ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)
– a form of pulmonary edema that causes acute respiratory failure resulting from increased permeability of the alveolo-capillary 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 patient’s airway forcing air into the alveoli – as a result the exhaled tidal volume exceeds the jet volume delivered.
• Drug Therapy – include he following
– 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
• Fluid Management – to maintain circulating blood volume
• Pulmonary Hygiene – suctioning, chest percussion, etc.
• Nutrition – proper diet to prevent progressive weakness of the respiratory muscles
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 patient’s respiratory status-auscultate breath sounds, watch for dyspnea, etc.
• Observe and document the hypoxemic patient’s 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 patient’s 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
• 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 patient’s 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 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
– excessive analgesics or anesthetics given to the mothers during labor and delivery
– general immaturity of the nervous system and the respiratory tract
• Inability to Handle Infections Adequately
– has a poorly developed immune system and response
• Tendency to Hemorrhage and Anemia – may be due to
– 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
– a poor sucking and swallowing reflexes
– an immature GI tract
• Impairment of the Renal Function – due to
– incomplete development of the kidney
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
– The nursery is isolated from all other units to minimize traffic and ensure protection from infection
Minimal Handling
– Lessens the danger of infection
– Conserves the infant’s 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 infant’s 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 wherein the infant’s 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.
Symptoms
• yellow, meconium-stained amniotic fluid and yellowish vernix caseosa
• pallor or cyanosis
• lack of muscle tone
• variable heart beat
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
• Interventions
– Administration of oxygen
– Administration of synthetic surfactant – via tracheal drip to premature infants
Other Complications
• Hypoglacemia – the infant’s 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 mg (3.5 mEq/L) – occurring because of the reduced calcium storage at birth
Symptoms
• 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 (life- long 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.
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