ACUTE BIOLOGIC CRISES HIGH RISK ADULT: RESPIRATORY DISORDERS 1.

PULMONARY EMBOLISM Occurs when a pulmonary embolus [thrombotic (blood clot) or nonthrombotic (fat) emboli] lodges in the pulmonary artery system. This blockage obstructs blood flow to the lung tissue supplied by the affected vessel. 2 types: 1. Thrombotic emboli mainly originate from the deep veins of the legs, right ventricle of the heart, or pelvis.

2. Nonthrombotic emboli mainly originate from fat release after skeletal injuries, amniotic fluid, air, and foreign bodies. The Virchows Triad - Three conditions and risk factors that can predispose a patient or that can precipitate the formation of venous thrombi. 1. Venous stasis eg. atrial fibrillation, heart failure immobility, polycythemia, pregnancy, varicose veins 2. Vessel wall injury eg. infection, trauma 3. Coagulation problems Pathophysiologic Changes Embolus lodge in the pulmonary vasculature-Pulmonary embolism (decreased/nonperfusion of alveoli distal to occlusion)- Infarction of pulmonary vessel <-----impaired gas exchange ---

decreased C02-bronchoconstriction-shunting of blood to ventilated areas of the lungs- increased pulmonary resistancehypoxiarelease of mediators at the injury siteincrease right ventricular workloadvasoconstrictionright ventricular failure pulmonary hypertensionventricular failure decreased cardiac output decreased blood pressureshockdeath Clinical Manifestations Shortness of breath and/or tachypnea- a response to the hypoxia that develops from impaired gas exchange

Cough Hemoptysis occurs when an infarction at or near the periphery of the lung begins to hemorrhage Chest pain generally comes from an infarction of the pulmonary vessel near the area in which the pleural nerves innervate. Usually worsen when the patient takes a deep breath. Tachycardia a response to the decrease in oxygenation and impaired gas exchange Jugular vein distention a result of pulmonary hypertension and the decreased effectiveness of the right ventricle Hypotension observed with large pulmonary embolism and is related to the decrease in cardiac output after ventricular dysfunction.

Diagnosis Chest radiograph excludes other reasons that may cause the same clinical manifestations. May show pulmonary artery distention, an elevation of the diaphragm, and small infiltrates or pleural effusions.

ABG analysis can reveal respiratory alkalosis, low partial pressure of oxygen, and low partial pressure of carbon dioxide Electrocardiogram involve transient nonspecific ST segment and T wave changes.

Management The best treatment for pulmonary embolism is PREVENTION. When patients are at risk for developing pulmonary embolism, prophylactic measures should be instituted such as intravenous or subcutaneous heparin (Lovenox) or oral anticoagulants such as warfarin (Coumadin). The goal of therapy is to prevent thrombi formation, limit thrombi growth, and encourage breakdown of existing thrombi. Management of hypoxia may require supplemental oxygen, intubation and mechanical ventilation. Heparin Therapy started with a bolus (usually based on patients weight) and a continuous infusion adjusted every 4-6 hours, depending on the institutions protocol. Activated partial thromboplastin time (apt) should be maintained at 1.5-2.0 times the normal value. generally continued for 7-14 days while the patient is on bedrest reversal agent (antidote) is protamine sulfate. The reversal agent for warfarin (Coumadin) is vitamin K or fresh frozen plasma.

Surgical intervention is rarely used and is considered a last resort.

Pulmonary embolectomy is the removal of a clot from the larger vessel of the pulmonary vasculature. This surgery carries a high risk of death and is only used in those patients who do not respond or have contraindications to other interventions. Nursing Responsibilities The main nursing goal is to prevent the development of deep venous thrombosis (DVT) that may lead to a thrombotic pulmonary embolism. Interventions should include early ambulation, use of pneumatic stockings, support hose, and passive rangeof-motion exercises. All of these improve venous blood flow and increase circulation. Other nursing interventions include the following:

Signs and symptoms of DVT are monitored in the lower extremities (calf pain or tenderness, redness, swelling, warmth, pain on dorsiflexion of foot [Homans sign]). If Homans sign is positive, DO NOT retest it; doing so may dislodge the clot. Prescribed oxygen therapy is maintained, and the patient is asked to cough and deep breath every 2 hours Signs and symptoms of respiratory distress or a worsening of pulmonary status (heart failure, pulmonary edema) are monitored, and the physician is notified of any developments. ABG analysis is monitored and pulse oximetry is continuously taken.

Patient is positioned for comfort and maximal oxygenation, as well as to promote the expulsion of secretions. Signs and symptoms of bleeding are monitored when anticoagulant or thrombolytic therapy is in progress. (eg. blood in stool or urine, pale mucous membranes, petechiae, echymosis, complaints of back or flank pain).

2. ACUTE RESPIRATORY DISTRESS SYNDROME

A clinical syndrome characterized by a sudden and progressive pulmonary edema, increasing bilateral infiltrates, hypoxemia refractory to oxygen supplementation and reduced lung compliance. A syndrome with inflammation and increased permeability of the alveolar capillary membrane that occurs as a result of an injury to the lungs. This inflammation causes noncardiogenic pulmonary edema with severely impaired gas exchange. Etiologic Factors Related to ARDS:

1. Aspiration (gastric secretions, drowning, hydrocarbons) 2. Drug ingestion and overdose 3. Hematologic disorders 4. Prolonged inhalation of high concentrations of oxygen, smoke, or corrosive substances 5. Localized infection (bacterial, fungal, viral pneumonia) 6. Metabolic disorders ( pancreatitis, uremia) 7. Shock (any cause) 8. Trauma ( pulmonary contusion, multiple fractures, head injury)

9. Fat or air embolism 10. Systemic sepsis Pathophysiology lung injury immune system initiates an inflammatory response activation of neutrophils, macrophages, and endotoxins into the lungs and the release of mediators increased alveolomembrane permeability fluid enters into the lung tissue Acute Respiratory Distress Syndrome alveolar collapse narrowing of airways pulmonary vasoconstriction hypoxia pulmonary hypertension hyperventilation right ventricular dysfunction respiratory failure decreased cardiac output Clinical Manifestations: 1. Rapid onset of severe dyspnea 2. Anxiety 3. Labored breathing and tachypnea Assessment: Intercostal retractions and crackles

In patients with ARDS, PaO2 will be low, despite oxygen administration, pCO2 will decrease as a result of hyperventilation.

Medical Management: - The main goals in the treatment of ARDS include improving and maintaining oxygenation, maintaining fluid and electrolyte imbalances, providing adequate nutrition, and preventing respiratory and metabolic complications. 1. Primary focus of management includes identification and treatment of the condition. 2. Supportive Therapy: Intubation and mechanical ventilation to maintain adequate gas exchange

3. Circulatory support, adequate fluid volume and nutritional support. -Fluid restriction is generally observed to prevent further leakage of fluid into the alveoli and to decrease pulmonary edema, but fluid restriction can also cause a decrease in cardiac output and blood pressure. 4. Supplemental oxygen is used as the patient begins the initial spiral of hypoxemia. Oxygen toxicity may develop if high concentrations of oxygen are used for longer than 2448 hours. 5. Positive end-expiratory pressure (PEEP)- generally leads to improved gas exchange and allows for lower concentrations of oxygen to be used. 6. Hypovolemia must be carefully treated. 7. Intravenous crystalloid solutions are administered. 8. Pulmonary artery pressure catheters are used to monitor patients fluid status Nursing Management: 1. Positioning is important. - Nurse should turn the patient frequently to improve ventilation and perfusion in the lungs and enhance secretion drainage. - Prone positioning is an intervention that may improve oxygenation by decreasing edema and atelectasis, thereby providing an improved distribution of oxygen throughout the lungs. 2. Nurse must closely monitor rapid changes in oxygenation with changes in position. 3. The nurse should explain all procedures and deliver care in calm, reassuring manner.

4. Rest is essential to reduce oxygen consumption Nursing Diagnosis: Impaired gas exchange r/t inadequate respiratory center activity, chest wall movement, airway obstruction, fluids in the lungs

RESPIRATORY FAILURE Respiratory failure is a sudden and life-threatening deterioration of the gas exchange function of the lung. Exists when the exchange of oxygen for carbon dioxide in the lungs can not keep up with the rate of oxygen consumption and carbon dioxide production by the cells of the body. ACUTE RESPIRATORY FAILURE (ARF) Defined as a fall in arterial oxygen tension and a rise in arterial carbon dioxide tension. The ventilation and/or perfusion mechanisms in the lung are impaired.

Respiratory system mechanisms leading to ARF include: 1. Alveolar hypoventilation 2. Diffusion abnormalities 3. Ventilation-perfusion mismatching 4 . S h u n t i n g Pathophysiology

 Common Causes of Acute Respiratory Failure: 1. Decreased Respiratory Drive May occur with severe brain injury, large lesions of the brain stem (multiple sclerosis), use of sedative medications, and metabolic disorders such as hyperthyroidism. This disorders impair the normal response of chemoreceptors in the brain to normal respiratory stimulation

2. Dysfunction of the Chest Wall

The impulses arising in the respiratory center travel through nerves that extend from the brain stem down the spinal cord to receptors in the muscles of respiration. Thus, any disease of the nerves, spinal cord, muscles or neuromuscular junction involved in respiration seriously affects ventilation and may lead to ARF

3. Dysfunction Of Lung Parenchyma Pleural effusion, hemothorax, pneumothorax, and upper airway obstruction are conditions that interfere with ventilation by preventing expansionof the lung. These conditions, which may cause respiratory failure, usually are produced by an underlying lung disease, pleural disease, trauma and injury.

Other diseases and conditions of the lung that lead to ARF pneumonia, status asthmaticus, lobar atelectasis, pulmonary embolism pulmonary edema

4. Other Factors In the postoperative period, esp. after major thoracic or abdominal surgery, inadequate ventilation and respiratory failure may occur. Causes of ARF during this period include the effects of anesthetic agents, analgesics, and sedatives; they may depress respiration and lead to hypoventilation.

Clinical Manifestations: Early signs are those associated with impaired oxygenation Restlessness fatigue headache dyspnea air hunger tachycardia tachypnea central cyanosis diaphoresis respiratory arrest Physical findings use of accessory muscles, decreased breath sounds Medical Management Objectives of treatment are to correct the underlying cause and to restore adequate gas exchange in the lung. Intubation and mechanical ventilation Nursing Management:

Assist with intubation

Assess respiratory status by monitoring patients level of response, arterial blood gases, pulse oximetry and vital signs Implement strategies to prevent complications: turning schedule, mouth care, skin care, ROM

CHRONIC RESPIRATORY FAILURE

Defined as deterioration in the gas exchange function of the lung that has developed insidiously or has persisted for a long period after an episode of ARF. Patients develop a tolerance to the worsening hypoxemia and hypercapnia. Patient with chronic respiratory failure may develop Acute respiratory failure seen in COPD patients who develops an exacerbation or infection that causes additional deterioration of the gas exchange mechanism. 2 Causes of Chronic Respiratory Failure: 1 . C O P D 2. Neuromuscular Diseases

Mechanical ventilation * is a form of artificial ventilation that takes over all or part of the work performed by the respiratory muscles and organs. * It is initiated when the patients ability to oxygenate and exchange carbon dioxide is impaired.

* Indicated for the following reasons: Hypoxemia Aspiration Atelectasis Pulmonary Edema Pulmonary Embolism Respiratory Distress To reduce intracranial pressure To stabilize the chest wall Respiratory Muscle Fatigue Acute Respiratory Distress Syndrome Over sedation *The main goal of mechanical ventilation is to support gas exchange until the disease process or condition is resolved. Positive pressure ventilation is the most common form of mechanical ventilation used in the acute care setting. This form of ventilation forces oxygen into the lungs, either through an endotracheal tube or a tracheostomy tube, mimicking respiration. Modes of Ventilation there are various modes of ventilation that may be used to ventilate and oxygenate the patient. these modes are ways in which ventilation is triggered; they allow the patient some or all control over his or her breathing. 1. Controlled ventilation (CV) delivers a preset volume or pressure at a preset rate. This mode takes away all control of breathing from the patient. it is primarily used for patients who have no respiratory effort at all.

2. Assist-control ventilation (ACV) delivers a preset volume or pressure whenever the patient initiates a breath. If the patient does not initiate a breath by a preset time, the ventilator will give one. This mode is used primarily for the patient with normal breathing but who has weak respiratory muscles or who cannot achieve an adequate volume on his or her own. 3. Synchronized intermittent mandatory ventilation (SIMV) delivers a preset volume at a preset rate and is synchronized with patients effort. This mode allows for spontaneous breathing between ventilated breaths and prevents competition between the patient and the ventilator. When a spontaneous breath occurs, it is at the patients own rate and tidal volume. SIMV is the most common mode used and allows for weaning from the ventilator. 4. Pressure-controlled ventiation (PCV) delivers a positive pressure breath until a maximum amount of pressure is reached; then the breath stops. The maximum pressure limit is preset and helps prevent barotraumas (damage from the pressure) to the lungs. The amount of volume that is delivered varies, based on airway resistance and lung compliance. Usually the maximal pressure limit is set to achieve a goal tidal volume that is designed by the physician. 5. Inverse-ratio ventilation (IRV) is used when the inspiratory time is increased and the expiratory time is decreased. With IRV the inspiration-expiration (I/E) ratios used most are 1:1 and 2:1. This mode of ventilation allows for a longer period for gas exchange toimprove

oxygenation. This mode is generally used in patients with ARDS. This type of ventilatory mode creates an abnormal breathing pattern for the patient; consequently the patient may become uncomfortable and anxious. 6. Constant positive airway pressure (CPAP) provided positive pressure during spontaneous breaths; the ventilator will not initiate any breaths. This mode increases oxygenation by opening any closed alveoli that may occur at end-expiration. CPAP generally ranges from5-10 cm water pressure. Greater than 10 cm water pressure may increase intrathoracic pressure to the point that it affects the patients venous return, decreasing cardiac output and blood pressure. CPAP at this level may also cause a pneumothorax to occur 7. Positive end-expiratory pressure (PEEP) adds positive pressure during expiration of each ventilated breath. Ventilator settings must be individualized to each patient to allow for optimal gas exchange. Settings are generally based on arterial blood gas (ABG) measurements and arterial oxygen saturation level.

VENTILATOR SETTING / DESCRIPTION / RANGES

1. VT ( Tidal Volume) Amount of oxygen delivered to patient with each

preset ventilated breath. 5-15ml/kg (average 10ml/kg)

2. Respiratory rate Number breaths per minute that ventilator is set

to deliver.

4-20 breaths/min

3. FIO2 (Fraction of Inspired Oxygen) Percentage of oxygen delivered by ventilator with

each breath. 21%-100%

4. I/E Ratio (Inspiratory to Expiratory) duration of I/E time 1:2 (unless IRV is used) 5. Sensitivity Determined how fast ventilator will delivered

during inspiration High: increase airway pressure Low: decrease airway pressure

6. Pressure Limits Regulates maximum amount of pressure the

ventilator will generate to deliver preset ventilator. Ventilated breath is stopped when pressure limit is reached.

Barotrauma occurs when high airway pressures cause overdistention of the alveoli, rupture and leakage of air. Barotrauma can cause pneumothorax, subcutaneous emphysema, or crepitus. Air can leak under the mediastinum or into the pericardium or peritoneum, causing problems with organs located in these areas. A patient needing long-term ventilatory management will need a tracheostomy placed at some point.

 Endotracheal tubes (oral or nasal) are not intended for long-term management and may lead to other problems such as mucosal breakdown, skin ulcerations (lips), sinusitis, and vocal cord paralysis or damage (or both). The following are practices performed for patients receiving mechanical ventilation:

The respiratory status is assessed every 4 hours and more frequently when a change in condition occurs. Close attention is paid to breathing sounds and the amount of patient effort. Signs of hypoxia are assessed. These signs include restlessness, anxiety, increased heart rate and blood pressure, increased respiratory rate, and oxygen saturation via pulse oximetry less than 90%. Endotracheal or tracheostomy tube placement is maintained by properly securing the tube and preventing inadvertent extubation by staff or patient. Placement is maintained until extubation. The endotracheal tube is repositioned per institutional policy to prevent pressure sores. Secretions are suctioned to maintain an open airway. Amount, color, and consistency of the secretions are noted, as well as how the patient tolerated the procedure. Ventilator settings and alarms are verified dehydration. Unlike patients with DKA, patients with HHNC do not develop ketoacidosis, but the reason for this is not known.

Contributing factors include:

The limitation on ketogenesis by hyperosmolarity the lower levels of free fatty acids available for ketogenesis the availability of insulin in amounts sufficient to inhibit ketogenesis but not sufficient to prevent hyperglycemia the hepatic resistance to glucagon in these patients.

Management: refer to DKA

THYROTOXIC CRISIS (THYROID STORM)

A severe form of hyperthyroidism marked by sudden release of thyroid hormone into the blood stream

Precipitating Factors

Stress such as injury, infection, thyroidal and nonthyroid surgery, tooth extraction, insulin reaction, diabetic acidosis, pregnancy, digitalis intoxication, abrupt withdrawal of anti-thyroid medications, extreme emotional stress, or vigorous palpation of the thyroid.

Clinical Manifestations 1. High fever 2. Diaphoresis 3. Cardiopulmonary symptoms: extreme tachycardia, HPN, arrhythmias, CHF, pulmonary edema 4. CNS symptoms: increasing feeling of tremulousness to severe agitation, psychosis with developing apathy, irritability, coma , heat intolerance 5. GI disturbance: weight loss, diarrhea, abdominal pain

6. Increased T3T4 and elevated BUN Medical Management 1. Immediate objectives: to reduced body temperature and heart rate and to prevent vascular collapse 2. Administration of humidified oxygen to improve tissue oxygenation and meet metabolic demands 3. Monitor respiratory status: arterial blood gas or pulse oximetry 4. PTU or methimazole is administered to impede formation of thyroid hormone and block conversion of T4 to T3 the more active form of thyroidhormone 5. Hydrocortisone is prescribed to treat shock or adrenal insufficiency. 6. Iodine is administered to decrease output of T4 from the thyroid gland 7. For cardiac problems: Sympatholytic agents may be administered. Propranolol in combination with digitalis, been effective in reducing severe problems has

cardiac

ADRENAL CRISIS: Pheochromocytoma

A tumor that originates from the chromaffin cells of the adrenal medulla Peak incidence is between ages 20 and 50 years old

The cause of high BP in 0.9% to 2.2% of patients with HPN One form of HPN that is usually cured by surgery

Clinical Manifestations Typical triad of symptoms: Headache, Diaphoresis, Palpitations HPN may be intermittent or persistent Tremor, flushing and anxiety Hyperglycemia may result from conversion of liver and muscle glycogen to glucose Clinical picture is usually characterized by: 1. Acute, unpredictable attacks, lasting seconds or several hours 2. Patient is anxious, tremulous and weak 3. Headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea 4. Polyuria, nausea, vomiting, diarrhea, abdominal pain 5. Feeling of impending doom 6. Palpitations and tachycardia 7. BP as high as 350/200 mm Hg Assessment/Diagnostic Findings: Signs of sympathetic nervous system over activity: 5 Hs (HPN, headache, hyperhidrosis (excessive sweating), hypermetabolism, and hyperglycemia) Medical Management: Pharmacologic Therapy

1. Close monitoring of ECG changes and careful administration of alpha-adrenergic blocking agents, muscle relaxants to lower BP quickly. 2. Long-acting alpha blocker to prepare patient for surgery 3. Beta-adrenergic blocking agents for patients with cardiac dysrhythmias Surgical Management

Adrenalectomy- surgical removal of the tumor

HEPATIC FAILURE (Hepatic Coma) An end stage of liver disease, usually arises as a complication of conditions that cause liver dysfunction although it can be idiopathic Also called Hepatic coma because the patients neurologic status gradually deteriorates Represents the most advanced stage of hepatic encephalopathy A life threatening crisis may occur if the serum ammonia level rises, causing cerebral ammonia intoxicationCauses:1. Cirrhosis2. Hepatitis3. Drug or toxin-induced damage4. Fatty liver 5. Portal HPN6. Surgically-created portal systemic shunts that bypass the liver and allow toxins into the

bloodPathophysiology:Liver disease alters liver structure and compromises essential functions. This leads to impaired protein, fat and carbohydrate metabolism, fluid andelectrolyte imbalance, poor lymphatic drainage, reduced coagulation and impaired detoxification of ammonia and of the metabolites. Ammoniaaccumulation and intoxication is the primary pathogenesis of hepatic failure and the ensuing encephalopathy. Ammonia accumulates because liver cells cannot detoxify and convert to urea the ammonia that is in constant supply in GI tract blood. Remaining liver functions may become impairedand may be difficult to treat or control. Hepatic failure may progress insidiously to a comatose state from which the patient rarely recovers. Clinical Findings: Stage 1 Slight personality and mood changes, disorientation, forgetfulness, slurred speech, slight tremors, periods of lethargy and euphoria, mildconfusion, inability to concentrate, hyperactive reflexes, sleep-wake patterns, handwriting starts to decline and mild asterixis (flapping tremorsof the hand) may appear Stage 2 The patient grows more disoriented and drowsy. He may display inappropriate behavior, mood swings, agitation, apraxia. His hand writingbecomes illegible and asterixes may become pronounced Stage 3 The patient becomes severely confused and may become combative, incoherent and hard to arouse. Sleeps most of the time. You may detecthyperactive deep tendon reflexes and rigid extremities Stage 4

The pupil is comatose and does not react to stimuli. Pupils are dilated and lack corneal and deep tendon reflexes. Extremities are flaccid andmay assume flexion or extension posturing, decebrate rigidity. The EEG is markedly abnormal.Assessment and Diagnostic Findings:1. Elevated arterial ammonia blood levels2. The encephalogram shows generalized slowing and an increase in amplitude of brain waves and the appearance of characteristic triphasicwaves3. Occasionally, fetor hepaticus, a characteristic breath odor like freshly mowed grass, acetone, or old wine, may be noticed.4. In a more advanced stage, there are gross disturbances of consciousness and the patient is completely disoriented with respect to time andplace5. With further progression of the disorder, the patient lapses into frank coma and may have seizures.Intervention:1. Anti-infective agents to decrease bacterial action in the colon.2. Ammonia detoxicants to reduce ammonia. Lactulose (Duphulac) is administered3. Cleansing enemas with diluted acetic acid or neomycin4. Discontinuation of any precipitating substance: Dietary proteins, sedatives, diuretic therapy, analgesics5. IV administration of glucose to minimize protein breakdown6. Oxygen administration7. Correction of any electrolyte imbalance8. Promote rest, comfort and quiet environmentNursing Diagnosis:1. Altered thought process2. Potential impaired skin integrity3. Impaired skin integrity RENAL DISORDER RENAL FAILURE Renal Failure is a systemic disease and is a final common pathway of many different kidney and urinary tract diseases. Results when the kidneys are unable to remove the bodys metabolic wastes or perform their regulatory functions The substances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal excretion and

lead to a disruption inendocrine and metabolic functions and fluid and electrolyte, an acid-base disturbances. ACUTE RENAL FAILURE Acute renal failure is a sudden and almost complete loss of kidney function over a period of hours to days. Categories of Acute Renal Failure:1. Prerenal Condition (hypoperfusion of kidney). Occurs as a result of impaired blood flow that leads to hypoperfusion of the kidney and a dropin the GFR. Common clinical situations are volume-depletion states (hemorrhage or gastrointestinal losses), impaired cardiac performance andvasodilation (sepsis or anaphylaxis) 2. Intrarenal . Intrarenal causes of acute renal failure are the result of actual parenchymal damage to the glomeruli or kidney tubules. Conditionssuch as burns crush injuries, and infections, as well as nephrotoxic agents, may lead to acute tubular necrosis and cessation of renal function.Severe transfusion reaction may also cause intrarenal failure. Medications may also predispose a patient to intrarenal damage, esp. nonsteroidalanti-inflammatory drugs and ACE inhibitors 3. Post renal conditions . Postrenal causes of acute renal failure are usually the result of an obstruction somewhere distal to the kidney. PHASES OF ACUTE RENAL FAILURE:1. Initiation period begins with the initial insult and ends when oliguria develops. 2. Period of Oliguria accompanied by a rise in the serum concentration of substances usually excreted by the kidney (urea, creatinine, uric acid,organic acids and the intracellular cations potassium and magnesium 3. Period of diuresis The patient experiences a gradual increase in urinary output, which signals that glomerular filtration has started to recover.Laboratory values start rising and eventually begin a

downward trend.Uremic symptoms may still be present. The patient must be closely monitoredfor dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase. 4. Period of Recovery signals the improvement of renal function. Laboratory values return to the patients normal level.Clinical Manifestations:1. May appear critically ill and lethargic2. Persistent nausea, vomiting and diarrhea3. The skin and mucous membranes are dry due to dehydration4. Uremic fetor breath have the odor of urine5. CNS manifestations: drowsiness, headache, muscle twitching, and seizuresAssessment and Diagnostic Findings:1. Changes in urine. The urinary output varies (from scanty to normal volume). Hematuria may be present and urine has lowspecific gravity.Patients with prerenal azotemia have a decreased amount of sodium. Those patients with intrarenal azotemia usually have urinary sodium levelsgreater than 40 mEq/L.2. Increased blood urea nitrogen and creatinine levels (Azotemia)3. Hyperkalemia4. Metabolic acidosis5. Calcium and Phosphorus Abnormalities Anemia due to reduced erythropoietin production, uremic gastrointestinal lesions, reduced Rbc lifespan, and blood lossPrevention:1. Renal function must be monitored closely if patient has been taking nephrotoxic antibiotic agents or has been exposed to environmental toxins.Blood should be drawn for determining baseline and monitoring serum BUN and creatinine levels by 24 hours after initiation of medication therapyMedical Management:1. Prerenal azotemia is treated by optimizing renal perfusion.2. Postrenal failure is treated by relieving the obstruction3. Overall, medical management includes maintaining fluid balance, avoiding fluid excesses, or performing dialysis4. The elevated potassium levels may be reduced by administering ion-exchange resins (sodium polystyrene sulfonate kayexalate)5. Diuretics are used for management of volume status6. Low-dose dopamine is

often used to dilate the renal arteries7. Atrial natriuretic peptide inhibits sodium and water absorption and dilates the afferent arteriole, thus improving blood flow to the glomerulus8. Correction of acidosis and elevated phosphate levels. When severe acidosis is present, the arterial blood gases or serum bicarbonate levelsmust be monitored because patient may require sodium bicarbonate therapy or dialysis. Patients elevated phosphate level may be controlled withphophate-binding agents (aluminum hydroxide).9. Nutritional Therapy. Dietary proteins are limited to about 1 g/kg during the oliguric phase. Highcarbohydrate meals to meet caloric requirements.Foods and fluids containing potassium and phosphorus are restricted.Nursing Management:1. Monitoring fluid and electrolyte balance. Hyperkalemia is the most immediate life-threatening imbalance seen in acute renal failure.2. Reducing metabolic rate. To reduce catabolism and the subsequent release of potassium and accumulation of endogenous waste products. Bedrest is indicated and fever and infection are prevented or treated promptly.3. Promoting pulmonary function. Patient is assisted to turn, cough and take deep breaths frequently to prevent atelectasis and respiratoryinfection.4. Preventing Infection. Asepsis is essential with invasive lines and catheters5. Providing skin care. Meticulous skin care is important. Massaging bony prominences, turning the patient frequently, and bathing the patient withcool water are comforting and prevent skin breakdown6. Providing support. The patient and family will need assistance, explanation and support during this time. CHRONIC RENAL FAILURE CRF is a progressive, irreversible deterioration in renal function in which the bodys ability to maintain metabolic and fluid and electrolytebalance fails, resulting in uremia or azotemia (retention of urea and other nitrogenous wastes in the blood)Pathophysiology:As renal function declines, the end products of protein metabolism (which are normally

excreted in urine) accumulate in the blood. Uremia developsand adversely affects every system in the body. 4 Stages of Chronic Renal Disease:Stage 1 Reduced renal reserve. Characterized by a 40 to 75% loss of nephron function. The patient usually does not have symptoms because theremaining nephrons are able to carry out the normal functions of the kidney. Stage 2 Renal Insufficiency. Occurs when 75 to 90% of nephron function is lost. At this point, the serum creatinine and blood urea nitrogen rise, the kidneyloses its ability to concentrate urine and anemia develops. The patient may report polyuria and nocturia. Stage 3 Renal Disease. Edema, metabolic acidosis, and hypocalcemia occur. Patient may exhibit overt uremia with cardiovascular, gastrointestinal, andneurologic complications. Stage 4End-stage renal Disease (ESRD). The final stage of CRF occurs when there is less than 10% nephron function remaining. All of the normalregulatory, excretory, and hormonal functions of the kidney are severely impaired. ESRD is evidenced by elevated creatinine and blood ureanitrogen levels as well as electrolyte imbalances. Once the patient reaches this point, dialysis is usually indicated.Signs And Symptoms Of CRF:1. Neurologic Weakness and fatigue; confusion; inability to concentrate; disorientation; tremors; seizures; asterixis; restlessness of legs; burning of soles of feet; behavior changes.2. Integumentary Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis; purpura; thin, brittle nails; coarse, thinning hair 3. Cardiovascular HPN; pitting edema (feet , hands, sacrum), periorbital edema; pericardial friction rub; engorged neck veins;

pericarditis; pericardial effusion;pericardial tamponade; hyperkalemia; hyperlipidemia4. Pulmonary Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic pain; shortness of breath; tachypnea; kussmaultype respirations; uremicpneumonitis; uremic lung5. Gastrointestinal Ammonia odor to breath (uremic fetor); metallic taste; mouth ulcerations and bleeding; anorexia; nausea and vomiting; hiccups; constipation or diarrhea; bleeding from GIT6. Hematologic Anemia; thrombocytopenia7. Reproductive Amenorrhea; testicular atrophy; infertility; decreased libido8. Musculoskeletal Muscle cramps; loss of muscle strength; renal osteodystrophy; bone pain; bone fractures; foot dropAssessment And Diagnostic Findings: Glomerular Filtration Rate. Decreased GFR can be detected by obtaining a 24-hour urine analysis for creatinine clearance. As GFR decreases,the creatinine clearance value decreases, whereas the serum creatinine and BUN levels increase. Sodium and Water Retention. The kidney is unable to concentrate or dilute the urine normally in ESRD. Some patients retain sodium and water,increasing the risk for edema, CHF, and HPN. Acidosis. With advanced renal disease, metabolic acidosis occurs because the kidney is unable to excrete increased loads of acid.

Anemia. Anemia develops as a result of inadequate erythoropoietin production, the shortened life span of RBCs, nutritional deficiencies, andthe patients tendency to bleed, particularly from GIT Calcium and Phosphorus Imbalance. The bodys serum calcium and phosphate levels have a reciprocal relationship in the body; as one rises,the other decreases. 14Complications:1. Hyperkalemia. Due to decreased excretion, metabolic acidosis, catabolism, and excessive intake (diet, medications, fluids)2. Pericarditis. Due to retention of uremic waste products and inadequate analysis3. Hypertension. Due to sodium and water retention and malfunction of the rennin-angiotensin-aldosterone system4. Anemia. Due to decrease erythropoietin, decreased RBC life span, GIT bleeding and blood loss during dialysis.5. Bone disease and metastatic calcifications. Due to retention of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, andelevated aluminum levelsMedical Management:1. Pharmacologic Therapy Antacids. Hyperphosphatemia and hypocalcemia are treated with aluminum based antacids that bind dietary phophorus in the GIT Antihypertensive and Cardiovascular agents. HPN is managed by intravascular control and a variety of hypertensive medications. CHF andpulmonary edema may require treatment with fluid restriction, low sodium diets, diuretics, inotropic agents such as digitalis, or dobutamine,and dialysis. Anticonvulsants. If seizures occurs. The onset of seizure is recorded along with the type, duration and general effect on the patient. IntravenousDiazepam or phenytoin is usually administered to control seizures. The side rails must be padded to protect the patient

 Erythropoietin. Anemia associated with CRF is treated with recombinant human erythropoietin (Epogen)2. Nutritional Therapy> Includes careful regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance sodium losses and some restriction of potassium3. Dialysis> Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with potassium removal and careful monitoring of all medications for their potassium intakeNursing ManagementNursing Diagnoses:1. Fluid volume excess r/t decreased urine output, dietary excesses, and retention of sodium and water 2. Altered nutrition; less than body requirements r/t anorexia, nausea and vomiting, dietary restrictions, and altered oral mucous membranes3. Knowledge deficit regarding condition and treatment regimen4. Activity intolerance r/t fatigue, anemia, retention of waste products, and dialysis procedure5. Self-esteem disturbance r/t dependency, role changes, changes in body image, and sexual dysfunction Nursing Care:1. Directed toward assessing fluid status and identifying potential sources of imbalance2. Implementing a dietary program to ensure proper nutritional intake within the limits of the treatment regimen3. Promoting positive feelings by encouraging increased self-care and greater independence CARDIOVASCULAR DISORDERS ANGINA PECTORIS literally translates as pain in the chest. This symptom occurs as a result of myocardial ischemia. Anginal chestpain is transient, lasting only 3-5 minutes and is usually relieved whenever the precipitating event is discontinuedor nitroglycerin is administered. The most common cause of angina is preexisting cardiovascular disease, whichnarrows or occludes the arteries that feed the heart muscle. Numerous disorders occur along thepathophysiologic continuum of cardiovascular disease; these include atheorsclerosis, angina, cerebrovascular accident, myocardial infarction (MI), and heart failure.The coronary

arteries, which arise from the ascending aorta immediately on exiting the heart, normally supplies the myocardium with adequateoxygen and nutrient-rich blood to meet metabolic demands. In the atherosclerotic heart, arteries are chronically dilated beyond narrowed or partially obstructed areas to meet the hearts metabolic demands at rest. Thus when the myocardium requires more oxygen during times of increased work, the coronary arteries cannot increase flow because they are already maximally dilated. An oxygen deficit is created as a result of the oxygen supply being less than the cellular demands.The oxygen imbalance created with angina can be quite precarious, and many factors can adversely affect this relationship. The demand for oxygen is increased whenever anyone of the following is increased: heart rate, afterload (hypertension), wall ension (ventricular volume or pressure), myocardial wall thickness (hypertrophy), or contractility. All of these factors make the heart work harder. Conversely, the oxygen supplyis decreased whenever any of the following occur: hypotension, anemia, respiratory insufficiency, or tachycardia, which allows minimal time for diastolic filling.In the absence of adequate oxygen and glucose, cellular metabolism shifts from the efficient oxidative phosphorylation, which yields a large amountof adenosine triphosphate (ATP) to the inefficient glycolysis; this action not only yields a very small amount of ATP but it also yields lactic acid as aby-product. This acidic environment activates chemical nociceptors, which transmit pain impulses to the brain, and the individual experienceschest pain. At this point the damage is reversible; in other words, if the flow of oxygen and glucose-rich blood is restored, no permanent damageresults. However, if the oxygen deficit continues and the lactic acid is allowed to build up, cellular metabolism and function can be altered to thepoint of irreversible cell death or myocardial infarction (MI). Types of Angina 1. Stable angina

(classic or exertional angina).The primary differentiating factor about this type of angina is that it is predictable and occurs intermittently over an extended period. It occurswith the same pattern of onset, duration, and intensity each time. Further, the same precipitating activity (most often physical in nature) usuallybrings on stable angina. The pain is relieved either when the precipitating event is discontinued or when nitroglycerin is administered in theprescribed fashion. If the pain is unrelieved by either rest or nitroglycerin, the patient may then be at risk for an MI. As previously discussed,stable angina is a result of atherosclerotic plaque that has narrowed the arteries. The chronically dilated vessel is unable to dilate further tomeet metabolic demands.2 . Unstable angina (progressive, crescendo, preinfarction angina, acute coronary insufficiency) This type is potentially life-threatening because it signifies advanced ischemic heart disease. This type of angina is most often unpredictable.Moreover, unstable angina attacks tend to occur with increasing frequency, intensity and duration. No precipitating event is necessary. In fact,these attacks are brought on at times of complete rest. An individual previously diagnosed with stable angina can progress to unstable angina;alternatively, unstable angina may be the first clinical manifestation in an individual with CAD.3. Prinzmetals angina (variant angina) The least common type of angina. It is unpredictable in onset, duration, and intensity and occurs almost exclusively at rest. Vasospasm of one or more of the coronary arteries is the underlying cause, which can occur with or without associated atherosclerosis. Clinical Manifestations

The cardinal symptom of angina is chest pain or discomfort. However, many patients describe feeling vague sensations of discomfort, tightness,

15pressure, heaviness, aching or squeezing. Others complain of heartburn or indigestion during an attack. The most common location is substernal;however, the pain or discomfort may radiate to the neck, jaw, back, shoulders, left arm, or occasionally the right arm.When asked to demostrate or point to the location of the pain, typically patients will clench one or two fists over the substernal region whenexperiencing myocardial ischemia. This display is known as the Levines sign . Other associated sighs and symptoms include pallor, diaphoresis,cold skin, shortness of breath, weakess, dizziness, anxiety, and feelings of impending doom.When an individual complains of chest pain, the source of pain should be considered cardiac until proven otherwise . However, it is prudentto consider both cardiac and noncardiac causes of chest pain as possible differentials. Electrocardiogram (ECG) remains the gold-standard for a first-line, noninvasive tool for diagnosis. Percutaneous transluminal coronary angioplasty (PTCA) involves the passage of an inflatable balloon catheter into the stenotic coronaryvessel, which is then dilated, resulting in compression of the atherosclerotic plaque and widening of the vessel Coronary artery bypass grafting (CABG) done by harvesting either a saphenous vein from the leg or the left internal mammaryartery and thenused to bypass areas of obstruction in the heart Nursing Responsibilities

In caring for patients with angina, the focus of the nurses role is two-fold. The first priority is appropriate treatment of the acute attack to alleviatediscomfort and, if possible, to avert untoward sequelae. The second priority is geared toward extensive education that not only empowers thepatient to become an active participant in his or her well being but also imparts practical tools with which the patient can effectively manage thecondition at home to achieve the highest level of wellness and independent functioning.During an acute anginal attack, it is imperative that the nurse performs a rapid and focused physical assessment and health history. Frequent vitalsigns and continuous cardiac monitoring are essential parts of the ongoing assessment. The most crucial part of the assessment focuses on thecurrent attack; emphasis must be placed on evaluating the pain itself and any precipitating events.The nurse must ask the following questions: How severe is the pain? (scale of 1-10) What does the pain feel like? Where is the pain? Does it move or radiate? Is it diffused or well localized? Did the pain start suddenly or gradually? How long does it last? How frequently does it occur? What makes the pain worse? What brings the pain on? What makes the pain better? What resolves the pain? Has the pain been increasingly worse with each attack? Another critical nursing function is prompt institution of

prescribed medical and pharmacologic therapies such as frequently used acronym MONA ,which stands for: M orphine, O xygen, N itroglycerine, and A spirin.Although nitrates are unable to dilate severely atherosclerotic vessels that are already maximally dilated, its administration during an unstableangina attack can prevent progression to an MI or death in 51% to 72% of patients.Other nursing measures that are beneficial to the patient who is suffering an anginal attack include helping the patient into a comfortable position,promoting rest and relaxation, and encouraging slow, deep breathing. ACUTE MYOCARDIAL INFARCTION As with angina, acute myocardial infarction occurs when the heart muscle is deprived of oxygen and nutrient-rich blood. However, in the case of MI, this deprivation occurs over a sustained period to the point at which irreversible cell death and necrosis take place. This deprivation leads tostructural and functional changes within the affected area of myocardial tissue. As with angina, too, underlying coronary artery disease (CAD) isthe most common cause of MI. With these basic similarities in mind, many components of the MI disease process and treatment either overlap tosome degree or further develop along the continuum of cardiovascular diseases. Infarction results from sustained ischemia and is irreversible causing cellular death and necrosis

.Circumstances that can cause an imbalance in supply and demand of oxygen and nutrient-rich blood: Physical exertion Emotional stress Weather extremes Digestion after a heavy meal Valsalva maneuver Hot baths or showers Sexual excitation Pathophysiologic chaaracteristics Clinical Manifestations The hallmark of MI is severe, unrelenting chest pain. As with angina, the pain is typically described as crushing, pressurefilled, vise-like, tight,constricting, or squeezing. The most common location of the pain is substernal, with radiation to the neck, jaw, or left arm. Leass frequently, painis reported in the shoulders, back, or right arm. In addition, a positive Levines sign (one or two fists clenched over the chest area when thepatient is asked to localize the pain) can contribute to the diagnosis.The major difference in the clinical presentation of MI compared with that of angina is the onset, severity, and duration. Chest pain aassociatedwith MI usually has an abrupt onset and can occur during activity, rest, or even sleep. The pain described during MI is typically more severe thananginal pain, lasting at least 20-30 minutes, and it is not relieved with either rest or nitroglycerin.However, not all patients will experience the same clinical presentation.During MI, associated clinical manifestations can range from vague sensations of just not feeling well to

the loss of consciousness or cardiacarrest. Often the skin is diaphoretic with a pale or ashen appearance, which occurs because of peripheral vasoconstriction as the body shunts

blood to the vital core. The initial surge of catecholamines can contribute to a variety of signs and symptoms such as tachycardia, hypertension,anxiety, palpitations, apprehension, and feelings of impending doom. Stimulation of the medulla is mediated via vasovagal reflexes and can resultin nausea and vomiting. Fever may be present secondary to the activation of the inflammatory process. As the infarction progresses and thehearts pumping ability becomes impaired, cardiac output drops. Associated with decreased cardiac output is hypotension, restlessness, dyspnea, jugular vein distention, oliguria, and confusion. Electrocardiogram capable of diagnosing MI in 80% of patients, making it an indispensable, noninvasive, and cost-effective tool.Evolving MI will show ST elevation which indicates acute myocardial necrosis. The development of Q wave may beobserved which signifies further electrical abnormalities. It may be an indication of worsening ischemia and necrosis. Cardiac Enzymes During the infarction process, cell membranes rupture, allowing intracellular enzymes to spill out into the blood stream. Blood sample drawn atcertain times during or after MI can be sent to the laboratory where enzymes can be measured and interpreted to determine the presence of aninfarction.Cardiac Enzyme Laboratory FindingsEnzymeEarliest Rise (in hours)Peak (in hours)Return to BaselineCreatinine kinase (CK)CK-MBMyoglobinTroponin 12-64-80.5-1.01-618-3615-246-97-243-6 days3-4 days12 hours10-14 days Troponin 1 is the newest cardiac marker and is a protein found only in myocardial cells. It is a quick, rapid test that, if elevated,

indicated MI.First-Line and Initial Treatment for Myocardial Infarction Provide oxygen Obtain a 12-lead ECG Monitor vital signs and pulse oximetry Monitor continuous cardiac rhythm with ST segment monitoring Conduct history and physical examinations Administer medications (thrombolytic therapy and anticoagulant therapyNursing Interventions:1. Bedrest must be enforced.2. The nurse should assist with all position changes and personal hygiene to avoid any exertional effort.3. Monitor I&O particularly urine output because this is a reliable indictor of cardiac output and systemic perfusion.4. Administer stool softener as ordered to prevent straining and vasovagal stimulation which can cause precipitous bradycardia CARDIAC FAILURECONGESTIVE HEART FAILURE (CHF) Often referred to as cardiac failure, is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygenation andnutrients. CHF is most commonly used when referring to left-sided and right-sided failure The incidence of CHF increases with agePathophysiology:Cardiac failure most commonly occurs with disorders of cardiac muscles that result in decreased contractile properties of the heart. Commonunderlying

conditions that lead to decreased myocardial contractility include myocardial dysfunction, arterial hypertension, and valvular dysfunction.Myocardial dysfunction may be due to coronary artery disease, dilated cardiomyopathy, or inflammatory and degenerative diseases of themyocardium. Atherosclerosis of the coronary arteries is the primary cause of heart failure. Ischemia causes myocardial dysfunction because of resulting hypoxia and acidosis (from accumulation of lactic acid). Myocardial infarction causes focal myocellular necrosis, the death of myocardialcells, and a loss of contractility; the extent of the infarction is prognostic of the severity of CHF.Dilated cardiomyopathy causes diffuse cellular necrosis, leading to decreased contractility. Inflammatory and degenerative diseases of themyocardium, such as myocarditis, may also damage myocardial fibers, with a resultant decrease in contractility.Systemic or pulmonary HPN increases afterload which increases the workload of the heart and in turn leads to hypertrophy of myocardial musclefibers; this can be considered a compensatory mechanism because it increases contractility.Valvular heart disease is also a cause of cardiac failure. The valves ensure that blood flows in one direction. With valvular dysfunction, valve hasincreasing difficulty moving forward. This decreases the amount of blood being ejected, increases pressure within the heart, and eventually leads topulmonary and venous congestion.Etiologic Factors : 1. Increased metabolic rate (eg. fever, thyrotoxicosis)2. Hypoxia3. Anemia VENTRICULAR FAILURELEFT-SIDED CARDIAC FAILURE Pulmonary congestion occurs when the left ventricle cannot pump the blood out of the chamber. This increases pressure in the left ventricleand decreases the blood flow from the left atrium. The pressure in the left atrium increases, which decreases the blood flow coming from thepulmonary vessels. The resultant increase in pressure in the pulmonary circulation forces fluid into the pulmonary tissues and alveoli; whichimpairs gas exchangeClinical Manifestations :1.

Dyspnea on exertion2. Cough3. Adventitious breath sounds4. Restless and anxious5. Skin appears pale and ashen and feels cool and clammy6. Tachycardia and palpitations7. Weak, thready pulse8. Easy fatigability and decreased activity tolerance RIGHT-SIDED CARDIAC FAILURE When the right ventricle fails, congestion of the viscera and the peripheral tissues predominates. This occurs because the right side of the heartcannot eject blood and thus cannot accommodate all the blood that normally returns to it from the venous circulation.Clinical Manifestations:1. Edema of the lower extremities (dependent edema) Amanuel/Pslidasan/Ksjuliano/MRCuenoNCM 104 1 st sem S.Y. 2007-2008 172. Weight gain3. Hepatomegaly (enlargement of the liver)4. Distended neck veins5. Ascites (accumulation of fluid in the peritoneal cavity)6. Anorexia and nausea7. Nocturia (need to urinate at night)8. WeaknessMedical ManagementThe basic objectives in CHF management are the following:1. Reducing the workload on the heart2. Increasing the force and efficiency of myocardial contraction3. Eliminating the excessive accumulation of body water by avoiding excess fluid, controlling the diet, and monitoring diuretic and angiotensin-converting enzyme (ACE) inhibitor therapyPharmacologic Therapy:If the patient is in mild failure, usually an ACE inhibitor is prescribed. A diuretic is added if there is no improvement or if there are signs of fluidoverload. Next, digitalis is added if the symptoms continue. If symptoms are severe, all three medications are usually started immediately.ACE Inhibitors. Promote vasodilation and diuresis by decreasing afterload and preload eventually decreasing the workload of the heart.Diuretic Therapy. A diuretic is one of the first medications prescribed to a patient with CHF. Diuretics

promote the excretion of sodium and water through the kidneys.Digitalis. This medication increases the force of myocardial contraction and slows conduction through the AV node. It improves contractility thus,increasing left ventricular output.Dobutamine.(Dobutrex) is an intravenous medication given to patients with significant left ventricular dysfunction. A catecholamine, it stimulates thebeta 1 -adrenergic receptors. Its major action is to increase cardiac contractility.Milrinone (Primacor). A phosphodiesterase inhibitor that prolongs the release and prevents the uptake of calcium. This in turn, promotesvasodilation, causing a decrease in preload and afterload and decreasing the workload of the heart.Other medications. Anticoagulants may be prescribed. Beta-adrenergic blockers maybe indicated in patients with mild or moderate failure.Nutritional Therapy:1. A low-sodium diet2. Avoidance of excessive amount of fluidsNursing Management:1. Record intake and output to identify a negative balance (more output than input)2. Weigh patient daily at the same time3. Auscultate lung sounds daily to detect a decrease or an absence of pulmonary crackles4. Determine the degree of jugular distention5. Identify and evaluate severity of dependent edema6. Monitor pulse rate and BP, and make sure the patient does not become hypotensive from dehydration7. Examine skin turgor and mucous membranes for signs of dehydration8. Assess for symptoms of fluid overload (orthopnea, paroxysmal nocturnal dyspnea, and dyspnea on exertion)Nursing Process: The Patient With Cardiac FailureAssessment The focus of the nursing assessment for the patient with cardiac failure is directed toward observing for signs and symptoms of pulmonary andsystemic fluid overload.Health History The nurse explores sleep disturbances, particularly sleep suddenly interrupted by shortness of breath.

 The nurse finds out about the number of pillows needed for sleep (indication of dyspnea) Find out also the activities of daily living and the activities that causes shortness of breathPhysical Examination The lungs are auscultated at frequent intervals to detect crackles and wheezes or their absence. The rate and depth of respiration are alsonoted. The heart is auscultated for an S 3 heart sound, a sign that the heart pump is beginning to fail and that increased blood volume remains in theventricle with each beat. HR and rhythm are also noted. Jugular vein distention is also assessed. Distention greater than 3 cm above the sternal angle is considered abnormal. Sensorium and level of consciousness must be evaluated Dependent parts of the patients body are assessed for perfusion and edema. The liver is examined for hepatojugular reflux. Output is measured carefully to establish a baseline against which to measure the effectiveness of diuretic therapy. Intake and output recordare maintainedNursing Diagnoses:1. Activity intolerance r/t imbalance between oxygen supply and demand secondary to decreased CO2. Excess fluid volume r/t excess fluid/sodium intake or retention secondary to CHF and its medical therapy3. Anxiety r/t breathlessness and restlessness secondary to inadequate oxygenation4. Non-compliance r/t to lack of knowledge5. Powerlessness r/t inability to perform role responsibilities secondary to chronic illness and

hospitalization.Potential Complications:1. Cardiogenic shock2. Dysrhythmias3. Thromboembolism4. Pericardial effusion and pericardial tamponadePlanning And Goals:1. Promoting activity while maintaining vital signs within identified range2. Reducing fatigue 183. Relieving fluid overload symptoms4. Decreasing the incidence of anxiety or increasing patients ability to manage anxiety5. Teaching the patient about the self-care program.6. Encouraging the patient to verbalize his ability to make decisions and influence outcomes.Nursing Interventions:1. Promoting Activity Tolerance The patient is encouraged to perform an activity more slowly than usual, for a shorter duration, or with assistance initially. Barriers that could limit abilities to perform an activity are identified Pacing and prioritizing activities will maintain the patients energy to allow participation in regular exercise. Vital signs should be taken before, during and immediately after an activity to identify whether they are within the predetermined range.2. Reducing Fatigue The nurse and patient can collaborate to develop a schedule that promotes pacing and prioritization of activities. The schedule should alternateactivities with periods of rest and avoid having two significant energy-consuming activities occur on the same day or in immediate succession.3. Managing Fluid Volume The nurse monitors the patients fluid status closely. Auscultating the lungs, comparing daily body weights,

monitoring intake and output andassisting the patient to adhere to a low-sodium diet. The nurse needs to position the patient or teach the patient how to assume a position that shifts fluid away from the heart. The nurse needs to assess for skin breakdown and institute preventive measures4. Controlling Anxiety The nurse should take steps to promote physical comfort and psychological support. A family members presence provides reassurance.Speaking in a slow, calm, and confident manner is helpful. Stating specific, brief directions for an activity is helpful in decreasing anxiety.5. Minimizing Powerlessness Patients need to recognize that they are not helpless and that they can influence their direction, their lives, and their outcomes. The nurse needs to assess for factors contributing to a perception of powerlessness and intervene accordingly. Contributing factors may includelack of knowledge, hospital policies, and lack of opportunities to make decisions. Taking time to listen to patient encourages them to express their concerns and questions Provide the patient with decision-making opportunities Provide encouragement and praiseExpected Outcomes:1. Demonstrates tolerance for increased activity2. Has less fatigue and dyspnea3. Maintains fluid balance4. Is less anxious5. Adheres to self-care regimen6. Makes decisions regarding care and treatment7. Absence of complications CARDIOGENIC SHOCK

Occurs when the heart cannot pump enough blood to supply the amount of oxygen needed by the tissues.Pathophysiology:The heart muscle loses its contractile power, resulting in a marked reduction in SV and CO, sometimes called forward failure. The damage tomyocardium results in a decrease in CO, which in turn reduces arterial blood pressure and tissue perfusion in the vital organs (heart, brain,kidneys). Flow to the coronary artery is reduced, resulting in decreased oxygen supply to the myocardium, which in turn increases ischemia andfurther reduces the hearts ability to pump. The inadequate emptying of the ventricle also leads to increased pulmonary pressures, pulmonarycongestion, and pulmonary edema, exacerbating the hypoxia and resulting ischemia of vital organs.Clinical Manifestations:1. Tissue hypoperfusion classic signs of cardiogenic shock manifested as cerebral hypoxia (restlessness, confusion, agitation), low bloodpressure, rapid and weak pulse, cold and clammy skin, increased respiratory crackles, hypoactive bowel sounds, and decreased urinary output.2. Initially, arterial blood gas analysis may show respiratory alkalosis.3. Dysrhythmias are commonAssessment and Diagnostic Findings:1. The use of a Pulmonary Artery catheter to measure left ventricular pressures and CO is important in assessing the severity of the problem andplanning management. The PA wedge pressure is elevated and the CO is decreased as the left ventricle loses its ability to pump.2. The systemic vascular resistance is elevated due to the sympathetic nervous system stimulation that occurs as a compensatory response to thedecrease in blood pressure.3. The decreased blood flow to the kidneys causes a hormonal response that causes fluid retention and further vasoconstriction.4. The increases in HR, circulating volume, and vasoconstriction occur to maintain circulation to the brain, heart and lungs, however, the workloadof the heart is increased.5. Continued cellular hypoperfusion eventually results in organ failure. The patient becomes unresponsive, severe hypotension occurs, and thepatient develops shallow respirations, cold, cyanotic or

mottled skin, and absent bowel sounds.6. Arterial blood gas analysis shows metabolic acidosis7. All laboratory results indicate organ dysfunction.Medical Management:1. Reduce any further demand on the heart2. Improve oxygenation and restore tissue perfusion3. Diuretics, vasodilators, and mechanical devices (filtration and dialysis)4. Intravenous volume expanders (normal saline, lactated Ringers solution, and albumin) are given for hypovolemia or low intravascular volume.5. Strict bed rest to conserve energy6. Oxygen administration is increased for hypoxemia7. Intubation and sedation may be necessary to maintain oxygenation balance.Pharmacologic Therapy: Most medication are administered IV because of the decreased perfusion to the gastrointestinal system 191. Pressor agents are medications used to raise BP and increase CO. Many pressor medications are catecholamines ( norepinephrine and high-dose dopamine) to promote perfusion to the heart and brain.2. Diuretics and vasodilators may be administered to reduce the workload of the heart.3. Positive inotropic medications are given to increase myocardial contractility4. Circulatory assist devices: Intraaortic balloon pump to augment the pumping action of the heart. The device inflates during diastole, increasingthe pressure in the aorta and therefore increasing perfusion. It deflates just before systole, lessening the pressure within the aorta beforeventricular contraction, decreasing the amount of resistance the heart has to overcome to eject blood and therefore decreasing the amount of workthe heart must complete to eject blood.Nursing Management:1. Nurse must carefully assess the patient, observe the cardiac rhythm, measure hemodynamic parameters, and record fluid intake and urinaryoutput.2. The patient must be closely monitored for responses to the medical interventions and for the development of complications3. The patient is always

treated in intensive care environment because of the frequency of nursing interventions and the technology required for effective medical management. THROMBOEMBOLISM The decreased mobility of the patient with cardiac diseases and the impaired circulation that accompany these disorders contribute to thedevelopment of intracardiac and intravascular thrombosis. Intracardiac Thrombus Detected by an echocardiogram and treated with anticoagulants, such as warfarin. A part of the thrombus may become detached and may be carried to the brain, kidneys, intestines, or lungs The most common problem is pulmonary embolism. The symptoms of pulmonary embolism include chest pain, cyanosis, and shortness of breath, rapid respirations and hemoptysis. (see discussion on pulmonary embolism) The pulmonary embolus may block the circulation to a part of the lung, producing an area of pulmonary infarction Systemic embolism may present as cerebral, mesenteric, or renal infarction An embolism can also compromise the blood supply to an extremity PERICARDIAL EFFUSION AND CARDIAC TAMPONADE Pathophysiology:Pericardial effusion refers to the escape of fluid into the pericardial sac. Normally, the pericardial sac contains less than 50 ml of fluid, which theheart needs to decrease friction for the beating heart. An increase in pericardial fluid raises the pressure within the pericardial sac and compressesthe heart. This results in :

Increased right and left ventricular-end diastolic pressures Decreased venous return Inability of the ventricles to distend adequatelyPericardial fluid may accumulate slowly without causing noticeable symptoms. A rapidly developing effusion, however, can stretch the pericardiumto its maximum size and, because of increased pericardial pressure, and reduce venous return to the heart, and decrease cardiac output. Theresult is cardiac tamponade .Clinical Manifestations:1. The patient may complain of a feeling of fullness within the chest. The feeling of pressure may result from stretching of the pericardial sac2. Engorged neck veins3. Shortness of breath4. A drop and fluctuation in BPAssessment and Diagnostic Findings:1. Pericardial effusion is detected by percussing the chest and noting an extension of flatness across the anterior aspect of the chest2. Echocardiogram to confirm diagnosisMedical Management:1. Pericardial Fluid Aspiration (pericardiocentesis) performed to remove fluid from the pericardial sac2. Pericardiotomy. A portion of pericardium is sliced to permit the pericardial fluid to drain into the lymphatic system. CARDIAC ARREST Occurs when the heart ceases to produce an effective pulse and blood circulation. It may be due to a cardiac electrical event, as when the HRis too fast or too slow or when there is no heart rate at all.Clinical Manifestations:1. Loss of consciousness, pulse and BP2. Ineffective respiratory gasping3. The pupils of the eyes dilate within 45 seconds.4. Seizures may or may not occur Emergency Management:Cardiopulmonary Resuscitation1. Airway maintain open airway2. Breathing provide artificial circulation by rescue breathing3. Circulation promoting artificial circulation by external cardiac compression4.

Defibrillation restoring the heart beatMaintaining Airway and Breathing The first step in CPR is to obtain an open airway. Any obvious material in the mouth and throat should be removed. The chin is directed up andback or the jaw (mandible) is lifted forward. The rescuer looks, listen. and feels for air movement. An oropharyngeal airway is inserted if available. Two rescue ventilations over 3 to 4 seconds are provided using a bag or mouth-mask device. If the first rescue ventilation enteredeasily, then the patient is ventilated with 12 breaths per minute and the open airway is maintained. Endotracheal intubation is performed toensure an adequate airway and ventilation.Restoring Circulation After performing ventilation, the carotid pulse is assessed and external cardiac compressions are provided when no pulse is detected. 1. Compressions are performed with the patient on a firm surface (Cardiac board, floor) 2. The rescuer (facing the patients head) places the heel of one hand on the lower half of the sternum, two fingerwidths from the tip of thexiphoid and positions the other hand on top of the first hand. The fingers should not touch the chest wall. 3. Using the body weight while keeping the elbows straight, the rescuer presses quickly downward from the shoulder area to deliver a forcefulcompression to the victims lower sternum toward the spine. 4. The chest compression rate is 80 to 100 times/minute Follow-up Monitoring 1. After successful resuscitation, the patient is transferred to an intensive care unit for close monitoring. Continuous

electrocardiographic monitoringand frequent BP assessment are essential until hemodynamic stability is reestablished. DYSRHYTHMIAS Disorders of the formation and/or conduction of the electrical impulse within the heart. This can cause disturbances of the heart rate, the heartrhythm, or both. Normal Electrical Conduction The electrical impulse that stimulates and paces the cardiac muscle normally originates in the sinus node, located near the vena cava in the rightatrium. Normally, the impulse occurs at a rate between 60 and 100 times a minute in the adult. The impulse quickly travels from the sinus nodethrough the atria to the atrioventricular (AV) node causing the atria to contract. The structure of the AV node slows the impulse, which allows timefor the atria to contract and the ventricles to fill with blood. From the AV node, the impulse travels quickly along the right and left bundle branchesand the Purkinje fibers, located in the ventricular muscle. The electrical stimulation of the ventricles, in turn, causes the ventricles to contract(systole). Then the electromechanical impulse completes the circuit and the cycle begins again. In this way, sinus rhythm promotes cardiovascular circulation. The electrical stimulus causes the mechanical event of the heart. Depolarization. The electrical stimulation: the mechanical contraction is called systole. Repolarization. The electrical relaxation and mechanical relaxation is called diastole. Influences on Heart Rate and Contractility Heart rate is influenced by the autonomic nervous system, which consists of sympathetic and parasympathetic fibers.

Stimulation of the sympathetic system increases heart rate. Sympathetic stimulation also causes the constriction of peripheral blood vessels and, therefore, an increase in BP Parasympathetic stimulation slows the heart rate Manipulation of the autonomic nervous system may increase or decrease the incidence of dysrhythmiasTypes of Dysrhythmias 1. Sinus Node DysrhythmiasA. Sinus Bradycardia Occurs when the sinus node creates an impulse at a slower than-normal rate.Etiology:1. Slower metabolic needs (sleep, athletic training, hypothyroidism)2. Vagal stimulation (vomiting, suctioning, severe pain, extreme emotions)3. Medications4. Increased intracranial pressure and MITreatment:1. Atropine 0.5 to 1.0 mg given quickly and IV as bolus medication of choice2. Catecholamines and emergency transcutaneous pacing B. Sinus Tachycardia Occurs when the sinus node creates an impulse at a fasterthan-normal rate. It may be caused by acute blood loss, anemia shock, hypovolemia, hypervolemia, CHF, pain, hypermetabolic state, fever, exercise, anxiety or sympathomimetic medications.Treatment:1. Calcium channel blockers (ex. Diltiazem)2. Beta-blockers (ex. Propranolol) C. Sinus Arrhythmia Occurs when the sinus node creates an impulse at an irregular rhythm; the rate increases with inspiration and decreases with expiration 2. Atrial DysrhythmiasA. Premature Atrial Complex (PAC)

This is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the SA node. The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium PACs are common in normal hearts. The patient may say My heart skipped a beat. A pulse deficit may exist. If PACs are infrequent, no treatment is necessary. B. Paroxysmal Atrial Tachycardia A term used to indicate a tachycardia characterized by abrupt onset and abrupt cessation and a QRS of normal duration. Now called AV nodal reentry tachycardia C. Atrial Flutter Occurs in the atrium and creates impulses at an atrial rate between 250 and 400 times per minute May cause serious signs and symptoms: chest pain, shortness of breath, and low blood pressure.Treatment:1. If patient is unstable, electrical cardioversion is indicated2. If patient is stable, diltiazem, verapamil, beta-blockers or digitalis may be administered IV to slow the ventricular rate. D. Atrial Fibrillation Causes a rapid, disorganized, and uncoordinated twitching of atrial musculature. The most common dysrhythmias Usually associated with advanced age, valvular heart disease, cardiomyopathy, hyperthyroidism, pulmonary

disease, moderate to heavyingestion of alcohol and the aftermath of open heart surgeryTreatment: Treatment depends on its cause and duration and the patients symptoms and instability In some cases, AF converts to sinus rhythm within 24 hours without treatment Both stable and unstable AF of short duration are treated the same as stable and unstable atrial flutter To prevent recurrence and to promote heart rate control over a long period, quinidine, procainnamide, flecainide, sotalol, or amiodatone may beprescribed 21 Anti-coagulation therapy is indicated if patient is elderly or has hypertension, heart failure or a history of stroke. Pacemaker or surgery is sometimes indicated for patients who are unresponsive to medications 3. Junctional DysrhythmiasA. Premature Junctional Complex An impulse that starts in the AV nodal area before the next normal sinus impulse. Causes include: digitalis toxicity, congestive heart failure, and coronary artery disease Rarely produce any significant symptoms Treatment is the same as for frequent PACs B. Junctional Rhythm Occurs when the AV node, instead of the SA node, becomes the pacemaker of the heart.

 Junctional rhythm may produce signs and symptoms of reduced cardiac output. If so, the treatment is the same as for sinus bradycardia. C. AV Nodal Reentry Tachycardia Occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate. Factors associated with the development of AV nodal reentry tachycardia include caffeine, nicotine, hypoxemia, and stress Signs and symptoms vary with the rate and duration of the tachycardia and the patients underlying condition. Usually of short duration,resulting only in palpitations. A fast rate may reduce cardiac output, resulting in significant signs and symptoms such as restlessness, chestpain, shortness of breath, pallor, hypotension and loss of consciousnessTreatment: Treatment is aimed at breaking the reentry of the impulse.1. Vagal maneuvers, such as carotid sinus massage, gag reflex, breath holding, and immersing the face in ice water increase parasympatheticstimulation, causing slower conduction through the AV node and blocking the reentry of the rerouted impulse. Because of the risk of a cerebral embolic event, carotid sinus massage is contraindicated in patients with carotid bruits.2. If vagal maneuvers are ineffective, the patient may then receive a bolus of adenosine, verapamil, or diltiazem.3. Cardioversion is the treatment of choice if the patient is unstable or does not respond to the medications.4. Intravenous adenosine may be prescribed to cause a conversion to sinus rhythm. 4. Ventricular DysrhythmiasA. Premature Ventricular Complex (PVC)

 PVC is an impulse that starts in a ventricle before the next normal sinus impulse. PVCs can occur in healthy people, esp. with the use of caffeine, nicotine, and alcohol. Also caused by cardiac ischemia or infarction, increased workload on the heart (ex. Exercise, fever. Hypervolemia, CHF, and tachycardia),digitalis toxicity, hypoxia, acidosis, and electrolyte imbalances, esp. hypokalemia In the absence of disease, PVCs are not serious. In the patient with acute MI, PVCs may indicate the need for more aggressive therapy. The following are warning or complex PVCs (precursors of ventricular tachycardia) : (1) more than 6/minute (2) multifocal (having differentshapes), (3) two in a row (pair), and (4) occurring on the T wave (the vulnerable period of ventricular depolarization)Treatment:1. Lidocaine is the medication most commonly used for immediate short-term therapy B. Ventricular Tachycardia Defined as three or more PVCs in a row, occurring at a rate exceeding 100 beats/minute. Ventricular tachycardia is usually associated with coronary artery disease and may precede ventricular fibrillation. Ventricular tachycardia is an emergency because the patient is usually unresponsive and pulseless.Treatment:1. Lidocaine is the initial choice2. Cardioversion maybe indicated if the medications are ineffective or if the patient becomes unstable3. Immediate defibrillation

Ventricular tachycardia in a patient who is unconscious and without pulse is treated in the same manner as ventricular fibrillation. C. Ventricular Fibrillation A rapid but disorganized ventricular rhythm that causes ineffective quivering of the ventricles. This dysrhythmias is always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations. Cardiac arrest and death are imminent if VF is uncorrectedTreatment:1. Immediate defibrillation and activation of emergency services. Placing a call for emergency assistance takes precedence over initiating CPR2. After a successful defibrillation, eradicating causes and administering anti dysrhythmics medication are treatments to prevent the recurrence of VF. D. Idioventricular Rhythm Also called ventricular rhythm, occurs when the impulse starts in the conduction system below the AV node Commonly causes the patient to lose consciousness and experience other signs and symptoms of reduced cardiac output. In such cases,treatment is the same as for any bradycardia, including identifying the underlying etiology, administering IV atropine, and initiating emergencytranscutaneous pacing. Bed rest is prescribed so as not to increase cardiac workload E. Ventricular Asystole Commonly called flatline, ventricular asystole is characterized by absent QRS complexes, although P waves may be apparent for a shortduration. There is no heartbeat, no palpable pulse, and no respiration.

 Without treatment, ventricular asystole is fatal.Treatment:1. CPR2. Rapid assessment to identify possible causes3. Intubation and establishment of IV access are the first recommended actions4. Bolus of IV epinephrine and to be repeated at 3-5 minutes intervals5. Sodium bicarbonate maybe administered IV Nursing Process: The Patient With A DysrhythmiaAssessment Major areas of assessment include possible causes of the dysrhythmias and the dysrhythmias effect on the hearts ability to pump an adequateblood volume When cardiac output is reduced, the amount of oxygen reaching the tissues and vital organs is diminished. This diminished oxygen producesthe signs and symptoms associated with dysrhythmias. A health history is obtained to identify possible causes and past incidences of syncope (fainting), lightheadedness, dizziness, fatigue, chestdiscomfort, and palpitations. Psychosocial assessment is also performed to identify the possible effects of dysrhythmia Physical assessment is conducted to confirm the data obtained from the history and to observe for signs of diminished cardiac output during thedysrhythmic event, esp. changes in level of consciousness. Skin may be pale and cool. Signs of fluid retention, such as neck vein distention,crackles and wheezes in the lungs may be detected during auscultation. The rate and rhythm of apical and peripheral pulses are assessed and any pulse deficit is noted. The chest is auscultated for extra heart sounds, esp. S

3 and S 4, measures BP and determines pulse pressures. A declining pulse pressureindicates reduced cardiac output.Diagnosis:1. Potential/actual decrease in cardiac output2. Anxiety related to fear of the unknown3. Lack of knowledge about the dysrhythmias and its treatment.Potential Complications: Ischemic Heart DiseaseNursing Interventions:1. Monitoring and Managing the Dysrhythmias Controlling the incidence or effect of dysrhythmias is often achieved by the use of ant-idysrhythmic medications A constant serum blood level of the medication is maintained to maximize beneficial effects and minimize adverse effects If the patient is hospitalized, an ECG is initiated and rhythm strips are analyzed to track dysrhythmias BP, rate and depth of respirations, pulse rate and rhythm are evaluated regularly to determine the hemodynamic effect of the dysrhythmias2. Minimizing Anxiety Nurse must maintain a calm and reassuring attitude Maximize the patients control and to make the unknown less threateningEvaluationExpected Outcomes:1. Cardiac output is maintained2. Anxiety is minimized3. The patient knows about dysrhythmias and its treatment Adjunctive Modalities and Management1. Cardioversion and Defibrillation Treatment for tachydysrhythmias. Used to deliver an electrical current to stimulate a critical mass of myocardial cells. This allows the sinus node to recapture its role as thehearts pacemaker.

 One major difference between cardioversion and defibrillation has to do with the timing of the delivery of electrical current. Defibrillation is usually performed as an emergency treatment, whereas cardioversion is usually a planned procedure Cardioversion involves the delivery of a timed electrical current to terminate a tachydysrhythmia. Defibrillation is the treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia. 2. Pacemaker Therapy An electronic device that provides electrical stimuli to the heart muscle. Usually used when a patient has a slower-than-normal impulse formation May also be used to control tachydysrhythmias that do not respond to medication therapyComplications of Pacemakers:1. Local infection at the entry site of the leads or at the subcutaneous site2. Bleeding and hematoma at the lead-entry sites or at the subcutaneous sites for permanent generator placement3. Hemothorax from puncture of the subclavian vein or internal mammary artery4. Ventricular ectopy and tachycardia from irritation of the ventricular wall by the endocardial electrode5. Movement or dislocation of the lead placed transvenously (perforation of the myocardium)6. Phrenic nerve, diaphragmatic (hiccupping) or skeletal muscle stimulation may occur if the lead is dislocated or if the delivered energy is set high7. Rarely, cardiac tamponade occurs after removal of epicardial wires8. Dislodgement of the pacing electrode most common

complication. Minimizing patient activities can help to prevent this complication. BURNS There are 4 major goals relating to burns:1. Prevention2. Institution of lifesaving measures for the severely burned person3. Prevention of disability and disfigurement through early, specialized, individual treatment4. Rehabilitation through reconstructive surgery and rehabilitative programsPathophysiology:Burns are caused by a transfer of energy from a heat source to the body. Heat maybe transferred through conduction or electromagnetic radiation.Burns are categorized as thermal (including electrical burns), radiation or chemical. Tissue destruction results from coagulation, proteindenaturation, or ionization of cellular contents. The skin and the mucosa of the upper airways are the sires of tissue destruction. Deep tissues,including the viscera, can be damaged by electrical burns or through prolonged contact.The depth of the injury depends on the temperature of the burning agent and the duration of contact with the agent. Classification of Burns Burn injuries are described according to the depth of the injury and the extent of body surface area (BSA) injured. Characteristics of Burns according to Depth Factors to consider in the determination of depth : 1. History of how the injury occurred2. Causative agent, such as flame or scalding liquid3. Temperature of the burning agent4. Duration of contact with the agent5. Thickness of the skin Extent of Body Surface Area InjuredRule of Nines An estimation of the total BSA involved in a burn is simplified using the rule of nines Lund and Browder Method A more precise method of estimating the extent of a burn

Recognizes that the percentage of BSA of various anatomic parts, especially the head and legs, changes with growth. By dividing the body into very small areas and providing an estimate of the proportion of BSA accounted for by such body parts, one can obtaina reliable estimate of the total BSA burned. The initial evaluation is made on the patients arrival at the hospital. Palm Method A method to estimate the percentage of scattered burns. The size of the patients palm is approximately 1% of BSA. The size of the palm can be used to assess the extent of burn injury. Local and Systemic Responses to Burns Burns that do not exceed 25% of the total BSA produce a primarily local response Burns that exceed 25% BSA may produce both a local and a systemic response, which is considered a major burn injury. Overview of physiologic changes after a major burn injuryCardiovascular Response Cardiac output decreases before any significant change in blood volume is evident. As fluid loss continuous and vascular volume decreases,cardiac output continuous to fall and blood pressure drops. This is the onset of burn shock. In response, the sympathetic nervous systemreleases catecholamines, resulting in an increase in peripheral resistance (vasoconstriction) and an increase in pulse rate. Peripheralvasoconstriction further decreases cardiac output. Prompt fluid resuscitation maintains the blood pressure in the low-normal range and improves cardiac output. Despite

adequate fluidresuscitation, cardiac filling pressures remain low during the burn-shock period. If inadequate fluid resuscitation occurs, distributive shock willoccur. Generally, the greatest volume of fluid leak occurs in the first 24 to 36 hours after the burn, peaking by 6 to 8 hours. As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment. As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases. If renal and cardiac function is adequate, urinary output increases. Patients with severe burns develop massive systemic edema. As edema increases in circumferential burns, pressure on small blood vesselsand nerves in distal extremities causes an obstruction of blood flow and consequent ischemia. This complication is known as compartmentsyndrome. The physician may need to perform an esharotomy, a surgical incision into the eschar (devitalized tissue resulting from a burn), torelieve the constricting effect of the burned tissue. Effects on Fluids, Electrolytes, and Blood Volume Circulating blood volume decreases dramatically during burn shock. Evaporative fluid loss through the burn may reach 3 to 5 L or more over aperiod of 24 hours until the burn surfaces are covered. During the shock, serum sodium levels vary in response to fluid resuscitation. Usually hyponatremia (sodium depletion) is present, as water shifts from the interstitial to the vascular space.

Immediately after burn injury, hyperkalemia (excessive K) results from massive cell destruction. Hypokalemia may occur later with fluid shiftsand inadequate potassium intake. At the time of burn injury, some red blood cells may be destroyed and/or damaged resulting in anemia. Despite this, patients hematocrit may beelevated due to plasma loss Blood transfusions are required periodically to maintain adequate hemoglobin levels for oxygen delivery. Abnormalities in coagulation, including a decrease in platelets (thrombocytopenia) and prolonged clotting and prothrombin time, also occur withburn injury. Pulmonary Response Inhalation injury is the leading cause of death in fire victims. One third of all burn injuries have a pulmonary problem related to the burn injury. Even without pulmonary injury, hypoxemia may be present. Early in the post burn period, catecholamine release in response to the stress of the burn injury alters peripheral blood flow, thereby reducing oxygen delivery to the periphery. Later, hypermetabolism and continuedcatecholamine release lead to increased tissue oxygen consumption, which can lead to hypoxemia. Categories of Pulmonary Injury:1. Upper Airway Injury Results from direct heat or edema. Manifested by mechanical obstruction of the upper airway, including the pharynx and larynx Because of the cooling effect of rapid vaporization in the pulmonary tract, direct heat injury does not normally occur below the level of thebronchus.

 Treated by early nasotracheal or endotracheal intubation. 2. Inhalation below the glottis Results from inhaling the products of incomplete combustion or noxious gases. These products include carbon monoside, sulfur oxides,nitrogen oxides, aldehydes, cyanide, ammonia, chlorine, phosgene, benzene, and halogens. The injury results directly from chemical irritation of the pulmonary tissues at the alveolar level. Inhalation injuries below the glottis cause loss of ciliary action, hypersecretion, severe mucosal edema, and possibly bronchospasm. The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alveoli). Expectoration of carbon particles in the sputum is the cardinalsign of this injury. Carbon monoxide is the most common cause of inhalation injury because it is a byproduct of the combustion of organic materials and istherefore present in smoke. Treatment usually consists of early intubation and mechanical ventilation with 100% oxygen. Using 100% oxygen is essential to accelerate theremoval of carbon monoxide from the hemoglobin molecule. Indicators of possible pulmonary damage: 241. History indicating hat the burn occurred in an enclosed area2. Burns of the face or neck3. Singed nasal hair 4. Hoarseness, voice change, dry cough, stridor, sooty sputum5. Bloody sputum6. Labored breathing or tachypnea (rapid breathing) and other signs of reduced oxygen levels (hypoxemia).7. Erythema and blistering of the oral or pharyngeal mucosa

Pulmonary Complications secondary to Inhalation Injury:1. Acute respiratory failure Occurs when impairment of ventilation and gas exchange is life-threatening. The immediate intervention is intubation and mechanical ventilation. If ventilation is impaired by restricted chest excursion, immediate escharotomy is needed. 2. Acute respiratory distress syndrome > May develop in the first few days after injury secondary to systemic and pulmonary responses to the burn and inhalation injury. Other Systemic Responses Renal function may be altered as a result of decreased blood volume. If there is inadequate blood flow through the kidney, the hemoglobin andmyoglobin occlude the renal tubules, resulting in acute tubular necrosis and renal failure. The immunologic defenses of the body are greatly altered by burn injury. The loss of skin integrity is compounded by the release of abnormalinflammatory factors. Immunosuppression places the patient at high risk for sepsis. Loss of skin also results in an inability to regulate body temperature. Burn patients may therefore exhibit low body temperature in the earlyhours after burn injury, but as hypermetabolism resets core temperatures, burn patients becomes hyperthermic for most of the postburnperiod, even in the absence of infection. Two potential gastrointestinal complications may occur: paralytic ileus (absence of intestinal peristalsis) and Curlings ulcer. Decreasedperistalsis and bowel sounds are

manifestations of paralytic ileus resulting from burn trauma. Gastric distention and nausea may lead tovomiting unless gastric decompression is initiated.Management Of The Patient With A Burn InjuryA. Emergent/Resuscitative Phase of Burn Care The first priority in on-the-scene care for a burn victim is to prevent injury to the rescuer.Airway, Breathing, Circulation It is important to remember the ABCs of all trauma care because the systemic effects pose a greater threat to life.1. Airway2. Breathing3. Circulation; Cervical spine immobilization for all high voltage electrical injury; Cardiac monitoring for all electrical injuries for at least 24 hoursafter cessation of dysrhythmias. Breathing must be assessed and a patent airway established immediately during the initial minutes of emergency care. Immediate therapy isdirected toward establishing an airway and administering humidified 100% oxygen. The circulatory system must also be assessed quickly. Apical pulse and blood pressure are monitored frequentlyManagement of Fluid Loss and Shock Next to respiratory difficulties, the most important is preventing irreversible shock by replacing lost fluids and electrolytes. Survival of burnvictims depends on adequate fluid resuscitation.1. Fluid Replacement Some combination of fluid categories may be used: Colloids (whole blood, plasma, and plasma expanders) and crystalloids/electrolytes(physiologic sodium chloride or lactated Ringers solution) Formulas have been developed for estimating fluid loss based on the estimated percentage of burns BSA and the

weight of the patient. Lengthof time is also very important in calculating estimated fluid needs. The formulas are individualized to meet the requirements of each patient The NIH Consensus Development Conference on Supportive Therapy in Burn Care established that salt and water are required in burnpatients, but that colloid may or may not be useful during the first 24 to 48 postburn hours The consensus formula provides for the volume of balanced saline solution to be administered in the first 24 hours in a range of 2 to 4 mL/kgper percent burn. Generally, 2mL/kg/ percent burn of lactated Ringers solution may be used initially for adults. This is the most common fluid replacement in usetoday. Studies show that with large burn, there is a failure of the sodium-potassium pump at the cellular level. Thus, patients with very large burns mayneed proportionately more milliliters of fluid per percent of burn than those with smaller burns Most fluid replacement formulas use isotonic electrolyte solutions. Another fluid replacement method requires hypertonic electrolyte solutions. This method uses concentrated solutions of sodium chloride andlactate (a balanced salt solution). The rationale for this replacement method is that by increasing serum osmolality, fluid will be pulled backinto the vascular space from the interstitial space. Reduced systemic and pulmonary edema results from administering hypertonic solutions.Goals of Fluid Replacement Therapy: A systolic blood pressure exceeding 100 mm Hg, pulse rate less than 110/minute, and urine output of 30 to50 ml/hour.

 Another gauge for fluid requirements and response to fluid resuscitation include hematocrit and hemoglobin and serum sodium levels.Nursing Process: Care during the Emergent/Resuscitative Phase Nursing assessment in the emergent phase of burn injury focuses on the major priorities for any trauma patient; the burn wound is a secondaryconsideration. Aseptic management of the burn wounds and invasive line continues. The nurse checks vital signs frequently. Respiratory status is monitored closely. Apical, carotid, and femoral pulses are evaluated Cardiac monitoring for patients with cardiac problems, electrical injury or respiratory problems or if the pulse is dysrhythmic or the rate isabnormally slow or rapid. Determining BP is a problem if all extremities are burned. A sterile dressing under the BP cuff will protect the wound from contamination. ADoppler UTZ or a non-invasive electronic BP may be helpful. In severe burns, an arterial catheter is used for BP measurement and for collecting blood specimen Peripheral pulses of burned extremities are checked hourly. Doppler is used. Elevation of burned extremities is crucial to decrease edema. Elevation of the lower extremities on pillows and of the upper extremities on pillows or by suspension using intravenous poles may be helpful.

25 Large-bore IV lines and Indwelling urinary catheter are inserted. Assessment includes monitoring of fluid intake and output. Urine output, an excellent indicator of circulatory status, is monitored carefully. The amount of urine first recorded may assist in determining the extent of preburn renal function and fluid status. Burgundy-colored urine suggests the presence of hemochromogen and myoglobin resulting from muscle damage. This is associated with deepburns caused by electrical injury. Glucosuria results from the release of stored glucose from the liver in response to stress. Infusion pumps and rate controllers are used to deliver a prescribed IV fluids Monitoring IV therapy is a major nursing responsibility. Body temperature, body weight, preburn weight, and history of allergies, tetanus immunization, past medical and surgical problems, currentillnesses, and use of medication are assessed. A head-to-toe assessment is performed, focusing on signs/symptoms of concomitant illness, injury, or developing complications. Patients with facial burns should have eye examination for potential injuries to the cornea

Assessment should include the time of injury, mechanism of burn, whether the burn occurred in closed space. The neurologic assessment focuses on the clients level of consciousness, psychological status, pain and anxiety levels, and behavior Acute or Intermediate Phase of Burn Care Begins 48 to 72 hours after the burn injury. Attention is directed toward continued assessment and maintenance of respiratory and circulatory status, fluid and electrolyte balance, andgastrointestinal function. Airway obstruction caused by upper airway edema can take as long as 48 hours to develop. Changes may occur as the effects of resuscitativefluid and the chemical reaction of smoke ingredients with lung tissues become apparent. The patients arterial blood gas values and other parameters determine the need for intubation and mechanical ventilation. If cardiac or renal function is inadequate, fluid overload occurs and symptoms of congestive heart failure may result. Vasoactive medications,diuretics, and fluid restriction may be used to support circulatory function and prevent congestive heart failure and pulmonary edema Cautious administration of fluids and electrolytes continuous because of the shifts in fluid from the interstitial to intravascular compartments.Blood components are administered as needed to treat blood loss and anemia A resetting of the core body temperature in severely burned patients results in a body temperature slightly higher than normal for several weeksafter the burn injury. Bacteremia and septicemia also causes fever in many patients.. Acetaminophen and hypothermia blankets may berequired

to maintain body temperature to reduce metabolic stress and tissue oxygen demand. Central venous, peripheral arterial or pulmonary artery thermodilution catheters may be required for monitoring venous and arterial pressures.However, invasive vascular lines are avoided because they provide an additional port for infection. Infection progressing to septic shock is the major cause of death in patients who have survived the first few days after a major burn injury. Theimmunosuppression places the patient at high risk for sepsis. The infection that begins within the burn site may spread to the bloodstream. Infection Prevention Burn wound is an excellent medium for bacterial growth and proliferation. Bacteria such as Staphylococcus, Proteus, Pseudomonas, Escherichia coli, and Klebsiella find optimal conditions for growth within the burnwound. The burn eschar is a nonviable crust, no blood supply; therefore, neither polymorphonuclear leucocytes or antibodies nor systemicantibiotics can reach the area. Phenominal numbers of bacteria- 1 billion per gram of tissue- may appear and spread to the blood stream or release their toxins, which reachdistant sites. Fungi such as Candida albicans also grow easily in burn wounds The primary source of bacterial infection appears to be the patients intestinal tract. Major secondary source is the environment.

Cap, gown, mask and gloves are worn while caring for patient with open burn wounds. Clean technique is used when caring directly for burnwounds. Antibiotics are seldom given prophylactically because of the risk of promoting resistant strains of bacteria. Tissue specimens are taken for culture regularly to monitor colonization of the wound by microbial organisms. Systemic antibiotics are administered when there is documentation of burn wound sepsis or other positive cultures such as urine, sputum, or blood. Wound Cleaning Hydrotherapy in the form of shower carts, individual showers and bed baths. Because of the high risk of infection and sepsis, the use of plastic liners and thorough decontamination of hydrotherapy equipment and woundcare areas are necessary to prevent cross-contamination. Tap water alone can be used for burn wound cleansing. Hydrotherapy in any form should be limited to 20 to 30 minute period to prevent chilling and additional metabolic stress. Hydrotherapy provides an excellent opportunity for exercising the extremities and cleaning the entire body. At the time of wound cleaning, all skin is inspected for any hints of redness, breakdown, or local infection. Hair in and around burn area, except the eyebrows, should be clipped short.

Intact blisters may be left, but the fluid should be aspirated with a needle and syringe Wound cleaning is usually performed daily. When the eschar begins to separate from the viable tissue beneath, more frequent cleaning and debridement may be necessary After burn wounds are cleaned, they are gently patted with towel and the prescribed method of wound care is performed. Whatever is the method of wound care, the goal is to protect the wound from overwhelming proliferation of pathogenic organisms. Patientcomfort and ability to participate are also important considerations. Topical Antibacterial Therapy Topical antibacterial therapy does not sterilize the burn wound; it simply reduces the number of bacteria so that the overall microbial populationcan be controlled by the bodys host defense mechanisms The three most commonly used topical agents are Silver sulfadiazine (Silvadene), silver nitrate, and Mafenide acetate (Sulfamylon) No single agent is universally effective. Using different agents at different times in the postburn period may be necessary. Prudent use andalternation of antimicrobial agents results in less-resistant strains of bacteria, greater effectiveness of the agents. Before a topical agent is applied, the previously applied topical agent must be thoroughly removed. Wound Dressing

After the wound is cleaned, patted dry and applied topical agent; the wound is then covered with several layers of dressings. A light dressing is used over joints to allow for motion, light dressing is also applied over areas for which a splint has been designed to conformto the body contour for proper positioning Circumferential dressings should be applied distally to proximal. If the hand or foot is burned, the fingers and toes should be individually wrapped to promote adequate healing. Exposure Method Occasionally, a wound is treated by exposing it to air. Wound care proceeds in the same manner and a topical agent is applied, but nodressings are applied. The success of exposure method depends on keeping the immediate environment free of organisms. Everything coming in contact with thepatient must be sterile. Those who come in direct contact must wear masks, caps, sterile gowns and gloves; visitors are instructed to wear protective garb and not to touch the bed or hand anything to the patient. The room must be maintained at warm temperature with 40 to 50% humidity to prevent excessive evaporative fluid losses. A cradle may be placed over the patient to prevent sheets from coming in contact with the burn area, to minimize the effects of air currents (towhich burn patient is sensitive) Occlusive Method

An occlusive dressing is a thin gauze that is either impregnated with a topical antimicrobial or that is applied after topical antimicrobialapplication Occlusive dressing are most often used over areas with new skin grafts. These are applied under sterile conditions in the operating room. Their purpose is to protect the graft, promoting an optimal condition for its adherence to the recipient site. Ideally, these dressings remain in place for 3 to 5 days. Precautions are taken to prevent two body surfaces from touching, such as fingers or toes, ear and scalp, areas under the breasts, any point of flexion, or between the genital folds. Dressing Changes > Dressings are changed approximately 20 minutes after an analgesic is administered.> A mask, hair cover, disposable plastic apron or cover gown, and gloves are worn by health care personnel. Dressings that adhere to the wound can be removed more easily if they are moistened with saline solution or if the patient is allowed to soak for a few moments in the tub. The patient may participate, providing some degree of control over this painful procedure. Wound Debridement Debridement has two goals:1.To remove contaminated tissue, thereby protecting the patient from invasion of bacteria2.To remove devitalized tissue or burn eschar in preparation for grafting and wound healing. Natural Debridement The dead tissue separates from the underlying viable tissue spontaneously. After partial and full- thickness burns occur,

bacteria that arepresent at the interface of the burned tissue and the viable tissue underneath gradually liquefy the fibrils of collagen that hold the eschar inplace for the first or second postburn week. Using antibacterial topical agents tends to slow down this natural process of eschar separation Mechanical Debridement Involves using surgical scissors and forceps to separate and remove the eschar. This is carried out to the point of pain and bleeding Dressings are also helpful debriding agents. Coarse-mesh dressings applied dry or wet-to-dry (applied wet and allowed to dry) will slowlydebride the wound of exudates and eschar when they are removed. Surgical Debridement An operative procedure involving either primary excision (surgical removal of tissue) of the full thickness of the skin or shaving the burned skinlayers gradually down to freely bleeding, viable tissue. Surgical excision is initiated early in burn wound management. This may be performed a few days after or as soon as the patient ishemodynamically stable and edema has decreased. Ideally, the wound is then covered immediately with a skin graft and an occlusive dressing. The use of surgical excision carries with it risks and complications, especially with large burns. The procedure creates a high risk for extensivebleeding (as much as 100 to 125 ml of blood per percent BSA excised). Grafting the Burn Wound

 If wounds are deep (full thickness) reepitheliazation is not possible. Therefore coverage of the burn wound is necessary until coverage with agraft of the patients own skin (autograft) is possible. The purpose of wound coverage is to decrease the risk for infection; prevent loss of protein, fluid, and electrolytes through the wound; andminimize heat loss through evaporation. The main areas for skin grafting include the face, for cosmetic and psychological reasons; the hands and other functional areas such as thefeet; and areas that involve joints. Grafting permits earlier functional ability and reduces contractures (shrinkage of burn scar through collagen maturation). When burns are extensive, the chest and abdomen maybe grafted first to reduce the burn surface. During wound healing, granulation tissue develops. It fills the space created by the wound, creates a barrier to bacteria, and serves as a bed for epithelial cell growth. Richly vascular tissue is pink, firm, shiny, and free of exudates and debris. It should have a bacterial count of less than 100,000 per gram of tissue to optimize graft take. A preoperative culture is mandatory before grafting, because enzymes of bacteria can dissolve a graft and lead to its failure. Beta hemolyticstreptococci are a major factor in graft failure. Biologic Dressings (Homografts And Heterografts)

In extensive burns, biologic dressings can be lifesaving by providing temporary wound closure and protecting the granulation tissue untilautografting is possible. Biologic dressing may also be used to debride untidy wounds after eschar separation. With each biologic dressing change, debridement occurs. Once the biologic dressing appears to be taking or adhering to the granulating surface with minimal underlying exudation, the patient is readyfor an autograft. Biologic dressing also provides immediate coverage for clean, superficial burns and decreases the wounds evaporative water and protein loss. Biologic dressing decrease pain by protecting nerve endings and are an effective barrier against water loss and entry of bacteria. When applied to superficial partial-thickness wounds, they seem to speed healing. Biologic dressings consist of homografts (or allografts) and heterografts(or xenografts). Homografts are skin obtained from living or recently deceased humans. The amniotic membrane (amnion) from the human placenta may alsobe used as a biologic dressing. Heterografts consist of skin taken from animals (usually pigs). Most biologic dressings are used as temporary coverings of burn wounds and are eventually rejected because of the bodys immune reaction tothem as foreign.

Homografts tend to be the most expensive biologic dressings. They are available from skin banks in fresh and cryopreserved (frozen) forms. Homografts are thought to provide the best infection control. Of all the biologic and bio synthetic dressings available. Revascularization occurswithin 48 hours, and the graft may be left place for several weeks. Amnion is low in cost, however, amnion grafts do not become vascularized by the patients vessels and can be left in place only briefly. Pigskin is available from commercial suppliers. Pigskin impregnated with a topical antibacterial such as silver nitrate is also available. One new biologic dressing that has shown promise for permanent burn wound coverage is Alloderm. Alloderm is processed dermis from human cadaver skin. When a donor site is taken for an autologous skin graft, both the epidermal and dermallayers of skin are removed from the donor site. However, Alloderm provides a permanent dermal layer replacement. Use of alloderm allows the surgeon to take a thinner skin graft consisting of the epidermal layer only. The patients epidermal layer is placeddirectly over the dermal base (Alloderm). Use of Alloderm has resulted in less scarring and contractures with healed grafts; donor sites heal much more quickly than conventional donor sites because only the epidermal layer has been taken. Biosynthetic And Synthetic Dressings

Currently, the most widely used synthetic dressing is Biobrane, which is composed of nylon. Silastic membrane combined with a collagenderivative. Less costly than homograft or pigskin. Biobrane dressings adhere to donor sites and meticulously clean debrided partial-thickness wounds; they will remain until spontaneousepitheliazation and wound healing occur. Like biologic dressing, Biobrane protects the wound from fluid loss and bacterial invasion. Biobrane is also useful for intermediate or long-term closure of a surgically excised wound until an autograft becomes available. Like Biologic dressing, Biobrane should not be used over grossly contaminated or necrotic wounds. Several other synthetic dressings are available: Op-site, a thin, transparent, polyurethane elastic film, can be used to cover clean partial-thickness wounds and donor sites. This dressing is occlusive and waterproof but permeable to water vapor and air; this permeability providesprotection from microbial contamination and allows for the exchange of gases. Other synthetic dressings are Tegaderm, N-Terface, andDuoderm. Artificial skin (Integra) is the newest type of synthetic dressing. A dermal analogue, Integra is composed of two main layers. The epidermallayer, consisting of Silastic, acts as a bacterial barrier and prevents water loss from the dermis. The dermal layer is composed of animalcollagen. It interfaces with the open wound surface and allows migration of fibroblasts and capillaries into the material. Autografts

The ideal means of covering burn wounds because they come from the patients own skin and thus are not rejected by the patients immunesystem. They can be split-thickness, full-thickness, pedicle flaps, or cultured epithelium. Full-thickness and pedicle flaps are commonly used for reconstructive surgery, months or years after the initial injury. Split-thickness autografts can be applied in sheets or in postage stamp-like pieces, or they can be expanded by meshing so that they can cover 1.5 to 9 times more than a given donor site area. Skin meshers enable the surgeon to cut tiny slits into a sheet of donor skin, making itpossible to cover large areas with smaller amounts of donor skin. These expanded grafts cling to the recipient site more easily than sheetgrafts and prevent the accumulation of blood, serum, air, or purulent material under the graft. Using expanded grafts may be necessary in large wounds but should be viewed as a compromise in terms of cosmetics.Care of the Patient with an Autograft Occlusive dressings are commonly used initially after grafting to immobilize the graft. Occupational therapists may be helpful in constructing splints to immobilize newly grafted areas to prevent dislodging the graft If the graft is dislodged, sterile saline compresses will help prevent drying of the graft until the physician reapplies it. The patient is positioned and turned carefully to avoid disturbing the graft or putting pressure on the graft site. If an extremity has been grafted, it is elevated to minimize edema.

 The patient begins exercising the area 5 to 7 days after grafting.Care of Donor site Moist gauze is applied at the time of surgery to maintain pressure and to stop any oozing. A thrombostatic agent such as thrombin or epinephrine may be applied directly to the site. The donor site may be applied with a single-layer gauze impregnated with petrolatum, scarlet red, or bismuth to new biosynthetic dressingssuch as Biobrane. Donor site must remain clean, dry, and free from pressure. Because a donor site is usually a partial-thickness wound, it will heal spontaneously within 7 to 14 days with proper carePain Management Pain management is the most difficult challenges facing the burn team. Many factors contribute to the patients burn pain experience: severity of the pain, health providers pain assessment, the appropriateness andadequacy of pharmacologic treatment of pain, the multiple procedures involved and assessment of the effectiveness of pain relief measures. The outstanding features of burn pain are its intensity and long duration. Wound care carries with it anticipation of pain and anxiety. In partial-thickness burn, the nerve endings are exposed, resulting to excruciating pain with exposure to air currents.

Although, nerve endings are destroyed in full-thickness burns, there is deep pain and pain in adjacent structures. The primary pain is intense in the initial acute post burn phase. This pain gradually subsides. However, until the skin heals or graft are appliedand taken, the pain level remains high because of treatment-induced pain. Wound cleaning, dressing changes, debridement, and physicaltherapy inflict intense pain. Discomforts related to tissue healing, such as itching, tingling, and tightness of contracting skin and joints adds tothe duration and intensity of pain. Because pain can not be eliminated short of anesthesia, the goal is to minimize the pain with analgesics before the patien faces wound careprocedures. Bolus doses of opioids, usually morphine, are often provided. Ketamine anesthesia administered IV are also used. Sedation with anti-anxiety agents such as lorazepam (Ativan) or midazolam(Versed) may be indicated in addition to analgesia. Patient-controlled analgesia, using both continuous and bolus morphine infusions, and sustained release oral morphine, given every 12 hourshave helped burn patients. Self-administered nitrous oxide also helps to make dressing changes tolerable to those patients who have sufficient hand function to hold amask to their faces intermittently during dressing changes. Early surgical excision with grafting under anesthesia may be the best way to reduce the overall pain experience for burn patients.Nutritional Support

Hypermetabolism persist after burn injury until wounds are closed, thereby increasing the basal metabolic need by as much as 100%. The goal of nutritional support is to promote a state of positive nitrogen balance. The nutritional support required is based on the patients preburn status and the extent of total BSA burned. Several formulas exist for estimating the daily metabolic expenditure and caloric requirements of burn patients. Protein requirements may range from 1.5 to 4 g of protein per kg of body weight every 24 hours Lipids are included in the nutritional support because of their importance for wound healing, cellular integrity, and absorption of fat-solublevitamins. Carbohydrates are included to meet caloric requirements as high as 5,000 cal per day Adequate vitamins and minerals are also needed. The proportions of fat, protein, and carbohydrate are planned for maximal use. Overfeeding can be detrimental. Therefore, a dietitian familiar with current concepts in nutrition for burn patients is necessary. As soon as GIT function resumes, nutritional support begins. The enteral route is preferred. In patients with extensive burns, tube feedings maybe indicated to ensure daily calories needed.

Indications for Total parenteral nutrition (TPN) include weight loss greater than 10% of normal body weight, inadequate intake of enteralnutrition prolonged wound exposure, and malnutrition or debilitated condition before injury. Amanuel/Pslidasan/Ksjuliano/MRCuenoNCM 104 1 st sem S.Y. 2007-2008 28 DISORDERS OF WOUND HEALINGSCARS Results from excessive abnormal healing or inadequate new tissue formation. Hypertrophic scars and wound contractures are more likely to occur if the initial burn injury extends below the level of the deep dermis. Healingof such deep wounds result in the replacement of normal integument Compression measures are instituted early in the burn wound treatment to prevent scar formation. Ace wraps are used to promote adequatecirculation, used as the first form of compression. Scar management occurs mainly in the rehabilitative phase, after the wounds are closed. KELOIDS A large, heaped-up mass of scar tissue. Keloids tend to be found in darkly pigmented people, grow outside of wound margins, and recur after surgical excision. FAILURE TO HEAL Failure to heal may be due to many factors, including infection and inadequate nutrition

A serum albumin level of less than 2g/dL is a usual factor CONTRACTURES The burn wound tissue shortens because of the force exerted by the fibroblasts and the flexion in natural wound healing. An opposing force provided by splints, traction, and purposeful movement and positioning must be used to counteract deformity in burnsaffecting joints.Nursing Process: Burn Care During The Acute PhaseAssessment Continued assessment focuses on hemodynamic alterations, wound healing, pain and psychosocial responses, and early detection of complications. Nurse assess VS frequently Continued assessment of peripheral pulses is essential for the first few post burn days while edema continuous to increase, potentiallydamaging peripheral nerves and restricting blood flow. Observation of the electrocardiogram may give clues to cardiac dysrhythmias resulting from potassium imbalance, preexisting cardiac disease,or the effects of electrical injury or burn shock Assessment focuses on hemodynamic alterations, wound healing, pain and psychosocial responses, and early detection of complications. Assessment of respiratory and fluid status is the highest priority for detection of complications. Assess VS

Assessment of peripheral pulses while edema continuous to increase, damaging peripheral nerves and restricting blood flow ECG may give clues to cardiac dysrhythmias resulting from potassium imbalance, preexisting cardiac disease, or the effects of electrical injuryor burn shock Assessment of residual gastric volumes and pH in the patient with a NGT- gives clues to early sepsis or the need for antacid therapy. Blood inthe gastric fluid or stools must also be reported Important wound assessment include size, color, odor, eschar, exudates, abscess formation under the eschar, epithelial buds (small pearl-likeclusters of cells on the wound surface), bleeding, granulation tissue appearance, progress of grafts and donor sites, and quality of surroundingskin Assessment on pain and psychosocial responses, daily body weights, caloric intake, general hydration, and serum electrolyte and hemoglobinlevels and hematocrit Assessment for excessive bleeding from blood vessels adjacent to areas of surgical site and debridement Potential Complications:1.Congestive heart failure and pulmonary edema2.Sepsis3.Acute Respiratory Failure4.Visceral DamagePlanning and Goals:The major goals: restoration of normal fluid balance, absence of infection, attainment of anabolic state and normal weight, improved skin integrity,

 reduction of pain and discomfort optimal physical mobility adequate patient and family coping adequate patient and family knowledge of burn treatment absence of complicationsNursing Interventions:Restoring Normal Fluid Balance Monitor IV and oral intake to reduce risk for fluid overload and consequent CHF1.Use IV infusion pumps2.Daily weights are obtained Low-dose dopamine to increase renal perfusion Diuretics to increase urine outputPreventing Infection A clean and safe environment Detect early signs of infection culture results and WBC counts are monitored Aseptic technique for wound care procedures. Hand washing before and after each patient contact Fresh flowers, plants or fresh fruit baskets should not be allowed inside the room because of the risk of microorganism growth Visitors are screened to avoid exposing the immunocompromised patient to pathogensMaintaining Adequate Nutrition

Oral fluids should be initiated slowly when bowel sounds resumes. If vomiting and abdominal distention do not occur, fluids may be graduallyincreased The nurse collaborates with the dietitian to plan a proteinand calorie-rich diet Amanuel/Pslidasan/Ksjuliano/MRCuenoNCM 104 1 st sem S.Y. 2007-2008 29 If caloric goals can not be met by oral feeding, a feeding tube is insertedPromoting Skin Integrity Assess and record changes or progress in wound healing Wound care Topical antibacterial agentsRelieving Pain and Discomfort Pain is more severe in partial-thickness burns than in fullthickness burns because the nerve endings are not destroyed. Cover exposed nerveendings to help reduce pain Analgesics and anti-anxiety medications Teach relaxation techniques Give patient control over wound care Pain-relieving distractions: video programs/games, hypnosis Complete treatments and dressings quickly. Analgesics before any painful procedures

Oral anti-pruritic agents, cool environment, frequent lubrication of skin with water or silica-based lotion to reduce discomfort in itching Exercise and splinting to prevent skin contracturePromoting Physical Mobility Early priority is to prevent complications resulting from immobility Deep breathing, turning, and proper positioning to prevent atelectasis and pneumonia, control edema and to prevent pressure ulcers andcontractures. Early sitting and ambulation When lower extremities are burned elastic bandage are applied before the patient is placed in an upright position. This bandages promotevenous return and minimize swelling Passive and active ROM to prevent contracture Splints or other functional devices are used for contracture control. Monitor splinted areas for signs of vascular insufficiency and nervecompressionStrengthening Coping Strategies The patient is facing the reality of burn trauma and is grieving over obvious loss. Depression, regression and manipulative disorders arecommon problems Develop effective coping strategies by:1.Setting specific expectations for behavior 2.Promoting truthful communications to build trust Patient always ventilates feelings of anger enlist someone to whom patient can vent feelings without fear of retaliationMonitoring and Managing Potential Complications:

Congestive Heart Failure and Pulmonary Edema Patient is assessed for pulmonary overload may occur as fluid is mobilized from the interstitial compartment back into the intravascular compartment. If the cardiac and renal system cannot compensate for the excess vascular volume, CHF and pulmonary edema may result. Crackles in the lungs and increased difficulty with respiration may indicate a fluid buildup in the lungs.1.Patient is positioned comfortably with the head of the bed raised to promote lung expansion and gas exchange2.Provide supplemental oxygen3.Administer IV diuretics Sepsis Early signs are increased in temperature, increased pulse rate, flushed dry skin, increased pulse rate, widened pulse pressure, and flushed dryskin in unburned areas Wound and blood cultures Antibiotics Acute Respiratory Failure and Acute Respiratory Distress Syndrome Patient is assessed for increased difficulty in breathing, change in respiratory pattern, onset of adventitious (abnormal) sounds Signs of hypoxia (decreased O2 to the tissues), decreased breath sounds, wheezing, tachypnea, stridor Patients receiving mechanical ventilation must be assessed for a decrease in tidal volume and lung compliance Key sign of ARDS is hypoxemia while receiving 100% oxygen, decreased lung compliance and significant shunting

Management includes intubation and mechanical ventilation Visceral Damage Assess for signs of necrosis of visceral organs due to electrical injury. Tissues affected are usually between the entrance and exit wounds of theelectrical burn All patients with electrical burns should undergo electrocardiographic monitoring Assess for pain relate to deep muscle ischemia Fasciotomies are performed to relieve the swelling and ischemia in the muscles Rehabilitation Phase Of Burn Care Rehabilitation begins immediately after the burn has occurred Wound healing, psychosocial support, and restoring maximal functional activity remain priorities Continued focus on maintaining fluid and electrolyte balance and improving nutritional status Reconstructive surgery to improve body appearance and function Psychological and vocational counseling and referral to support groups SHOCK a serious abnormal physiologic state characterized by an imbalance between the amount of circulating blood volume and the size of the vascular bed resulting in insufficient blood flow to the tissues

a life-threatening medical emergency and is considered one of the most common causes of death for critically-ill patients body's response to shock: 1. hyerventilation leading to respiratory alkalosis 2. vasoconstriction--> shunts blood to heart and brain 3. intracellular to intracellular fluid shifts 4. tissue anoxia--> anaerobic metabolism--> increased capillary permeability and lactic acid build-up-->metabolic acidosis 5. impaired organ function: renal failure and ARDS (adult respiratory distress syndrome) types of shock (note: think C-H-A-N-S) 1. cardiogenic--> failure of heart to pump properly 2. hypovolemic--> decreased circualting blood volume 3. anaphylactic shock--> massive dilatation caused by an allergic reaction leading to release of histamine and related substances 4. neurogenic shock--> failure of arteriolar resistance, leading to massive dilatation and pooling of the blood 5. septic shock--> lethal drop in blood pressure as a consequence of bacteremia Assessment Findings

skin--> cool, pale, and moist for cardiogenic and hypovolemic shock; warm, dry , and pink in septic and neurogenic shock tachycardia weak and thready pulse blood pressure: normal during early stages but will drop in late stages rapid, shallow respirations--> due to tissue anoxia and increase in CO2 levels restlessness and apprehension--> may progress to coma decreased urinary output due to impaired circulation to the kidneys decreased temperature (except in septic shock)

Medical

Management

1. fluid replacement using crystalloid solutions (Ringer's lactate, normal saline), colloid solutions (albumin, plasmanate, dextran) and/or blood products ( whole blood, packed RBC, fresh frozen plasma) 2. drugs such as dopamine, dobutamine, isoproterenol, norepinephrine, sodium nitroprusside, corticosteroids and antibiotics (for septic shock) Nursing Management 1. maintain patent airway 2. administer oxygen as ordered 3. resuscitate as

necessary

4. continuously monitor : VS,respiratory status, CVP, ECG, ABG, CBC, electrolytes, BUN, creatinine, urine output, and other parameters as indicated 5. administer fluid and blood replacement as ordered 6. administer medications as ordered 7. elevate extremities to 45 deg.--> promotes venous return to the heart (avoid trendelenburg position as it increases respiratory impairment) 8. if narcotics will be administered for pain, use cautiously via IV and in small doses only--> incomplete absorption due to vasoconstriction may lead to overdose when circulation improves 9. promote rest and maintain a quiet, warm environment 10.provide psychological support for client and family Prognosis Prognosis depends on the underlying cause and the extent of complications. Hypovolemic, anaphylactic, and neurogenic shock repond well to therapy. Septic shock has a mortality rate of 30% to 50%. Cardiogenic shock has the poorest prognosis.

Prevention Shock can be prevented by minimizing factors that favor a specific type of schock. Treatment goals include reestablishing perfusion to the organs by restoring and maintaining the blood circulating volume, ensuring oxygenation and blood pressure are adequate, achieving and maintaining effective cardiac function, and preventing further complications. -ENDCatherine P. Tapales, RNMAN SY 2011-2012 ACUTE BIOLOGIC CRISES (24 HOURS) High Risk Adult (8 hours) A. Respiratory Disorders i.Pulmonary Embolism ii.Acute Respiratory Distress Syndrome (ARDS) iii.Respiratory Failure a . A c u t e R F b . C h r o n i c R F

iv.Mechanical

Ventilators

B.Endocrine/ Metabolic Disorders

i.Diabetic Ketoacidosis (DKA) ii.Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) iii.Thyrotoxic Crisis (Thyroid Storm) iv.Adrenal Crisis (Peochromocytoma) v.Hepatic Failure (Hepatic Coma) C.Renal Disorders i.Renal Failure a . A c u t e R F b . C h r o n i c R F

D.Cardiovascular Disorders i.Angina Pectoris ii.Myocardial Infarction iii.Congestive Heart Failure a.Right-sided CF b.Left-sided CF iv.Cardiogenic Shock v.Thromboembolism vi.Pericardial Effusion & Cardiac Tamponade vii.Cardiac Arrest viii.Dysrhythmias a . S i n u s N o d e 1.Sinus Bradycardia 2.Sinus Tachycardia

b.Atrial Dysrhythmias 1.Premature Atrial Complex (PAC) 2.Atrial Flutter 3.AtrialFibrillation c.Junctional Dysrhythmias d.Ventricular Dsyrhythmias 1.Premature ventricular Complex 2.Ventricular Tachycardia 3.Ventricular Fibrillation

4.Ventricular E . B u r n s F . A B C : S h o c k

Asystole