ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) a form of pulmonary edema that causes acute respiratory failure resulting from

m increased permeability of the alveolocapillary membrane. Fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lungs to stiffen. Effective ventilation is thus impaired, prohibiting adequate oxygenation of pulmonary capillary blood.

ASSESSMENT FINDINGS rapid, shallow breathing dyspnea tachycardia hypoxemia intercoastal and suprasternal retractions crackles and rhonchi restlessness apprehension mental sluggishness motor dysfunction

INTERVENTIONS Mechanical Ventilation improves the gas exchange between the alveoli and pulmonary capillaries by delivering tidal volume under positive pressure (while the patient is sedated), expanding the alveoli, halting the atelectasis and an adequate gas exchange resumes. Types of ventilators used for patients with ARDS include
Volume Cycled Ventilator ends inspiration after a preset volume High Frequency Jet Ventilator delivers a small tidal volumes (up to 300 ml) at a respiratory rate of 60 to 100 beats per minute the small tidal volume intensifies in the patients airway forcing air into the alveoli as a result the exhaled tidal volume exceeds the jet volume delivered.

 Drug Therapy include he following

Fluid Management to maintain circulating blood volume Pulmonary Hygiene suctioning, chest percussion, etc. Nutrition proper diet to prevent progressive weakness of the respiratory muscles

Sedatives Neuromuscular Blockers to paralyze the patient on the ventilator to keep them from fighting the ventilator to help minimize oxygen consumption. Steroids in high doses to reduce inflammation Antibiotics depending on the culture and sensitivity tests

NURSING DIAGNOSES Impaired Gas Exchange related to interstitial and alveolar edema Potential For Fluid Volume Excess related to interstitial and alveolar edema Altered Nutrition, Decreased Less Than The Body Requirements related to a heightened body metabolism and inability to eat as a result of dyspnea and hypoxemia Self-Care Deficits related to mental sluggishness and motor dysfunction Knowledge Deficit related to inadequate information regarding the disease process, treatment options Ineffective Coping related to the disease process, or the inability to communicate while on a ventilator.

NURSING INTERVENTIONS Frequently assess the patients respiratory status-auscultate breath sounds, watch for dyspnea, etc. Observe and document the hypoxemic patients neurologic status LOC, mental sluggishness Maintain a patent airway by suctioning, using sterile, non-traumatic technique Closely monitor heart rate and rhythm, and blood pressure Monitor serum electrolyte levels and correct imbalances MIO, weigh patient daily Check ventilator settings frequently, and empty condensation from tubing promptly to ensure maximum oxygen delivery Monitor ABG studies. Give sedatives as needed to reduce restlessness. Reposition the patient

 THYROID STORM an extreme exaggeration of the clinical manifestation of hyperthyroidism; a life-threatening complication of hyperthyroidism that may lead to cardiac failure. The manifestation of the patient rapidly develops triggered by such conditions such as infection, especially pulmonary infection, sepsis, trauma, sever stress, abrupt thyroid medication withdrawal or overuse and diabetes mellitus.

ASSESSMENT FINDINGS fever usually above 100oF marked tachycardia with arrhytmias agitation and anxiety hot, flushed skin systolic hypertension abdominal pain nausea and vomiting profuse diaphoresis diarrhea dehydration As the thyroid storm progresses, the patient may enter a stupor, then a coma. Hypertension and vascular collapse may follow.

INTERVENTIONS Drug therapy high doses of anti-thyroid drugs Propylthiouracil, Methimazole, iodine Glucocorticorticoids Temperature control with hyperthermia blanket Replacement of fluid volume NURSING DIAGNOSES Altered Body Temperature, Increased related to the disease process Potential For Alteration In Nutrition, Less Than The Body Requirements related to increased metabolic body rate Ineffective Copping related to excessive anxiety Potential For Decreased Cardiac Output related to hypermetabolic responses Potential For Alterations In Bowel Elimination related to diarrhea

NURSING INTERVENTIONS Maintain a patent airway and adequate breathing Maintain IV fluid rate as ordered Administer medications as ordered Reduce fever with cooling blankets and nonslicylate antipyretics Continuous assessment and monitoring for changes in the patients condition.

DIABETIC KETOACIDOSIS an acute metabolic emergency characterized by significant hyperglycemia and ketonemia which result directly from an absolute or relative insulin lack, leading to severe dehydration (from osmotic diuretic), metabolic acidosis (from hyperketonemia), electrolyte depletion (from osmotic diuresis), and hyperosmolarity (from hyperglycemia and dehydration). Assessment Findings Early symptoms include: polyuria, polydipsia, fatigue, malaise, drowsiness anorexia, headache, abdominal pain muscle cramps, nausea, vomiting, constipation

Late symptoms include

Kussmaul breathing
deep, rapid respiration characteristic of diabetic or other causes of acidosis. Syn: Kussmaul-Kien respiration.

Sweetish odor of the breath (due to ketonemia) Hypertension and weak, thready pulse Stupor and coma

Intervention

Insulin Fluid and electrolyte replacement Treat acidosis if necessary

Nursing Diagnosis Potential for fluid volume deficit related to polyuria, dehydration Altered nutrition, less than the body requirements related to nausea, vomiting Potential for electrolyte imbalance related to polyuria Nursing Interventions Monitor fluid and electrolyte balance MIO, Monitor laboratory studies Continuous assessment for changes in the patients status Administer medications

ASSESSMENT FINDINGS changes in the ECG waveforms unconsciousness in V-tach, Asystole TREATMENT Heart Block First Degree No treatment Second Degree atropine, pacemaker, Isuprel Third Degree Pacemaker, Maintain on atropine and Isuprel

(ISOPROTERENOL) while awaiting pacemaker insertion

Ventricular Tacycardia Cardioversion, Lidocaine Ventricular Fibrillation Defibrillation; If unsuccessful with defibrillation, Epinephrine 1 mg. Ventricular Asystole Initiate CPR, Epinephrine, Atropine or Isopreterenol, Pacemaker insertion

NURSING DIAGNOSIS Alteration in cardiac output, less, related to arrythmias Alteration is in tissue perfusion related to a reduced cardiac output Fear or Anxiety related to possible death Knowledge deficits related t inadequate information regarding treatment options, disease process NURSING INTERVENTION Asses for rhythm disturbances Watch for signs of hypoperfusion (such as hypotension, diminished urine output) for patients with abnormally rapid, slow or irregular pulse Look for indications of predisposing factors, such as signs of drug toxicity, especially digoxin report to the doctor and withold next dose

ACUTE MYOCARDIAL INFARCTION ASSESSMENT FINDINGS Severe, persistent chest pain unrelieved by rest or NTG Changes in vital signs such as the pulse may become rapid, iregular or slow, BP may be normal , elevated or lowered, Elevated temperature during the first 24 to 48 hours due to tissue necrosis Others symptoms such as feeling of an impending doom, nausea and vomiting, shortness of breath, cool extremities, perspiration, anxiety, palpable precordial pulse, muffled heart sounds

INTERVENTIONS Morphine or Meridine for pain and sedation Strict bedrest with bedside commode Oxygen administration at a modest flow rate for 24 to 48 hours Thrombolytic therapy up to 6 hours after infarction PCTA Drug Therapy NTG Lidocaine or other antiarrythmic drugs Dobutamine (inotropic drug to treat reduced myocardial contractility) Betablockers to prevent further reinfarction Atropine to treat bradycardia

NURSINGDIAGNOSES Alteration In Cardiac Output related to problems with the preload, afterload or contractility; structural problems such as aneurysms Acute Pain related to disease process / ischemia Anxiety related to fear death, acuteness of the illness Alteration In Cardiac Tissue Perfusion related to a decreased cardiac output Potential for injury related to myocardial ischemia and development of complications such as cardiogenic shock, arrhythmias

NURSING INTERVENTIONS Prevent, detect and treat complications continuous ECG monitoring Assess pain, administer analgesics as ordered Administer oxygen Check vital signs, assess heart sounds Start ECG for new episode of chest pain Control anxiety, provide emotional rest and sleep by sedation Bedrest on proper positioning for 24 hours until hemodynamically stable then progress activity

 Prevent venous stasis leg exercises, TED hose Elimination without strain stool softeners, bedside commode Appropriate diet Sodium and fluid restriction, Fat controlled diet I and O Organize patient care and activities to maximize periods of uninterrupted rest Begin rehabilitation while in CCU

 PREMATURITY the termination of pregnancy in the period from approximately the twenty eighth week to the end of the 37th week of gestation. Approximately 10% of all live births are premature. Weight often indicative of prematurity and physiologic immaturity.

A Premature Infant is one who weighs 2500 Gms (5 lbs. 8oz.) or less at birth; his length from the crown to the heel is likely to be close to 18.5 inches (47cm). His behavior shows immaturity
lacking in normal reflexes and in a general ability to carry on vital functions.

The incidence of prematurity is highest among the low socioeconomic status, and accounts for the highest mortality rate among infants in the first year of life.

FACTORS ASSOCIATED WITH PREMATURITY multiple births premature separation of the placenta maternal diseases such as infectious diseases, cardiac diseases, diabetes mellitus fetal anomalies toxemia of pregnancy placenta previa premature rupture of the membranes drug abuse chronic poor nutrition IUD in the gravid uterus PREVENTION OF PREMATURITY Adequate prenatal care for all prospective mothers

PHYSICAL CHARACTERSITICS of Premature Infants small and limp Skin wrinkled and red, excess lanugo and little or no vernix caseosa; very thin, capillaries visible Head relatively large with prominent eyes, soft ears, and receding chin Thorax less firm and small Abdomen relatively large and protrudes; the genitalia are small undescended testes in males, undeveloped labia minora in females Extremities thin and small muscles; fingernails and toenails are abnormally soft and short Subcutaneous tissue is deficient, his face gives him an old man appearance Normal reflexes such as sucking, swallowing and gag reflexes are absent Poor ear cartilage

PHYSIOLOGIC HANDICAPS OF A PREMATURE INFANT Poor Control of Body Temperature due to

an Immature nervous system, thus the heat regulating is also immature subcutaneous tissue is deficient, thus lacks the insulation provided by such has poor muscular development thus he is inactive very slow metabolic rate

 Difficulty in respiration due to an immature lungs Cyanosis may be due to an increased ICP as a result of birth trauma obstruction of the respiratory tract by mucous secretions poorly developed lungs (immature) abdomen is relatively large and appear distended, thus may interfere with the movement of the diaphragm

Apnea may result from

Inability to Handle Infections Adequately

may be due to

excessive analgesics or anesthetics given to the mothers during labor and delivery general immaturity of the nervous system and the respiratory tract has a poorly developed immune system and response

Tendency to Hemorrhage and Anemia

fragile blood vessels lacking in the normal supply of Vitamin K RBCs are easily destroyed tendency to loss blood more because he lack iron and the other hematogenous factors

 Tendency for rickets to develop

lacks the ability to absorb fat-soluble vitamins (Vit. A, D, E, K) from his feeding due to an immature GI tract lacks the Calcium, Phosphorus and Vitamin D which is stored in the body of a full term infant

Disturbance in nutrition due to

Impairment of the Renal Function due to

incomplete development of the kidney

a poor sucking and swallowing reflexes an immature GI tract

CARE AND MANAGEMENT OF PREMATURE INFANTS Immedately After Birth

Warmth Place infant in an incubator provided with necessary facilities for increasing environmental oxygen and humidity Initiation Of Respiration Respiration should be cleared by suctioning mucous from the airway very gently Position the infant with head down for natural drainage of position Administer artificial respiration with a mechanical devise (resuscitator), if the infant is hypoxic

 Oxygen Administration
Should be given if respiration are not established in the first few seconds and the infants become cyanotic

Medications Commonly Used in treating unusual conditions in the premature

Epinephrine Cardiac stimulant given IM Caffeine sodium benzoate given IM as respiratory stimulant Vitamins K given IM to reduce bleeding tendencies

Within The Nursery Environment

Minimal Handling

The nursery is isolated from all other units to minimize traffic and ensure protection from infection Lessens the danger of infection Conserves the infants strength

Maintenance Of Body Temperature

The infant is placed in an incubator in a warm nursery to provide the required environmental heat in order to maintain the infants body temperature

 Maintenance Of Respirations
Vaporizers are used to provide high humidity Positioning the infant on his side to get the maximum amount of air into the lungs change his position every 3-4 hours Administer oxygen if necessary concentration should not exceed 40%

 Nutrition

Formulas should be high in protein, low in

fat and of average carbohydrate content

The premature infant has a small gastric capacity but a great need for calories; thus he can tolerate small frequent feedings Methods of feeding include gavage feeding for small prematures without good sucking or swallowing reflexes; Dropper or nipple feeding for vigorous premature infants with a good sucking and swallowing reflex; or gastrostomies, if indicated. Allow the infant to rest prior to feeding he easily tires from procedures and will eat better if rested.

 Medications Necessary For Growth and development

Vitamin C 50 mg Vitamin D 1000 I.U. given within 2 weeks Iron by about six weeks when the infant is 1.5 to 2 times birth weight

Prevention Of Infection

Sterile feeding equipment to prevent GI infection. Scrupulous hand washing by all personnel handling the infant and entering the nursery.

 Such infant must have his own equipment, supplies used should be sterile as much as possible. Use gown and mask technique as prescribed by hospital protocol. Minimize the number of persons who come in contact with the premature infant. Nurses or other health personnel who come in contact with these infants should be free of any type of infection. There should be no dry dusting or sweeping in the nursery.

SPECIAL HEALTH PROBLEMS OF THE PREMATURE INFANT Retrolental Fibroplasia the abnormal replacement of the sensory retina by fibrous tissue and blood vessels occurring mainly in premature infants who are subjected to a high oxygen environment. Oxygen given beyond the point of infant need will cause the retinal arteries to constrict resulting to anoxia. The retina detach from the surface of posterior chambers and a fibrous mass forms, resulting in an ability to receive visual stimulation. This is the chief cause of blindness among infants under 1500 gm of birth weight and of gestational age of six to seven months.

Respiratory Conditions

Anoxia Of The Newborn a condition

Symptoms yellow, meconium-stained amniotic fluid and yellowish vernix caseosa pallor or cyanosis lack of muscle tone variable heart beat

wherein the infants vital organs, especially the brain receives less oxygen than they need for optimum functioning due to any cause which limit the oxygen supplied by way of the maternal and fetal circulation from reaching the brain of the fetus.

Interventions
Respiratory resuscitation Oxygen administration Administer Nalorphine Hydrochloride (Nalline) a powerful emergency respiratory stimulant when the cause of dpression is a narcotic CPR

Respiratory Distress Syndrome also

known as Infant Respiratory Distress Syndrome (IRDS), previously called Hyaline Membrane Disease

Results from a deficiency of the alveolar surfactant as caused by an immature surfactant production the synthesis of surfactant in the utero takes place for lung maturation to be complete at about 35 weeks gestation. Healthy full term infants produce more surfactant that they actually need the excess spills into the amniotic fluid where it is lost or discarded when the amniotic sac ruptures during delivery.

 Symptoms
cyanosis tachypnea retractions nasal flaring and see-saw respiration diminished breath sounds hypotension
Administration of oxygen Administration of synthetic surfactant via tracheal drip to premature infants

Interventions

Other Complications Hypoglacemia the infants serum sugar levels are less than 25 mg/100 ml dil occur as a result of the reduced glycogen storage of the premature infant at birth and his limited carbohydrate tolerance Symptoms
jitterness lethargy tachypnea or apnea cyanosis convulsions high pitched, week cry pallor sweating

Intervention

Increase blood sugar intake by oral feeding or IV slowly

Hypocalcemia serum level are less than 7

Symptoms

mg (3.5 mEq/L) occurring because of the reduced calcium storage at birth

twitching convulsions hypotonia lethargy high-pitched cry increased apneic spells abdominal distention with ileus Interventions

Oral or IV administration of calcium

NURSING DIAGNOSES AND SPECIFIC NURSING INTERVENTIONS for the premature infants and family Potential For Impaired Gas Exchange related to lack of sufficient surfactant Potential for Fluid Volume Deficit related to insensible water loss and inadequate fluid intake Alteration in nutrition less than the body requirements, related to actual intake less than the caloric requirements High Risk for Infection related to Immature Immune System Parental Knowledge Deficit related to the care of the preterm infants

POSTMATURITY - The postmature infant is one who remains in the uterus from one to three weeks or more after the expected date of delivery beyond 42 weeks or 300 days of gestation and who may show signs of weight loss with placental insufficiency.

About 5% of the newborn infants are born postmature. These infants may experience the effects placental insufficiency as a result of aging, intrauterine malnutrition and hypoxia. Normally, before the termination of the pregnancy, at the point when birth should have occurred, the placental function begins to diminish, resulting in impaired oxygen and inadequate nutrient transfer to the fetus.

PHYSICAL CHARACTERISTICS OF PREMATURE INFANTS reduced or absent vernix caseosa and lanugo abundant scalp hair reduced subcutaneous tissue loose skin especially on the buttocks and thighs cracked, thin skin wrinkled macerated skin greenish-yellow staining of the skin, nail and cord-indicating fetal distress having an alert, wide-eyed look just like a 2 to 3 week old infant, following delivery

CLINICAL PROBLEMS OF POSTTERM INFANTS Hypoxia Meconium aspiration Perinatal asphyxia Polycythemia Thermal regulation problems Pulmonary problems such as pneumonia, pneumothorax MANAGEMENT OF POSTMATURITY concerned with the termination of pregnancy either by Induction of labor Ceasarean section

NURSING DIAGNOSES and NURSING INTERVENTIONS Impaired Gas Exchange related to Hypoxia or Meconium Aspiration secondary to placental insufficiency Alteration In Nutrition, Less Than The Body Requirement related to an increased caloric requirement Parental Knowledge Deficit Related to the care of their postterm infants Potential for Injury related to problems associated with the complications common among post term infants.

GRAVIDA-CARDIAC PATIENT IN LABOR The diagnosis of cardiac disease is not an indication for the early induction of labor. Clients are usually allowed to go into spontaneous labor. However, an interdisciplinary team effort is needed to appropriately manage the pregnant woman with cardiac disease
MANAGEMENT OF GRAVIDA-CARDIAC PATIENTS IN LABOR Hospitalization for a short period prior to the expected onset of labor is occasionally recommended.

 Relief of Discofort and Anxiety during the labor effective intrapartum pain relief may reduce cardiac workload by as much as 20%

Systematic analgesics combined with sedatives may be administered early in the first stage of labor Caudal or epidural anesthesia may be initiated, as the labor will progress

Maintain the patient on a Left side-lying position to improve cardiac circulation and maximize oxygenation Administer oxygen if pulmonary complications arise Perform continuous fetal monitoring Attach the patient to continuous ECG monitoring and perform continuos hemodynamic monitoring as indicated.

 Administer medications as needed

Prophylaxis antibiotics for patients who will undergo ceasarean section For patients with prosthetic valves and receiving anticoagulant therapy (lifelong treatment) hold before delivery and resume 6 12 hours after delivery

Controlled Vaginal Delivery preferred CS

Delivery is done is the lateral position of in a supine position with the client tilted to the left to decrease the risk of hypoventilation Use of high stirrups is contraindicated or inappropriate. Forceps or vacuum extractor commonly applied during the second stage of labor to avoid the stress of increased abdominal pressure created by the maternal pushing