SHOCK

is a life threatening condition with a variety of underlying causes. Characterized by inadequate tissue perfusion that ,if untreated ,results in cell death. Systematic blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cellular functions.

SIGNIFICANCE OF SHOCK
Shock affects all body systems. It may develop rapidly or slowly, depending on the underlying cause. During shocks the body struggles to survive, calling on all its homeostatic mechanism to restore blood flow and tissue perfusion. Any insult to the body can create a cascade of events resulting in poor tissue perfusion. Therefore, almost any patient with any disease state maybe at risk for developing shock.

CLASSIFICATION OF SHOCKS
 Hypovolemic shocks occurs when there is a decrease in the intravascular volume  Cardiogenic shocks occurs when the heart impaired pumping ability ,it maybe a coronary or non coronary origin.  Circulatory or distrivutive shocks result from a maldistribution osr mismatch of blood flows to the cells.

STAGE OF SHOCKS
 COMPENSATORY STAGE
The patients blood pressure remains with a normal limits. Vasoconstrictions, increase heart rate and increased contractility of the heart contribute to maintaining adequate cardiac output. This result from stimulations of the sympathetic nervous system and subsequent release of catecholamines (epinephrine and norepinephrine). The patient displays the often-described “fight to fight” response.
CLINICAL MANIFESTATIONS

Despite a normal blood pressure, the patients shows numerous clinical signs indicating inadequate organ perfusions. The result of inadequate perfusions is anaerobic metabolism and a buildup of lactic acid, producing metabolic acidosis.
MEDICAL MANAGEMENT

Medical treatment is directed toward identifying the cause of the shocks, correcting the underlying disorder so that shocks does not progress, and supporting those physiologic processes that thus far have responded successfully to the threat.

NURSING MANAGEMENT

a. monitoring tissue perfusion b. reducing anxiety c. promoting safety

 PROGRESSIVE STAGE
In the progressive stage of shocks, the mechanisms that regulate blood pressure can no longer compensate and the MAP falls below normal limits, with an average systolic blood pressure of less than 90mm Hg.
ASSESSMENT AND DIAGNOSTIC FINDINGS

a. b. c. d. e. f. g.

Chances of survival depend on the patients general health before the shocks state as well as the amount of time it takes to restore tissue perfusion. As shocks progresses, organs systems decompensate. respiratory effects cardiovascular effects neurologic effects renal effects hepatic effects gastrointestinal effects hematologic effects

MEDICAL MANAGEMENT

These include use of appropriate intravenous fluids and medications to restore tissue perfusion by: 1. optimizing intravascular volume 2. supporting the pumping action of the heart 3. improving the competence of the vascular system
NURSING MANAGEMENT

a. preventing complications b. promoting rest and comport c. supporting family members

 IRREVERSIBLE STAGE
The irreversible stage(or refractory) stage of shocks represent the point along the shocks continuum at which organ damage is so severe that the patients does not respond to treatment and cannot survive.

MEDICAL MANAGEMENT

During the irreversible stage of shock is usually the same as for the progressive stage. Although the patients conditions may have progressed from the progressive to the irreversible stage, the judgment that the shocks is irreversible can be made of only retrospectively on the basis of the patients failure to respond to treatment.
NURSING MANAGEMENT

The nurse focuses on carrying out prescribed treatments, monitoring the patients, preventing complications, protecting the patients from injury, and providing comport. Offering brief explanations to the patients about what is happening is essential even if the ther is no certainty that the patients hears or understand what is being said.

Overall Management Strategies in Shock
(management in all types and all phases of shocks includes the ff.) a. fluid replacement to restore intravascular volume b. vasoactive medications to restore vasomotor tone and improve cardiac function c. nutritional support to address the metabolic requirements that are dramatically increased in shock
FLUID REPLACEMENT

Is administered in all types of shocks. The type of fluids administered And the speed of delivery vary, but fluids are given to improve cardiac and tissue oxygenation, may include CRYSTALLOIDS (electrolyte solutions that move freely between intravascular and isterstitial space), COLLOIDS (large-molecule intravenous solutions) or blood components.
CRYSTALLOID AND SOLUTIONS

The best fluid to treat shocks remains controversial. In emergrencies , the “best” fluid that is readily available. Both crystalloids and the colloids, can be given to restore intravascular volume. Blood component therapy is used most frequently in hypovolomic shock.
COMLICATIONS OF FLUID ADMINISTRATION

Close monitoring of the patients during fluid is necessary to identify side effects and complications. The most common and serious side effect of fluid replacement are cardiovascular overload and pulmonary edema.
VASOACTIVE MEDICATION THERAPY

Administered in all forms of shocks to improve the patients hemodynamic stability when fluid therapy alone cannot maintain adequate MAP. Vasoactive medications are selected for their action on receptors of the symphatetic nervous system.when vasoactive medications are administered, vital sign must be monitored frequently(at least every 15min until stable or more often if indicated)
NUTRITIONAL SUPPORT

Nutritional support is an important aspect of care for the patient with shocks. Increased metabolic rates during shock increase energy requirements. The patients in shocks requires more than 3000 calories daily. the release of catecholamines early in the shocks continuum causes glycogen atores to the depleted in about 8 to 10 hours.  HYPOVOLEMIC SHOCKS >> The most common type of shocks, is characterized by a decreased intravascular volume . Risk Factor for Hypovolemic Shock External: Fluid losses Trauma Surgery Vomiting Diarrhea Diabetes insipidus
MEDICAL MANAGEMENT

Internal: Fluid Shifts hemorrhage burns ascites peritonitis dehydration

Major goals in treating hypovolemic shocks are to : 1. restore intravascular volume to reverse the sequence of events leading to inadequate tissue perfusion 2. redistribute fluid volume 3. correct the underlying cause of the fluid loss as quickly as possible. Depending on the severity of shocks and the patients conditions, it is likely that the efforts will be made to address all three goals simultaneously. a. b. c. d. treatment of the underlying cause fluid and blood replacement redistribution of fluid pharmacologic therapy

NURSING MANAGEMENT

Primary prevention of shocks is an essential focus of nursing intervention. General nursing measures include ensuring safe administration of prescribed fluids and medications and documenting their administration and effects

 CARDIOGENIC SHOCK
Cardiogenic shocks occurs when the hearts ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues. The cause of cardiogenic shocks are known as either coronary or noncoronary.
PATHOPHYSIOLOGY

In cardiogenic shocks, cardiac output, which is a function of both stroke volume and heart rate, is compromised. when stroke volume and heart rate decreased or become eratic, blood pressure drops and tissue perfusion is compromised.
CLINICALY MANIPESTATIONS

Patients in cardigenic shocks may experience angina pain and develop dysrhythmias and hemodynamic instability.
MEDICAL MANAGEMENT

The goals of medical management are to: 1. limit further myocardial damage and preserve the healthy myocardium 2. improve the cardiac function by increasing cardiac contractility
CORRECTION OF UNDERLYING

The underlying cause of cardiogenic shock must be corrected. It is necessary first to treat the oxygenation needs of the heart muscle to ensure its continued ability to pump blood to other organs.
INITIATION OF FIRST LINE TREATMENT

Involves the following actions: a. supplying supplemental oxygen b. controlling chest pain c. providing selected fluid support d. administering vasoactive medications e. controlling heart rate with medications or by implementations of a thranstoracic or intravenous pacemaker f. implementing mechanical cardiac support (intra-aortic balloon counterpulsation therapy, ventricular assist systems,or extracorporeal cardiopulmonary bypass)

OXYGENATION

In the early stages of shocks, supplemental oxygen is administered by nasal cannula at a rate 2 to 6 L/min to achieve ab oxygen saturation exceeding 90%

PAIN CONTROL

If the patients experiences chest pain, morphine sulfate is administered intravenously for pain relief. In addition to relieving pain, morphine delates the blood vessels . This reduces the workload of the heart by both decreasing the cardiac filling pressure (preload)and reducing the preassure against which the heart muscle has to eject blood (afterload)
HEMODYNAMIC MONITORING

Is initiated to asses the patients to response to treatment .this is performed in the intensive care unit, where an arterial line can be inserted. The arterial line enables accurate and continuous monitoring of blood pressure and provides a port from which to obtain frequent arterial blood samples without having to perform repeated arterial punctures.
PHARMACOLOGIC THERAPY

Vasoactive medication therapy consist of multiple pharmacologic strategies to restore and maintain adequate cardiac output.
DOBUTAMINE

(dobutrex) produces inotropic effects by stimulating myocardial beta receptors, increasing the strength of myocardial activity and improving cardiac output.
NITROGLYCERIN

(tridil) in low doses acts as a venous vasodilator and therefore produces preload. At higher doses nitroglycerin causes arterial vasodilation and therefore reduces afterload as well.
DOPAMINE

(intropine) is a symphathomimetic agent that has varying vasoactive effects depending on the dosage.
OTHER VASOACTIVE MEDICATIONS

Additional vasoactive agents that may be used in managing cardiogenic shocks include norepinephrine(lephoped),epinephrine(adrenalin), milrinone(primacor), amrinone( inocor) vasopressin( pitressin), and phenylephrine (neo-synephrine)

ANTIARRHYTHMIC MEDICATIONS

Is also part of the medication regimen in cardiogenic shocks.
FLUID THERAPY

In addition to medications appropriate fluid is necessary in treating cardiogenic shocks. A fluid bolus should never be given quickly because rapid fluid administration with cardiac failure may result in acute pulmonary edema.
MECHANICAL ASSISTIVE DEVICES

a. b. c. d. e.

increased stroke volume improved coronary artery perfusion decreased preload decreased cardiac workload decreased myocardial oxygen demand

NURSING MANAGEMENT
PREVENTING CARDIOGENIC SHOCK

Identifying patients at risk early and promoting adequate oxygenation of the heart muscle and decreasing cardiac workload can prevent cardiovascular shocks.
MONITORING HEMODYNAMIC STATUS

A major role of the nurse is monitoring the patients hemodynamic and cardiac status.
ADMINISTERING MEDICATIONS AND INTRAVENOUS FLUIDS

The nurse has a critical role in safe and accurate administration of intravenous fluid and medications.
MAINTAINING INTRA-AORATIC BALLOON COUNTERPULSATION

The nurse plays a critical role in caring for the patient receiving intra-aoratic balloon counterpulsation.the nurse makes ongoing timing adjustment of the balloon pump to maximized its effectiveness by synchronizing it with the cardiac cycle.
ENHANCING SAFETY AND COMPORT

Throughout care the nurse must take an active role in safe guarding the patient,enhancing comport and reducing anxiety.

 CIRCULATORY SHOCK
Circulatory or distributive shocks occurs when the blood volume is abnormally displaced in the vasculature.

Three type

1. septic shock 2. neurogenic shocks 3. anaphylactic shocks

SEPTIC SHOCKS
Is the common type of circulatory shock and is caused by widespread infection. Septic shocks typically in two phases. • reffered to as the hyperdynamic ,progressive phase • reffered to as the hypodynamic, irreversible phase

NEUROGENIC SHOCK
In neurogenic shocks vasodilation occurs as a result of symphathetic tone. May have a prolonged course (spinal cord injury) oa a short one (syncope fainting)it is characterized by dry, rather than the cool , moist skin seen in hypovolemic shocks,may have a prolonged course (spinal cord injury) or a short one (syncope or fainting).
MEDICAL MANAGEMENT

Treatment of neurogenic shock involves restoring symphatetic tone either trough the stabilization of a spinal cord injury or in the instance of spinal anesthesia, by positioning the patient properly .specific treatment of neurogenic shock depends on its cause.
NURSING MANAGEMENT

It is important to elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when a patient is receiving spinal or epidural anesthesia. Elevation of the head of the bed helps to prevent the spread of the anesthetic agent up the spinal cord.

ANAPHYLACTIC SHOCK
Cause by a severe allergic reaction when a patient who has already produced antibodies to a foreign substance (antigen) develops a systematic antigen-antibody reaction.

MEDICAL MANAGEMENT

Treatment of anaphylactic shock requires removing the causative antigen,administering medications that restore vascular tone,amd providing emergency support of basic life functions . Epinephrine is given for its vasoconstrictive action. Diphenhydramine(benadryl) is administered to reverse the effect of histamine .
NURSING MANAGEMENT

The nurse has an important role in preventing anaphylactic shock: assessing all patients for allergies or previous reactions to antigen and communicating the existence of these allergies or reactions to other. The must be knowledgeable about the clinical signs of anaphylaxis, must take immediate actions if sings and symptoms occur, and must be prepared to begin cardiopulmonary resuscitation if cardiorespiratory arrest occurs.

Burn
The incidence of burn injuries had been declining during the past several decades. Approximately 2 million people require medical attention for burn injury. Young children and elderly people are at particularly high risk for burn injury. The skin in people in these two age groups is thin and fragile; therefore, even a limited period of contact with a source of heat can create a full thickness of burn. Most injuries occur in the home, usually in the kitchen while cooking and in the bathroom by means of scalds or improper use of electrical appliances around water sources. Careless cooking is the one of the leading cause of fires in all over the world.

Classification by degree
• The most common system of classifying burns categorizes them as first-, second-, or third-degree. Sometimes this is extended to include a fourth or even up to a sixth degree, but most burns are first- to third-degree, with the higher-degree burns typically being used to classify burns post-mortem. The following are brief descriptions of these classes:[5] First-degree burns are usually limited to redness (erythema), a white plaque and minor pain at the site of injury. These burns only involve the epidermis. Second-degree burns manifest as erythema with superficial blistering of the skin, and can involve more or less pain depending on the level of nerve involvement. Second-degree burns involve the superficial (papillary) dermis and may also involve the deep (reticular) dermis layer. Third-degree burns occur when most of the epidermis is lost with damaged to underlying ligaments, tendons and muscle. Burn victims will exhibit charring of the skin, and sometimes hard eschars will be present. An eschar is a scab that has

• •

• • • •

separated from the unaffected part of the body. These types of burns are often considered painless, because nerve endings have been destroyed in the burned area. Hair follicles and sweat glands may also be lost due to complete destruction of the dermis. Third degree burns result in scarring and may be fatal if the affected area is significantly large. Fourth-degree burns damage bone tissue and may result in a condition called compartment syndrome, which threatens the life of the limb. Fifth-degree burns are burns in which most of the hypodermis is lost, charring and exposing the muscle underneath. Sometimes, fifth-degree burns can be fatal. Sixth-degree burns, the most severe form, are burn types in which almost all the muscle tissue in the area is destroyed, leaving almost nothing but charred bone. Often, sixth-degree burns are deadly.

Other classifications
A newer classification of "Superficial Thickness", "Partial Thickness" (which is divided into superficial and deep categories) and "Full Thickness" relates more precisely to the epidermis, dermis and subcutaneous layers of skin and is used to guide treatment and predict outcome. • Table 1. A description of the traditional and current classifications of burns. • Traditional • Nomenclature • Depth • Clinical findings nomenclature • Erythema, minor • Superficial • Epidermis • First-degree pain, lack of thickness involvement blisters • Superficial • Partial thickness — • Blisters, clear • Second-degree (papillary) superficial fluid, and pain dermis • Whiter appearance, with • Partial thickness — • Deep (reticular) decreased pain. • Second-degree deep dermis Difficult to distinguish from full thickness • Dermis and • Hard, leather-like underlying tissue • Third- or fourtheschar, purple • Full thickness and possibly degree fluid, no sensation fascia, bone, or (insensate) muscle • Main article: Total body surface area • Burns can also be assessed in terms of total body surface area (TBSA), which is the percentage affected by partial thickness or full thickness burns (superficial thickness •

burns are not counted). The rule of nines is used as a quick and useful way to estimate the affected TBSA. Causes of burns • • Burns may be caused by a wide variety of substances and external sources such as exposure to chemicals, friction, electricity, radiation, and extreme temperatures, both hot and cold. Most chemicals (but not all) that can cause moderate to severe chemical burns are strong acids or bases.[6] Chemical burns are usually caused by caustic chemical compounds, such as sodium hydroxide, silver nitrate, and more serious compounds (such as sulfuric acid and Nitric acid).[7] Hydrofluoric acid can cause damage down to the bone and its burns are sometimes not immediately evident.[8] Electrical burns are generally caused by an exogenous electric shock, such as being struck by lightning or defibrillated or cardioverted without a conductive gel. The internal injuries sustained may be disproportionate to the size of the burns seen, and the extent of the damage is not always obvious. Such injuries may lead to cardiac arrhythmias, cardiac arrest, and unexpected falls with resultant fractures.[9] Radiation burns may be caused by protracted and overexposure to UV light (as from the sun), tanning booths, radiation therapy (as patients who are undergoing cancer therapy), sunlamps, and X-rays. By far the most common burn associated with radiation is sun exposure, specifically two wavelengths of light UVA, and UVB, the latter being the more dangerous of the two. Tanning booths also emit these wavelengths and may cause similar damage to the skin such as irritation, redness, swelling, and inflammation. More severe cases of sun burn result in what is known as sun poisoning.

• [edit] Scalding

• • • •

Two day-old scald caused by boiling radiator fluid. Scalding is a specific type of burning that is caused by hot fluids or gases. They most commonly occur in the home from exposure to high temperature tap water.[10] Steam is a common gas that causes scalds. The injury is usually regional and usually does not cause death. More damage can be caused if hot liquids enter an orifice. However, deaths have occurred in more unusual circumstances, such as when people have accidentally broken a steam pipe. The demographics that are of the highest risk to suffering from scalding are young children, with their delicate skin, and the elderly over 65 years of age.

Cold burn

• • • •

Frostbitten hands A cold burn (see frostbite) is a kind of burn which arises when the skin is in contact with a low-temperature body. They can be caused by prolonged contact with moderately cold bodies (snow and cold air for instance) or brief contact with very cold bodies such as dry ice, liquid helium, liquid nitrogen, or canned air. In such a case, the heat transfers from the skin and organs to the external cold body. The effects are very similar to that of a burn caused by extreme heat. The remedy is also the same. For a minor cold burn, it is advisable to keep the injured organ under a flow of water of comfortable temperature. This will allow heat to transfer slowly from the water to the organs.

Management
• A local anesthetic is usually sufficient in managing pain of minor first-degree and second-degree burns. However, systemic anti-inflammatory drugs such as naproxen may be effective in mitigating pain and swelling. Additionally, topical antibiotics such as Mycitracin are useful in preventing infection to the damaged area.[11] Lidocaine can be administered to the spot of injury and will generally negate most of the pain. Regardless of the cause, the first step in managing a person with a burn is to stop the burning process at the source. For instance, with dry powder burns, the powder should be brushed off first. With other burns, such as those caused by exposure to chemicals, the affected area should be rinsed throughly with a large amount of clean water to remove the caustic agent and any foreign bodies. Cold water should not be applied to a person with extensive burns, however, as it may compromise the burn victim's temperature status. If the patient was involved in a fire accident, then it must be assumed that he or she has sustained inhalation injury until proven otherwise, and treatment should be managed accordingly. At this stage of management, it is also critical to assess the airway status. Any hint of burn injury to the lungs (e.g. through smoke inhalation) is considered a medical emergency. Survival and outcome of severe burn injuries is remarkably improved if the patient is treated in a specialized burn center/unit rather than a hospital. Serious burns, especially if they cover large areas of the body, can result in death. Once the burning process has been stopped, the patient should be volume resuscitated according to the Parkland formula, since such injuries can disturb a person's osmotic

balance. This formula dictates the amount of Lactated Ringer's solution to deliver in the first twenty four hours after time of injury. This formula

excludes first and most second degree burns. Half of the fluid should be given in the first eight hours post injury and the rest in the subsequent sixteen hours. The formula is a guide only and infusions must be tailored to urine output and central venous pressure. Inadequate fluid resuscitation causes renal failure and death.

Burn Prevention Tips • • • • • • • • • • • • • Keep matches and lighters out of reach of the children Never leave unattended around fire or in bathroom/bathtub Install and maintain smoke detectors in the home Develop and practice and practice home exit fire drill Set the water heater temperature no higher than 120F Do not smoke in bed. Do not fall asleep while smoking Do not throw flammable liquids on to an already burning fire Do not use flammable liquids to start fires Do not remove radiator cap from a hot engine Watch for overhead electrical wires and underground wires when working outside Never store flammable liquids near a fire source, such as a pilot light Use caution while cooking Keep a working fire extinguisher in your home

Characteristics of Burn According to Depth Burn and causes Superficial Partial Thickness (1st degree burn) Deep Partial Thickness (2nd degree burn) Skin involvement Epidermis; possibly a portion of dermis Epidermis; upper dermis’ portion of deeper dermis Symptoms Tingling Hyperesthia Pain that is soothed by cooling Pain Hyperesthia Sensitive to cold air Wound appearance Reddened; blanches w/pressure dry Minimal or no edema Possible blisters Blistered; mottled red base; broken epidermis; weeping surface Edema Recuperative course Complete recovery within a week, no scarring Peeling Recovery in 2 to 4 weeks Some scarring and depigmentation contractures Infection my convert it to full thickness Eschar sloughs Grafting Scarring and loss of contour and fxn; contractures Loss of digits or extremity possible

Full Thickness (3rd degree burn)

Epidermis; entire dermis, and sometimes subcutaneous tissue; may involve connective tissue, muscle, and bone

Pain free Shock Hematuria (blood in the urine)and possibly hemolysis (blood cell destruction) Possibly entrance and exit wounds (electrical burn)

Dry; pale white leathery, or charred Broken skin with fat exposed Edema

Local and Systemic Response to Burns • • Burns that do not exceed 25% TBSA produce a primarily local response Burns that exceed 25% TBSA may produce both a local and systemic response and are considered major burn injuries

Cardiovascular Response • • • Hypovolemia is tha immediate consequence of fluid loss resulting in decreased perfusion and oxygen delivery Cardiac output decrease before any significant change in blood volume is evident The greatest volume of fluid leak occurs in the first 24-36 hours after the burn, peaking by 6-8 hours

Burn Edema • • • Edema maximal after 24 hours It begins to resolve 1-2 days post burs and usually is completely resolved in 710 days post injury Edema increase in circumferential burns, pressure on small blood vessels and nerve in distal extremities cause and obstruction of blood flow and consequent ischemia

Effects on Fluids and Electrolytes and Blood Volume • • • Evaporative fluid loss through the burn wound may reach 3 to 5 L or more over a 24 hour period until the burn surfaces are covered Hyponatremia is most common during the first week of the acute phase, as water shifts from the interstitial to the vascular space Immediately after burn injury, hyperkalemia (excessive potassium) results from massive cell destruction. Hypokelamia (potassium depletion) may occur later with fluid shifts from the interstitial to the vascular space

Pulmonary Response • • • Inhalation, bronchoconstriction caused by release of histamine, serotonin and thrombaxane a powerfull vasoconstrictor, as well as chest constriction secondary o circumferential full thickness chest burns caused this deteoriation Pulmonary, upper airway injury results from direct heat or edema, manifested by mechanical obstruction of the upper airway Carbon monoxide, the pathophysiologic effects due to tissue hypoxia, a result of carbon monoxide combining with hemoglobin to form carboxyhemoglobin, which competes with oxygene for available hemoglobin binding sites

Other Systemic Response • • • • Renal fxn may be altered as a result of decreased blood volume, destruction of red blood cells at the injury site results in free hemoglobin in the urine Significant impairment of the production and release of granulocytes and macrophages from bone marrow after burn injury. The resulting immunosup resion places the burn patient at high risk of sepsis Loss of skin also results in an ability to regulate body temperature. Burn patients may therefore exhibits low body temp. in the early hours after injury Two potential gastrointestinal complications may occur, paralytic ileus and Curling ulcer, gastric distention and nausea my lead to vomiting unless gastric decompression is initiated.

Phases of Burn Care Phase Emergent or immediate resuscitative Duration From onset of injury to completion of fluid resuscitation Priorities • First aid • Prevention of shock • Prevention of respiratory distress • Detection and tx of comcominant injuries • Wound assessment and initial care • Wound care and closure • Prevention or tx of complication, including of infection • Nutritional support • Prevention of scars and contractures • Physical, occupational, and cosmetic reconstruction • Psychosocial counselling

Acute

From beginning of diuresis to near completion of wound care

Rehabilitation

From major wound closure to return to individuals optimal level of physical and psychosial adjustment

Emergency Procedure at the Burn scene • • • • • Extinguish the flames Cool the burn Remove restricted objects Cover the wound Irrigate chemical burns

Emergency Medical Management • • • • • • • • • • • • • Transport to the nearest emergency department Priorities the airway, breathing, and circulation Administer humidification, bronchodilator, mucolytic agents Continuous + airway pressure and mechanical ventilation may also be required to achieve adequate oxygenation Asses for cervical spinal injuries Asses for burn and wound Insert IVP and NGT, and suction the pt. to prevent vomiting Practice aseptic technique to prevent infection Asses for TBSA Fluid replacement Asses for Acute Respiratory and Renal Failure Transfer to a burn center Management of fluid loss and shock

Acute or Intermediate Phase of Burn Care Infection prevention • • • • • • • • Phase occur 48-72 hours after burn injury Asses for electrolytes imbalance, and gastrointestinal fxn Infection prevention wound cleaning, topical antibacterial therapy, wound dressing, wound debridement, and wound grafting Pain management and nutritional support Asses for airway obstruction caused by upper airway edema Asses for capillaries integrity Monitor fever for the signs of infection Monitor for infection like staphylococcus, proteus, pseudomonas, Escherichia coli, kliebsuella, candida albicans,

Wound Cleaning • Hydrotherapy • Use tap water • Tub baths

Topical Antibacterial Therapy • • • • Silver sulfadiazine (silvadene) Mafenide acetate (sulfamylon) Silver nitrate Acticoat

Wound Dressing • • 1st topical agent is applied then covered by a several layers of dressing A light dressing is also applied areas for which a splint has been designed to conform to the body contour the proper positioning

Dressing Change • • Dressings are changed in the pt. units hydrotherapy room, or tx approximately 20 min after and analgesics agent administered They may also changed in the OR after the pt. administered anesthesia

Wound Debridement • • • • • To remove tissue contaminated by bacteria and foreign bodies, thereby protecting the pt. from invasion of bacteria To remove devitalized tissue or burn eschar in preparation for grafting and wound healing Natural debridement Mechanical debridement Surgical debridement

Angina Pectoris
 Chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply  Caused by imbalanced between oxygen supply demand  Caused include obstruction of coronary blood flow because of atherosclerosis, coronary artery spasm and conditions increasing myocardial oxygen consumption

 The goal of treatment is to provide relief of an acute attack, correct imbalance between the myocardial oxygen supply and demand, and prevent progression of the disease and further attack to reduce the disk of MI. Precipitating Factors  Physical exertion  Exposure to cold  Eating a heavy meal  Stress or any emotion provoking situation TYPES 1. Stable Angina  Predictable and consistent pain that occurs on exertion and relieved by rest or nitroglycerine  Stable pattern of onset, duration, severity and relieving factors 2. Unstable Angina/Preinfraction Angina  Occurs with an unpredictable degree of exertion or emotion and increases in occurrence, duration and severity overtime  May not be relieved with rest and nitroglycerine 3. Variant/ Prinzmetal’s/ Vasospastic Angina  Result from coronary spasm  Similar to classic angina but last longer  May occur at rest  ECG- ST segment elevation 4. Intractable or refractory Angina  Severe incapacitating chest pain

CLINICAL MANIFESTATIONS 1. Chest Pain  Varying severity from indigestion to choking or heavy/tightness sensation  Range from discomfort to agonizing pain  Substernal or retrosternal  Poorly localized

 

May radiate to the neck, jaw, shoulder, and inner aspects of the upper arms Feeling of numbness in the arm wrist or hands  DM patient may not experience pain  Elderly may not exhibit typical pain profile -may present with dyspnea

2. Associated symptoms  Dyspnea  Pallor  Sweating  Palpitation and tachycardia  Dizziness and faintness  Hypertension Diagnostic Studies 1) ECG: normal during rest  ST depression or elevation and T wave inversion during episode of pain 2) Stress test: Chest pain or changes in the ECG or vital signs during testing indicating ischemia 3) Cardiac enzymes: normal 4) Cardiac Catheterization  Provide definitive diagnosis by providing information of the patency of the coronary artery Medical Management Objective: decrease O2 demand and increase O2 supply 1) Pharmacologic therapy a. Nitrates: Nitroglycerine  Mainstay of the treatment of the angina  MOA: dilates the coronary artery Decrease preload and afterload Routes: SL, topical, IV

Nursing Interventions:  Pre-procedure  Obtain consent  Assess for allergies to seafood’s, iodine and radioapaque dyes  Withhold meals before the procedure

 Document baseline vital signs  Have the client void  Administer sedatives as order

 Mark distal pulses  Inform the client that a warm flushing sensation may be felt as the contrast medium is injected  Inform the client that he may feel fluttery feeling as the catheter passes through the heart  Prepare insertion site by shaving or cleaning  Post-procedure  Monitor VS and cardiac rhythm for dysrhythmias  Assess for the chest pain and notify the physician  Monitor peripheral pulses color, warmth and sensation distal to insertion sites  Monitor bleeding and hematoma  Extremity extended for 4-6 hours  Strict bed rest for 6-12 hours  Encourage fluids  Monitor for the signs of hypersensitivity Immediate management a. Assess pain b. Provide bed rest c. Administer O2 at 3L nasal cannula as prescribed to dilate coronary arteries, reduced the O2 requirements of the myocardium, and relieve the chest pain d. Obtain a 12 lead ECG e. Provide continuous cardiac monitoring Following Acute Episode a. Instruct the client regarding the purpose of the diagnostic medical surgical procedure and post procedure expectation. b. Assist the client to identify angina precipitating event c. Instruct the client to stop activity and the rest if the chest pain occurs and to take nitroglycerine as prescribe d. Instruct the client to seek medical attention if pain persist e. Instruct the client regarding the prescribe medication f. Provide diet instruction to the client, stressing the dietary changes re not temporary and must be maintain for life

g. Assist the client to identify risk factor that can be modified h. Assist the client to set goals that will promote changes in lifestyle to reduce impact of risk factor i. Assist the client identify barriers to compliance with therapeutic plan to identify methods to become barriers j. Provide community resources to the client regarding exercise reduction and stress reduction.

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