair feels soft and silky in hyperthyroidism while coarse, dry, brittle in hypothyroidism EyesEyes- exopthalmus is an important characteristic of hyperthyroidism, one serious complication of DM is blindness Bone and joint problem- people with hyperparathyroidism often develop bone pain, problemcyst and fractures, cushing syndrome produces a rapid breakdown of bone When assessing a person with endocrine disorder inquire into the family history. A number endocrine disorders are inherited or at least associated with a familial trend
ADDISONS DISEASE
Adrenal gland ( suprarenal gland ) - small vital endocrine structures that cap the kidneys 2 LAYERS A. adrenal medulla- inner core, sometimes medullacalled symphatoadrenal system - the brain ( hypothalamus ) controls the release of two potent hormones epinephrine and norepinephrine ( symphatomimetics )
ADDISONS DISEASE
Epinephrine during stressful situation - converts glycogen to glucose for energy - increase cardiac output - produces cold sweat, pounding heart, deep rapid breathing and wide eyed alertness in times of emergency
ADDISONS DISEASE
Norepinephrine during stress reactions - extensive vascular constriction - increase blood pressure * Overactivity of the adrenal medulla can be life threatening usually caused by cathecolamine producing tumor called pheochromocytoma which produces oversecretion of epinephrine and norepinephrine, should the medulla destroyed or removed, the SNS compensates for its loss
ADDISONS DISEASE
B. adrenal cortex- makes up the outer shell, cortexunlike the adrenal medulla, is essential for survival without therapeutic replacement of adrenocortical hormones, destruction or removal of this vital structure causes death within few days - produces adrenocortical hormones/ steroid hormones ( corticosteroids ) * Both are important for survival and well being but only the adrenal cortex is essential for life
ADDISONS DISEASE
3 CLASSIFICATIONS OF CORTICOSTEROIDS A. mineralocorticoids- includes aldosterone, mineralocorticoidsdesoxycorticosterone, corticosterone - they regulate electrolyte balance by promoting sodium retention and potassium excretion - helps maintain normal blood pressure and cardiac output
ADDISONS DISEASE
- decrease levels of mineralocorticoids(addison s disease) person suffers hypotension, decrease cardiac output and hyperkalemia - increase levels of mineralocorticoids leads hypertension and hyperkalemia B. Glucocorticoids- regulate blood glucose levels Glucocorticoidsincludes cortisol, cortisone and corticosterone - produces anti insulin effect
ADDISONS DISEASE
Effects of glucocorticoids on the body * glucose metabolism- amino acids, lactate, pyruvates metabolismare converted in the liver to glucose(gluconeogenesis) which raises the blood glucose levels * excessive secretion can produce DM * fluid and electrolyte balance- overabundance of balanceglucocorticoid secretion results in hypovolemia and hypertension owing to sodium water retention * inflammatory and immunity- acts to suppress immunityinflammation in response to stress but too much impedes healing and lowers resistance to infection
ADDISONS DISEASE
* stressors- release of glucocorticoids during stressorsstress the person can cope up but insufficient production of gucocorticoids(addison s disease) decrease the resistance to stress C. Sex hormones- adrenal cortex secretes very hormonessmall amount of androgens and even smaller amounts of estrogen than the large amount release by the gonads. - too much release of adrogens causes virilism, while too much estrogen causes gynecomastia
I. ADDISON S DISEASE
Adrenal hypofunction is a deficiency of adrenocortical hormones. Etiology: Addison s disease 1. autoimmune process- circulating autoantibodies react specifically processagainst adrenal tissue 2. hemorrhage into the adrenal gland 3. adrenalectomy 4. neoplasm 5. fungal infection & tuberculosis Secondary adrenal insufficiency 1. suppression of the hypothalamic- pituitary axis from exogenous hypothalamicsteroid use 2. pituitary destruction or removal 3. inadequate cortisol replacement, especially during time of stress
ADDISON S DISEASE
Clinical Manifestation: a. addison disease 1. anorexia, nausea, vomiting, abdominal pain or diarrhea 2. fatigue, muscle weakness & arthralgias 3. decreased alertness & confusion 4. weight loss 5. dry skin, decreased body hair & possible increased pigmentation with excessive ACTH stimulation
ADDISON S DISEASE
b. addisonian crisis (acute adrenal insufficiency)insufficiency)often unrecognized 1. hypotension 2. rapid, weak pulse 3. rapid respiratory rate 4. pallor & extreme weakness 5. hyperthermia Laboratory & diagnostic study: Suggestive findings 1. serum blood glucose 2. serum sodium level 3. serum potassium level 4. white blood cell count
ADDISON S DISEASE
Definitive findings: 1. serum cortisol levels are decreased 2. ACTH stimulation test reveals a low to normal cortisol response Nursing Management: 1. Administer prescribed medications - glucocorticoids (hydrocortisone Na succinate, cortisone, dexamethasone, prednisone, methylprednisolone) - mineralocorticoids (fludrocortisone)
ADDISON S DISEASE
2. Provide immediate treatment for an addisonian crisis. - IVF, glucose & electrolytes administration - Corticosteroid replacement & vasopressors may be administered - client must avoid exertion 3. Help prevent addisonian crisis - take precautions to avoid unnecessary activity & events that may be stressful - ensure hospitalized & acutely ill client on long term glucocorticoid therapy receive additional doses to compensate for stress
ADDISON S DISEASE
4. Provide client & family teaching. a. discuss hormonal therapy (purpose, side (purpose, effects, duration) b. symptoms of abnormalities report to medical doctor c. report to health care providers about the steroid replacement therapy d. if overreplacement of glucocorticoids is indicated, explain the purpose & side effects (cushingoid appearance, weight gain, hirsutism, diabetes mellitus, osteoporosis, infection, muscular weakness, mood swings, cataracts & hypertension
ADDISONS DISEASE
PHARMACOLOGIC INTERVENTION - synthetic corticosteroids taken daily - cortisone or hydrocortisone on a daily basis correct metabolic imbalances - administer oral cortisol with meals or antacids to lessen gastric irritation and possible development of peptic ulcer - administer parenteral cortisol deep into gluteal muscle not into deltoid - cortisol injected SQ causes sterile abscess, tissue atrophy, abnormalities in pigmentation - assess for signs of cushing syndrome due to long term cortisol therapy - fludrocortisone taken daily causes sodium retention -deoxycorticosterone correct electrolyte imbalance
II. CUSHING S SYNDROME

Cushing syndrome ( glucocorticoid oversecretion )- hyperfunction of the adrenal cortex causes excessive production of glucocorticoids, mineralocorticoids and sex hormones Etiology 1. cortisol secreting adrenal tumor- 30 % of tumorcases 2. hyperplasia of adrenal cortex caused by overproduction of ACTH
CUSHING S SYNDROME
Clinical Manifestation: 1. weight gain & altered fat distribution moon face & buffalo hump at C7, truncal obesity, slender limbs- cardinal S/S limbs2. potassium depletion leading to hypokalemia, arrythmias, muscle weakness and renal disorders 3. frequent infections, poor wound healing and lowered resistance to stress owing to suppressed inflammatory response 4. hyperglycemia result to DM 5. mental status changes & mood swings due to increase levels of glucocorticoids and ACTH 6. menstrual disturbances (amenorrhea) 7. diminished libido 8. striae, bruises, acne & thinning of scalp hair
CUSHING S SYNDROME
Laboratory & diagnostic study findings: 1. serum potassium level 2. serum glucose level 3. eosinophils & lymphocyte counts 4. plasma cortisol & 24-hour urine cortisol 24results ACTH5. ACTH (indicative of ACTH-mediated cushing syndrome) 6. selected radiographic & axial CT studies may determine the site of ectopic ACTH production (e.g. bronchogenic oat cell carcinoma)
CUSHING S SYNDROME
Nursing Management: 1. Administer prescribed medications. a. adrenocortical steroid inhibitors ketoconazole (nizoral), aminoglutethimide (cytadren), mitotane (lysodren) 2. Take measures to protect the client from injury & infection a. assess skin integrity regularly
CUSHING S SYNDROME
b. Avoid agents that can damage skin (e.g. tape, strong soaps) c. promote good hygiene d. modify the environment to remove or minimize hazards 3. Prepare the client for surgery, if indicated (bilateral adrenalectomy) 4. Encourage the client & family to ask questions & verbalize concerns about disease pathology, body image, treatment & mental status
DIABETES MELLITUS
Pancreas large fish shaped organ that lies behind the stomach both an exocrine and endocrine gland Exocrine function- secrete enzyme that catalyze the digestion of proteins, functioncarbohydrates and fats Endocrine function- carried out by the islets of langerhans which contains functionalpha and beta cells 2 Hormones secreted by the islet : a. insulin- synthesize by the beta cells, controls fat and protein metabolism insulin- powerful hypoglycemic agent - lowers the blood sugar levels by promoting the passage of glucose into cell b. glucagon- synthesize by alpha cells glucagon- a hyperglycemic agent - raises blood sugar level by promoting the conversion of glycogen( principal storage form of carbohydrate ) to glucose with in the liver
DIABETES MELLITUS
Specific function of insulin . Stimulate the active transport of glucose into muscle and adipose tissue cells. To cross the cell membrane glucose must be bound to insulin and hook up with the receptor sites on cell * Some people with DM have enough insulin but few receptor sites which reduces insulin to transport into the cell *Others have inadequate insulin, glucose remains outside the cell raising the blood glucose concentration above normal . Regulates the rate at which carbohydrates are used by cells for energy . Promotes the conversion of fatty acids into fat which can be stored as adipose tissue . Inhibit conversion of fats to ketone bodies . Stimulate protein synthesis with in tissues
NORMAL CARBOHYDRATE METABOLISM

Carbohydrate glucose( composed of carbon, hydrogen and oxygen ) is one of the body s major fuel Carbohydrates, proteins and fats can all be catabolized by the body for energy but the body uses carbohydrates for energy Glycogen is converted to glucose in the liver for energy In cases body obtain energy protein or fats, fats are metabolized in the liver to ketones which can be released into the circulation Increased amount of ketones in circulation due to decrease insulin can lead to ketoacidosis and coma
III. DIABETES MELLITUS

Diabetes mellitus is a disorder of carbohydrate metabolism resulting from deficiency of or resistance to available insulin & is characterized by hyperglycemia. . Imbalance between insulin demand and supply . It s either the pancreas produces subnormal insulin or the person requires high amounts(obese) INCIDENCE . 3rd leading cause of death in the US because of complications . Average life expectancy decrease about one third . Even diabetes does not kill it produces permanent disabilities ETIOLOGY .heredity .age 40 yrs old .overweight body needs more insulin to metabolize food and decrease insulin receptor sites Types: 1. Type 1 Insulin dependent diabetes mellitus (IDDM) insulin deficiency & risk of ketosis characterize it, accounts 5% to 10% of cases & typically occurs in person younger than 25 years of age.
DIABETES MELLITUS
2. Type II non-insulin dependent diabetes nonmellitus (NIDDM) accounts for 90% of cases & most commonly affects persons older than 40 years old, defects in insulin release & use, insulin resistance & little risk of ketosis characterize it. 3. Gestational diabetes is a transitory glucose intolerance during pregnancy that resolves after delivery, accounts 2% to 5% of all pregnancies, high risk of developing overt diabetes later in life.
DIABETES MELLITUS
4. Diabetes associated with other conditions is described as glucose intolerance caused by other diseases, drugs, or agents. Etiology: 1. Type I (IDDM) a. exact cause unknown b. autoimmune caused by virus c. genetic factors
DIABETES MELLITUS
2. Type II (NIDDM) a. obesity b. genetics 3. Gestational diabetes a. antiinsulin effects of progesterone, cortisol, & human placenta lactogen, which increases the amount of insulin needed to maintain glycemic control. 4. Diabetes associated with other conditions a. pancreatic diseases b. hormonal abnormalities estrogenc. drugs (glucocorticoids, estrogen-containing preparations)
DIABETES MELLITUS
Acute complications: 1. Diabetic ketoacidosis (DKA) an acute insulin deficiency resulting in metabolic acidosis from ketone bodies (acid end-products of fat endbreakdown), occurring in clients with type I diabetes Causes: a. failure to take prescribed insulin b. increased physical stress (infection & surgery) c. psychological stress 2. Hyperglycemic hyperosmolar nonketotic coma (HHNK) occurring in older client s with type II diabetes, is a severe hyperglycemia & hypertonic dehydration without significant ketoacidosis.
DIABETES MELLITUS
Common in type II DM because of enough insulin to prevent development of ketoacidosis Extremely elevated blood glucose levels can lead to polyuria, dehydration and coma Extremely elevated blood sugar with no ketosis causes profound hyperosmolar state that leads to serios volume depletion and shock TPN may precipitate HHNK if person receives solutions containing large amounts of glucose
DIABETES MELLITUS
Causes: a. Stress (infection, surgery & hyperalimentation) b. ingestion of certain drugs (thiazide diuretics, glucocorticoids, phenytoin & sympathomimetics) 3. Hypoglycemia is an excessive insulin to blood glucose ratio linked to excessive use of hypoglycemic drugs agents (e.g. insulin, oral agents), decreased food intake, increased physical activity, excessive alcohol consumption or renal failure , it occur in client s with type I or type II diabetes
Early manifestations
Headache Weakness Irritability Lack of muscular coordination Apprehension DiaphoresisDiaphoresis- due to epinephrine released when blood glucose drops abnormally low Drunk or bizarre psychotic fashion Brain damage develops when deprived of glucose after a drastic drop in blood sugar. Hypoglycemic shock is more dangerous than diabetic coma INTERVENTION . Depends on severity . Mild- glass of orange juice, sugar cubes, candies Mild. Severe- IV glucose ASAP, 20 to 50 ml of D 50% glucose Severe. Never force an unconscious or semi conscious person to drink liquids . ID card or bracelet tags
DIABETES MELLITUS
Chronic complications: 1. Microangiopathy is thickening of capillary basement membrane, most prominently in the eyes causing vascular degeneration in the retina leading to microaneurysm, retinal hemorrhage and blindness whereas in the kidneys it leads to intercapillary glumerulosclerosis and renal failure. 2. Macroangiopathy is atherosclerotic changes accelerated by lipid abnormalities exacerbated by elevated blood glucose level. . May lead to premature CAD . Results in reduced blood supply to the feet causing intermittent claudication, cold feet, infections, inadequate healing of foot lesions, ulceration and gangrene of extremities. 3. Neuropathy is abnormal nerve function, possibly caused by alteration in enzyme systems & affecting nerve sheaths or neural cell function. . Vascular insufficiency and high blood sugar levels both lead to metabolic disturbance in the neuron . Painless neuropathy is a dangerous condition people may be unaware of the injury particularly of the lower extremity 4. Increased susceptibility to infection results from an impaired ability of granulocytes to respond to infectious agents. . Infected areas heal slowly due to damaged vascular system due to insufficient oxygen, nutrients and antibodies to the injured site
DIABETES MELLITUS
Clinical Manifestations: a. Diabetes Mellitus 1. polyuria, polydipsia & polyphagia 2. weight loss 3. fatigue & weakness 4. visual disturbance 5. recurrent skin, vulva & urinary tract infections b. DKA 1. dehydration 2. tachycardia 3. kussmaul respiration 4. acetone breath & decreased LOC 5. nausea & vomiting, abdominal pain
DIABETES MELLITUS
c. HHNK or HHNC 1. dehydration 2. decreased LOC 3. tachycardia 4. hypotension d. Hypoglycemia 1. Cool, moist skin or pallor 2. tachycardia 3. tremor, paresthesia, confusion 4. headache leading to loss of consciousness & seizure
DIABETES MELLITUS
Laboratory & diagnostic study findings: a. Diabetes mellitus 1. FBS level above 140 mg/dL. or postprandial blood glucose level above 200 mg/dL. Measured on more than one occasion 2. Glycosylated hemoglobin (A1C) reveals an elevated blood glucose level over the previous 2 to 4 months 3. Glucose tolerance test reveals blood glucose over 200 mg/dL. At the 2-hour sample 2-
DIABETES MELLITUS
b. DKA 1. serum K levels are elevated 2. arterial blood gas (ABG) values indicate acidosis c. HHNK or HHNC 1. serum blood glucose is higher than 700 mg/dl 2. serum blood osmolarity is higher than 330 mOsm/kg 3. urine specimen reveals an absence of ketosis 4. ABG studies reveals possible mild lactic acidosis 5. renal function test detects azotemia 6. serum electrolytes reveals hypernatremia & hypokalemia
d. Hypoglycemia 1. serum blood glucose level is less than 70 mg/dL. Nursing Management: 1. Administer prescribed medications a. Type I (IDDM) insulin insulin b. Type II (NIDDM) sulfonylureas, thiazolidinediones, biguanides 2. Intervene as indicated for a client exhibiting signs & symptoms of DKA a. administer IVF NSS (0.90% NSS) at high rate followed by hypotonic NSS (0.45% NSS) b. monitor & administer electrolytes as prescribed, major electrolyte concern is potassium
DIABETES MELLITUS
DIABETES MELLITUS
c. infuse regular insulin intravenously at a slow, continuous rate d. monitor blood glucose values hourly e. assess vital signs, lungs, intake & output & monitor ketones f. assess for precipitating factors 3. intervene as indicated to manage HHNK a. provide treatment similar to that of DKA b. because clients are usually older, monitor for CHF & cardiac arrhythmias
DIABETES MELLITUS
4. provide care for a client experiencing hypoglycemia a. monitor blood glucose levels b. administer glucose, sources include - 2 to 3 tsp. sugar or honey - 4 to 6 oz. fruit juice or regular soda - 2 to 4 tablets of commercially prepared glucose - 6 to 10 Life-savers Life- intravenous glucose (50% dextrose) - glucagon (IM or SQ administration)
DIABETES MELLITUS
c. administer a source of long-acting longcarbohydrate to prevent subsequent episodes d. advise the client to carry simple sugar at all times. e. protect the client injury 5. Provide teaching to client & family 6. Provide referrals - American diabetes Association, National Diabetes Information Clearinghouse, American Association of Diabetes Educators & Medic-Alert MedicFoundation
ORAL HYPOGLYCEMIC AGENTS

Insulin is given parenterally because it is destroyed by the GI enzymes 2 classifications a. sulfonylureas- lowers the blood sugar by stimulating sulfonylureaspancreatic beta cells to release insulin, it also increases the number of insulin receptor sites ex. Tolbutamide(Orinase) Chlorpropramide(Diabenase) Glipizide(Glucotrol) b. Biguanides- banned in 1977 due to increase risk of Biguanideslactic acidosis
IV. LIVER CIRRHOSIS

Liver cirrhosis is a chronic, degenerative liver disease marked by diffuse destruction & fibrotic regeneration of hepatic cells. Disorganization of liver architecture by widespread fibrosis and nodule formation and scarring of the liver Hepatocytes(major liver cells) die and replaced by scar tissue Liver regenerate in abnormal pattern forming tiny balls known as nodules Peak incidence occurs between ages 40 & 60 years The incidence of cirrhosis is twice as high among men as women. Types: 1. Laennec cirrhosis(micronodular) . Common in individual who chronically abuse alcohol . Also in non drinkers and ddue to hepatotoxins substance intake 2. Postnecrotic cirrhosis(macronodular) . Most common worldwide, massive loss of liver cells with irregular pattern of regenerating cells 3. Biliary cirrhosis . Bile flow is decreased with concurrent cell damage to hepatocytes around bile ducts
LIVER CIRRHOSIS
2 major clinical problems a. decrease liver function b. portal hypertension- develop in severe cirrhosis hypertensionPortal vein- receives blood from intestine and spleen veinnormal blood flow to and from liver depend on the proper functioning portal vein . It carries nutrients,metabolites and toxins from the digestive organs to the liver for processing and detoxification Portal hypertension- a disease process that alter the flow of blood through the hypertensionliver or it s major vessels Increase pressure in the portal vein causes the ff : . Reverse blood flow and enlargement of esophageal veins . Ascites . Incomplete clearing of metabolic waste
Etiology: 1. Alcoholism & chronic nutritional deficiencies (Laennec cirrhosis) 2. Bile duct disorders (Biliary cirrhosis) 3. Hepatitis (Posthepatic cirrhosis) Clinical Manifestation: 1. enlarged, firm liver 2. chronic dyspepsia & splenomegaly 3. constipation or diarrhea 4. gradual weight loss & ascites 7. dilated abdominal blood vessel 8. S/S of portal hypertension (late) 9. Ascites- plasma leaks directly from the liver Ascitescapsule and congested portal vein into the peritoneal cavity
LIVER CIRRHOSIS
LIVER CIRRHOSIS
Laboratory & diagnostic study findings: 1. Liver biopsy detects destruction & fibrosis of liver tissue 2. liver scan reveals abnormal thickening & masses 3. liver function test results for ALT, AST & LDH levels are elevated 4. serum protein levels reveal hypoalbuminemia 5. PT is elevated
LIVER CIRRHOSIS
Nursing Management: 1. Promote adequate nutrition. a. ensure a nutritious, diet supplemented with vitamins as prescribed 2. Protect client from injury a. turn the client every 2 hours b. use mild, soft soap c. minimize metabolic derangements that can cause further deterioration of mental status d. restrict dietary CHON e. limit visitors & orient the client to date, time & place f. assist with ambulation & raise side rails
LIVER CIRRHOSIS
3. Develop a nursing care plan to address the complications of liver (e.g. jaundice, portal hypertension, hepatic encephalopathy, bleeding esophageal varices) 4. Provide health education 5. Provide referrals a. American Liver Foundation & Alcoholics Anonymous
COMPLICATION OF LIVER CIRRHOSIS

JaundiceJaundice- excessive formation of bile pigments in the blood(hyperbilirubinemia) and in the skin Portal hypertension Bleeding esophageal varices- portal HPN rise to varicesabdominal wall veins and esophagogastric veins dilate and distend Hepatic encephalopathy- elevation of ammonia encephalopathylevels in the blood and CSF due to inability of the liver cells to convert ammonia to urea and damage liver cells and necrosis occurs
HYPERTHYROIDISM
Thyroid gland- located at the neck, just below the cricoid cartilage glandShaped like a letter H ThyroxineThyroxine- one of the 3 major hormones produced Major role . Regulate body metabolism . Regulate growth and development both physical and mental . Carbohydrate, fat and protein metabolism . Resistance to infection . Ensures that oxygen consumption and heat production keep pace with the body s needs and activities * Too much thyroxine causes dangerous speeding of metabolism and high rate of oxygen consumption. In contrary too little results in sluggish metabolism, a slowing physical and mental function in adults and retardation of growth and development in child
HYPERTHYROIDISM
Thyroxine production depends on a. ingestion of sufficient protein and iodine b. release of anterior pituitary hormone called TSH Factors that depress thyroxine secretion . Excessive intake of goitrogens known to inhibit thyroxine production . Ingestion of certain drugs(sulfonamides,salicylates) . Exposure to prolong heat Triiodothyronine(T3)Triiodothyronine(T3)- much more potent than thyroxine Thyrocalcitonin(TCT) capable of lowering both plasma calcium and phosphate
V. HYPERTHYROIDISM
Hyperthyroidism is a metabolic imbalance resulting from excessive thyroid hormone production. Grave s disease is the most common form, disease is greatest between the ages 30 to 40 & is higher among women than men. Etiology: 1. Autoimmune dysfunction- antibodies react against dysfunctionthyroglobulin(storage form of thyroxine)that lead to enlargement of the thyroid gland and secretion of excess thyroid hormone 2. Genetic factors and other factors like a. toxic nodular goiter b. exposure to iodine c. TSH-secreting pituitary tumor (rare) TSHd. Thyroiditis, which may be acute, subacute or chronic (e.g. Hashimoto disease)
HYPERTHYROIDISM
Clinical Manifestation: a. Hyperthyroidism 1. nervousness, irritability, hyperactivity, emotional lability & decreased attention span 2. weakness, easy fatigability & exercise intolerance 3. heat intolerance and profuse diaphoresis 4. weight changes (loss or gain) & increased appetite 5. insomnia & interrupted sleep 6. frequent stools & diarrhea 7. menstrual irregularities & decreased libido
HYPERTHYROIDISM
8. warm, sweaty, flushed skin with a velvety-smooth texture & velvetyspider telangiectasias owing to an accelerated circulation to tissues 9. tremor, hyperkinesia & hyperreflexia 10. exopthalmos, retracted eyelids & staring gaze 11. hair appears thin and soft 12. goiter 13. bruits over thyroid gland 14. elevated systolic blood pressure, widened pulse pressure & S3 sound 15. heart failure & AF (elderly clients) 16. cyclic moods- mild euphoria to extreme hyperactivity or delirium moods17. excessive hyperactivity leads to extreme fatigue and depression
HYPERTHYROIDISM
b. Thyroid storm 1. hyperthermia 2. hypertension 3. delirium 4. vomiting 5. tachyarrhythmias Laboratory & diagnostic study findings: 1. Increased serum T4 & T3 2. Radioactive iodine uptake test shows an increased uptake 3. Serum TSH assay reveals a nondetectable TSH level 4. Thyroid scan reveals increased function in the thyroid gland (hot areas)
HYPERTHYROIDISM
Nursing management: 1. Administer prescribed medications a. antithyroid drugs (levothyroxine: synthroid, SSKI: lugols solution) .PTU.PTU- block thyroid hormone synthesis .Methimazole.Methimazole- more potent than PTU .Adrenergic blocking agent- lessen palpitation and agenttremors 2. Assist the client & family members or significant others in exploring treatment options a. Pharmocotherapy b. Radioactive iodine therapy c. Surgery (subtotal or total thyroidectomy)
HYPERTHYROIDISM
3. Promote rest a. calm & quite environment b. minimize client s energy expenditure by assisting ADL as necessary c. encourage client to alternate periods of activity with rest 4. Promote adequate nutrition a. monitor nutritional status b. provide increased calories & other nutritional support
HYPERTHYROIDISM
5. Prevent injury a. assess the client s mental status & decision-making decisionability, intervene as needed to ensure safety b. provide eye protection with exopthalmos (patches, drops, artificial tears) ExopthalmosExopthalmos- protruding eyes and fixed stare due to accumulation of fluids in the fat pads and muscles that lies behind the eyeballs that push out the eyes that can lead to corneal ulceration and loss of vision 6. Maintain normothermia a. use cooling mattress & acetaminophen, avoid aspirin b. supply sufficient fluids to offset losses from diaphoresis c. provide appropriate comfort measures for the febrile patient
HYPERTHYROIDISM
7. Provide client & family teaching a. reassure the family that any abrupt changes in the client s behavior probably are disease related b. encourage the client to comply with long-term longmedical follow-up therapy follow8. Provide postoperative care a. support the head & avoid tension on sutures b. monitor for complications & intervene as needed (thyroid storm, hemorrhage, tetany, laryngeal nerve injury & edema of the glottis) 9. Provide referrals: Thyroid Foundation of America & National Graves disease Foundation
NEUROLOGIC DISORDERS
I. MYASTHENIA GRAVIS
Myasthenia gravis is a progressive disorder affecting neuromuscular transmission of impulses in voluntary muscle. The incidence is 1 case per 25,000 persons & is higher among women than men, initial symptoms occur between the ages of 20 & 40 years old Etiology: 1. Autoimmune response
MYASTHENIA GRAVIS
Clinical Manifestation: 1. Severe fatigue 2. Drooping facial muscle & ptosis 3. Diplopia 4. Impaired chewing & swallowing 5. Breathing difficulty because of weak respiratory muscle Laboratory & diagnostic study findings: 1. Positive Tensilon test that confirm diagnosis 2. Serum anti-ACHR antibodies are present anti-
MYASTHENIA GRAVIS
Nursing Management: 1. Administer prescribed medications a. anticholinesterase (pyridostigmine: mestinon, neostigmine: prostigmine) 2. If indicated assist the client undergoing medical procedure - plasmapheresis (plasma exchange to reduce titer of circulating antibodies) - thymectomy (decrease formation of anti-ACHR antiantibodies)
MYASTHENIA GRAVIS
3. Prevent problems associated with swallowing difficulty a. provide small, frequent meals & keep suctioning equipment readily available 4. Prevent problems associated with respiratory function a. monitor pulmonary function test b. Promote measures to maintain adequate c. encourage effective coughing, chest physiotherapy & suctioning of secretions 5. Encourage adjustment in lifestyle to prevent fatigue
MYASTHENIA GRAVIS
a. administer medications 30 mins. Before activities b. plan adequate rest period throughout day c. set realistic daily schedule 6. Maximize functional abilities a. prevent complications of immobility b. promote self-care selfc. maximize effective communication 7. Prevent problems associated with impaired vision resulting from ptosis of eyelid a. encourage client to tape eyes open for short intervals
MYASTHENIA GRAVIS
b. instill artificial tears & wear sunglasses when outside 8. Be prepared for emergency treatment of myasthenic or cholinergic crisis a. Determine the type of crisis by administering intravenous edrophonium (tensilon) , if crisis is myasthenic there is improvement & if cholinergic there is no improvement. Treat myasthenic crisis with intravenous anticholinesterase, cholinergic with atropine
II. INCREASED INTRACRANIAL PRESSURE

ICP is the result of the amount of brain tissue, intracranial blood volume & CSF within the skull at any time. The normal ICP depends on the position of the client & is 15 mmHg or less, increased ICP is more than 15 mmHg Etiology: 1. Head injury 2. Stroke 3. Inflammatory 4. Brain tumor 5. Intracranial surgery
INCREASED INTRACRANIAL PRESSURE

Clinical Manifestation: 1. Lethargy (earliest sign), altered LOC, restlessness, slowing of speech 2. Pupil changes (fixed, dilated, slowed response, inequality) 3. Bradycardia & Increase pulse pressure (called cushing reflex) 4. Bradypnea & irregular breathing pattern 5. Hyperthermia (late sign of increasing ICP) 6. Headache 7. Blurred or double vision, photophobia

Laboratory & diagnostic study findings: 1. ICP monitoring reveals an ICP greater than 15 mmHg 2. MRI scans, radiographs, & CT scans may identify the cause of the increased pressure (e.g. tumor, ischemic area) Nursing Management: 1. Administer prescribed medications a. Osmotic diuretics, corticosteroids, analgesic, & sedatives 2. Monitor neurologic status (VS, LOC, Oculomotor nerve, motor & sensory status)

3. Provide safety measures when administering sedatives & analgesics that may depress respiration & decrease LOC a. reduce or eliminate noxious stimuli b. elevate the head of the bed 30 degrees c. hyperoxygenate the client before suctioning 4. Maintain a patent airway a. suction PRN b. position the client to prevent airway obstruction

5. Manage hyperthermnia a. provide only minimal bed coverings & clothing b. use a hypothermia blanket, avoid rapid cooling c. administer antipyretics as prescribed d. force fluids unless contraindicated 6. Prevent infection a. sterile technique for wound care b. insertion of ICP monitoring device & keeping it intact

7. Maintain fluid & electrolyte balance a. monitor intake & output b. monitor for signs of dehydration 8. Help orient the client & reduce confusion a. reduce external stimuli b. provide for adequate c. give simple directions d. provide familiar objects in the client s environment
III. SPINAL CORD INJURIES

Spinal cord injury is a fractures, contusions or compression of the vertebral column with damage to the spinal cord. Common sites of injury include the cervical spine & the junction of the thoracic & lumbar areas (T1 to L1) Etiology: 1. Motor vehicle accidents 2. Diving accidents 3. Falls 4. Sports injuries 5. Gunshot wounds
SPINAL CORD INJURIES

Clinical Manifestations: 1. Pain 2. Paresthesia 3. Loss of consciousness 4. Loss of sensation & altered motor functions Neurologic damage: 1. Below C4 loss of motor & sensory function from the neck down, including independent respiratory function & bowel & bladder control

2. Below C6 loss of motor & sensory function below the shoulders, loss of bowel & bladder control, impaired intercostal muscle function. 3. Below C8 loss of motor control & sensation to parts of the arms & hands, loss of bowel & bladder control 4. Below T6 loss of motor control & sensation below the mid-chest but with motor control & midsensation preserved in the arms & hands, loss of bowel & bladder control 5. Below T12 loss of motor control & sensation in the legs & pelvis, loss of bowel & bladder control

6. Below L2 loss of motor control & sensation in the legs & pelvis, loss of bowel & bladder control 7. Below L4 loss of motor control & sensation in parts of the thighs & legs, loss of bowel & bladder control Laboratory & diagnostic study findings: 1. Spinal radiography can locate the area of cord damage 2. CT scanning can locate the area of cord damage & search for other injuries that often accompany spinal trauma

Nursing Management: 1. Provide emergency treatment a. do not move the client b. keep the neck aligned c. immobilize the head & neck d. maintain a patent airway (e.g. O2 therapy, ABG s & pulse oximeter) 2. Administer prescribed medications a. osmotic diuretics b. muscle relaxants (e.g. Baclofen) c. high dose corticosteroids (e.g. reduces disability if given within 8 hours after injury)

3. Assist with immobilization & reduction of dislocations & stabilization of the cervical vertebral column a. applying skeletal traction (e.g. skeletal Tongs: GardnerGardner-Wells or Crutchfield tongs, halo tongs) 4. Prepare the client for surgery a. usually for repair of fractures or dislocations to stabilize the spinal column. 5. Prevent complication of immobility a. perform passive ROM exercises on paralyzed limbs to maintain joint mobility

6. Prepare client & family for ambulation & home maintenance management a. work with other discipline in securing needed assistive devices b. teach the client transfer skills if appropriate c. collaborate with the clients family to identify ways to adapt the home environment to the client s needs 7. Promote client and family coping a. teach new coping strategies b. evaluate the client s & family members coping strategies

c. encourage the client & family members to verbalize concerns 8. As appropriate, provide information on alternative means for achieving sexual satisfaction 9. Provide a referral a. National Spinal Cord Injury Association

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ACUTE BIOLOGIC CRISIS

SUDDEN INFANT DISTRESS SYNDROME (SIDS)

SUDDEN INFANT DISTRESS SYNDROME

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

STRUCTURE & FUNCTION of the HEART

NURSING PROCESS OVERVIEW for the CARDIOVASCULAR SYSTEM

Pathophysiology of Myocardial Infarction

Cardiogenic shock death

BODY S REACTION TO SHOCK

decrease periphery perfusion - cool & pale skin

Reduced renal perfusion - oliguria

NORMAL SINUS RHYTHM

II. SINUS BRADYCARDIA

III. PAROXYSMAL ATRIAL TACHYCARDIA and SUPRAVENTRICULAR TACHYCARDIA

PAT & SVT

PAT & SVT

PAT & SVT

IV. ATRIAL FIBRILLATION

VI. PREMATURE VENTRICULAR CONTRACTIONS

PREMATURE VENTRICULAR CONTRACTION

VII. VENTRICULAR TACHYCARDIA

VIII. VENTRICULAR FIBRILLATION

IX. VENTRICULAR ASYSTOLE

MANIFESTATIONS THAT DEVELOP IN SOME ENDOCRINE DISORDERS

II. CUSHING S SYNDROME

NORMAL CARBOHYDRATE METABOLISM

III. DIABETES MELLITUS

ORAL HYPOGLYCEMIC AGENTS

IV. LIVER CIRRHOSIS

COMPLICATION OF LIVER CIRRHOSIS

II. INCREASED INTRACRANIAL PRESSURE

INCREASED INTRACRANIAL PRESSURE

INCREASED INTRACRANIAL PRESSURE

INCREASED INTRACRANIAL PRESSURE

INCREASED INTRACRANIAL PRESSURE

INCREASED INTRACRANIAL PRESSURE

III. SPINAL CORD INJURIES

SPINAL CORD INJURIES

SPINAL CORD INJURIES

SPINAL CORD INJURIES

SPINAL CORD INJURIES

SPINAL CORD INJURIES

SPINAL CORD INJURIES

SPINAL CORD INJURIES

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