EMERGENCY NURSING CARE
OF PATIENTS WITH SHOCK
CHAPTER I
INTRODUCTION
A. Background
Shock refers to a condition in circumstances where there is loss of body fluids quickly so that the occurrence of multiple organ failure due to inadequate perfusion. Shock occurs most often occur after heavy bleeding (hemorrhagic shock). Acute external bleeding caused by penetrating trauma and severe bleeding due to gastrointestinal kelianan 2 causes hemorrhagic shock is most often found. Hemorrhagic shock can also result from acute internal bleeding into the thoracic cavity and the abdominal cavity. Internal bleeding is the leading cause of trauma on organs and rupture of abdominal aortic aneurysm. Shock may result from loss of body fluids other than blood in significant amounts. Examples of hypovolemic shock caused by the loss of other fluids are refraktrer gastroenteritis and severe burns. Overall objective of this journal is focused to hypovolemic shock caused by bleeding and the many controversies that arise around how to handle.
Most trauma merbahaya when the war around 1900 has given the impression that a significant detriment to the development of the principles of treatment of hemorrhagic shock resuscitation. When World War I, W.B. Cannon recommends fluid resuscitation to slow so the main cause of shock addressed surgically. Giving blood kristalloid and used extensively during World War II to deal with patients with unstable conditions. Can experience in wartime against Korea and Vietnam showed bahawa fluid resuscitation and early surgical intervention is an important step to save trauma patients with hemorrhagic shock causing. This and some other principle helps in the development of guidelines for the treatment of hemorrhagic shock face of opposition from trauma. However, most researchers have questioned these guidelines, and today it has raised many controversies about how to handle the most optimal hemorrhagic shock.
B. Destination
1. General Purpose
Students can learn nursing care to patients syock
2. Special Purpose
Students can learn: understanding syock, cause shock, syock pathophysiology, signs and symptoms syock, manifestations kllinis syock, syock types, management syock
Chapter II
review theory
Nursing care in patients with SHOCK
A. Definition
A state / tissue perfusion disorder syndrome that is not optimal, complete metabolic networks. (Rupii, 2005)
Critical state due to failure of the circulatory system in sufficient nutrients and oxygen in terms of both supply and use for cellular metabolism of body tissue, causing an acute deficiency of oxygen in acute secular level. (Tash Ervien S, 2005)
A form of dynamic syndrome caused by tissue damage because ultimately be necessary substrate for aerobic metabolism at the microcellular level removed at a pace that does not adekuatoleh very little blood flow or flow maldistribusi (Candido, 1996)
Weight form of lack of oxygen supply compared to the needs. This situation is caused by a decrease in tissue oxygenation or changes in the capillary circulation. Lack of oxygen will be in touch with lactate acidosis, which is an indicator of body lactat levels of severity level syock
Shock resistance in the peripheral blood circulation leading to tissue perfusion is not sufficient to meet the nutrient needs of the cell and threw the rest metabolism (Theodore, 93), or a less than perfect tissue perfusion.
The first step is to be able to overcome the shock should be able to recognize the symptoms of shock. There is no laboratory test that can diagnose shock immediately. Diagnosis is made based on an inadequate understanding of clinical organ perfusion and tissue oxygenation.
The second step in tackling the shock is trying to find out possible causes of shock. In patients with trauma, shock is directly related to the introduction of the mechanism of trauma. All types of shock can occur in trauma patients and the most common is of hypovolemic shock due to bleeding. Cardiogenic shock can also occur in patients who experience trauma in the diaphragm and neurogenic shock can be caused by trauma to the central nervous system and spinal cord. Septic shock should also be considered in trauma patients who arrive too late to get help.
B. Stadium Syock
Compensation
Body composition by increasing reflex syarpatis ie increased systemic resistance which occurs only in the selective detruksi vital organs. TD sistokis normal, dioshalik systemic arterial resistance is increased due to an increase in addition TN skresi vaseprsin and activation of RAA system. special menitestasi talekicad, rowdy restless, pale skin, kapir retail> 2 docks.
Decompensation
Composition mechanisms begin to fail, made strong sulfuric cadiac worsen tissue perfusion, anaerobic metabolism occurs. because lactic acid accumulates there asidisif who gain weight with intracellular formation of carbonate asan. It inhibits the heart kontraklilitas already on the mechanism of Na + K Pompo energy at the cellular level. At syock also occur due to histamine release smesvar but when syock continues to aggravate the situation, which occurs disfori vasodilation and increased capillary permeability so volumevenous retwn reduced incidence of depression that occurs muocard. Clinical Maniftrasi: TD decreased, porfsi bad teriter olyserci, acidosis, kusmail napus.
3. Irreversible
Compensation failed terlanjut with cell death and multiorgan system dysfunction, ATP reserves in keper and heart out (new synthesis 2 hours). recent death of circulation can be recovered even if the clinical manifestations: TD taktenkur, no palpable pulse, consciousness (coma), anuria.
C. Occurrence of Shock Pathophysiology
D. Signs And Symptoms
1. Cardiovascular System
· Impaired peripheral circulation - pale, cold extremities. Lack of peripheral venous more meaningful than a decrease in blood pressure.
· Rapid pulse and smooth.
· Low blood pressure. It can not be hold, due to compensatory mechanisms occur losing one third of the volume of circulating blood.
· Peripheral veins collapse. Neck veins are best judgment.
· Low CVP.
2. Respiratory System
Breathing fast and shallow.
3. Central nervous system
Mental changes vary widely shock patients. If low blood pressure causes hypoxia to the brain, the patient became agitated until unconscious. Sedative and analgesic drugs should not be given to believe that the patient is restless because of the pain.
4. Digestive System
Nausea and vomiting can occur.
5. Urethral System
Reduced urine production. Normal urine production average adult patient was 60 ml / hour (1/5-1 ml / kg / hour).
E. Clinical Manifestations
In general, the clinical manifestations syock that arise include: pale, confused, tachicardy coma, cyanosis, congestive heart failure Arithnia, sweating, tachypnea, temperature changes, pulmonary edema, Restlessness, disorientation. Other clinical manifestations being that can arise
1. Decline in glomerular filtration
2. decreased urine output
3. keeping the increased blood
4. metabolic acidosis
5. hyperglikemi
F. Shock Type
1. Shock Hypovolemik
Circumstances hypovolemic shock refers to a condition in which there is loss of body fluids quickly so that the occurrence of multiple organ failure due to inadequate perfusion. Hypovolemic shock is most often happen after a severe bleeding (hemorrhagic shock). Acute external bleeding caused by penetrating trauma and severe bleeding due to gastrointestinal kelianan 2 causes hemorrhagic shock is most often found. Hemorrhagic shock can also result from acute internal bleeding into the thoracic cavity and the abdominal cavity
a. Causes
In general, hypovolemic shock due to bleeding, while other causes are extreme discharge of salt (NaCl). Such as occurs in shock: long-bone fracture, rupture spleen, hematothorak, arterial dissection, pangkreatitis weight. Being due to hypovolemic shock secondary to the gathering of fluid in the interstitial space due to: increased capillary permeability due to heat injury, allergic reactions, toxins bekteri.
Internal bleeding is the leading cause of trauma on organs and rupture of abdominal aortic aneurysm. Hypovolemic shock may result from loss of body fluids other than blood in significant amounts. Examples of hypovolemic shock caused by the loss of other fluids are refraktrer gastroenteritis and severe burns. Overall objective of this journal is focused to hypovolemic shock caused by bleeding and the many controversies that arise around how to handle.
Most trauma merbahaya when the war around 1900 has given the impression that a significant detriment to the development of the principles of treatment of hemorrhagic shock resuscitation.
When World War I, W.B. Cannon recommends fluid resuscitation to slow so the main cause of shock addressed surgically. Giving blood kristalloid and used extensively during World War II to deal with patients with unstable conditions. Can experience in wartime against Korea and Vietnam showed bahawa fluid resuscitation and early surgical intervention is an important step to save trauma patients with hemorrhagic shock causing. This and some other principle helps in the development of guidelines for the treatment of hemorrhagic shock face of opposition from trauma. However, most researchers have questioned these guidelines, and today it has raised many controversies about how to handle the most optimal hemorrhagic shock.
b. Pathophysiology
The human body responds to acute hemorrhage by activating the body's physiology 4 major systems: the hematologic, cardiovascular system, renal system and hematologic neuroendokrin.system system responds to severe bleeding which occurred acutely by activating the blood clotting cascade and mengkonstriksikan blood vessels (with release of thromboxane Local A2) and form a blockage immatur the source of bleeding. The damaged vessel will expose the collagen layer, which will subsequently lead to fibrin deposition and stabilization of subatan formed. About 24 hours required for the formation of fibrin obstruction perfect and mature formations.
Cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, myocardial contractility raised, and mengkonstriksikan heart blood vessels. This response arises due to the elevation of the release of norepinephrine and decreased vagal tone (which is regulated by the arch baroreceptors located in the carotid, aortic arch, left atrium and pulmonary veins. Cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys, and carries blood from the skin, muscle, and GI.
Urogenital system (kidneys) responds to stimulation that increases the release of renin from justaglomerular apparatus. Of renin release then proceed then the formation of angiotensin II, which has two main effects memvasokontriksikan blood vessels and stimulates the secretion of aldosterone in the adrenal cortex. Adrenal responsible for the reabsorption of sodium and water conservation perpetually active.
Neuroendocrine system responds to hemorrhagic shock by increasing the secretion of ADH. ADH is released from the posterior hipothalmus responds to a decrease in blood pressure and a decrease in sodium concentration. Reabsorsi ADH directly improve water and salt (NaCl) in the distal tubule. Colletivus ductus and the loop of Henle.
Patofisiology of hypovolemic shock more than what has been mentioned. for mengexplore more about patofisiology, bibliographic references on a reference bias. Mechanisms that have been described sufficiently effective to maintain perfusion of vital organs due to heavy blood loss. Without the blood and fluid resuscitation and correction of the cause of hemorrhagic shock, cardiac perfusion usually fail and multiple organ failure
c. Hypovolemic Shock stage
1) Phase I:
· Occurs bika 0-10% blood loss (approx 500ml)
· Compensation which occurs usually Cardiak output and blood pressure can still be maintained
2) Phase II:
· Occurs when blood kehilanagan 15-20%
· Drop in blood pressure, PO2 down, tachycardia, tachypnea, diaforetik, restless, pale.
3) Phase III
· If there is blood kehilengan more than 25%
· Decline: blood pressure, Cardiak output, PO2, perfusion rapid network
· Occurs in the ischemic organ
· Fluid extravasation occurs
2. Cardiogenic Shock
a. Definition
Cardiogenic shock caused by the failure of the pump function of the heart resulting in cardiac output to be reduced or stopped altogether.
Cardiogenic shock is defined as the presence of tissue hypoperfusion signs of heart failure caused by low preload corrected. There is no clear definition of hemodynamic parameters, but cardiogenic shock is usually characterized by a decrease in blood pressure (systolic less than 90 mmHg, or a decrease in mean arterial pressure over 30 mmHg) and or a decrease in urine output (less than 0.5 ml / kg / hour) with a pulse rate of more than 60 times per minute with or without the presence of organ congestion. There is no clear boundary between the low cardiac output syndrome with shock kerdiogenik. (Www.fkuii.org)
Cardiogenic shock is an end-stage left ventricular dysfunction or congestive heart failure, occurs when the left ventricle suffered extensive damage. Contractility of heart muscle loses strength, causing a decrease in cardiac output with inadequate tissue perfusion to vital organs (heart, brain, kidneys). Comparable degree of shock with left ventricular dysfunction. Although cardiogenic shock usually occurs as a complication of MI often, but can also terajdi on temponade cardiac, pulmonary embolism, cardiomyopathy and dysrhythmias. (Brunner & Suddarth, 2001)
Cardiogenic shock is shock caused adekua cardiac function, as in myocardial infarction or mechanical obstruction of the heart; manifestations include hypovolemia, hypotension, cold skin, weak pulse, mental confusion, and anxiety. (Dorland's Medical Dictionary, 1998)
b. Etiology
Cause of cardiogenic shock have a coronary and non-coronary etiology. Coronary, caused by myocardial infarction, while non-cardiomyopathy caused by coronary, valve damage, cardiac tamponade, and dysrhythmias.
Lab / SMF Anesthesiology FKUA / Hospital Dr. M. Djamil, Padang classify the cause of cardiogenic shock following:
· Ischemic heart disease (IHD)
· Drugs that depress the heart
· Heart Rhythm Disorders.
c. Clinical Manifestations
Cardiogenic shock is characterized by impaired left ventricular function resulting in impaired resulting in impaired function of the left ventricular lead to severe impairment of tissue perfusion and oxygen delivery to the tissues that are characteristic of cardiogenic shock due to acute myocardial infarction was 40% or more loss of muscle tissue in the left ventricle and necrosis of vocal throughout the ventricle because of the imbalance between myocardial oxygen demand and supply. Gmbaran clinical left heart failure:
· Shortness of breath dyspnea on effert, paroxymal nocturnal dyspnea
· Breathing cheyne stokes
· Cough-cough
· Cyanosis
· Hoarseness
· Ronchi wet, smooth is not loud in the lung basal hydrothorax
· Abnormalities of the heart such as cardiac enlargement, gallop rhythm, tachycardia
· BMR may rise
· Abnormalities in X-rays
d. Pathophysiology
Signs and symptoms of cardiogenic shock reflects the nature of the circulatory pathophysiology of heart failure. Damage to the heart resulting in decreased cardiac output, which in turn lowers blood pressure arteries to vital organs. Blood flow to the coronary arteries is reduced, so that the intake of oxygen to the heart decreases, which in turn increases ischemia and further decreased the heart's ability to pump, finally there was a vicious circle. Cardiogenic shock is a classic sign of low blood pressure, rapid and weak pulse, brain hypoxia manifested by the confusion and agitation, decreased output of urine, and the skin cool and moist.
Dysrhythmias often occur due to decreased oxygen to jantung.seperti in heart failure, the use of a pulmonary artery catheter to measure left ventricular pressure and cardiac output are very important to assess the severity of the problem and evaluate the management has done. Increased left ventricular diastolic tekananakhir sustainable (LVEDP = Left Ventricular End Diastolic Pressure) showed that the heart fails to function as an effective pump.
e. Diagnostic Examination
Trigger factors of diagnostic test include:
· Electrocardiogram (ECG)
· Sonogram
· Scan heart
· Cardiac catheterization
· Roentgen chest
· Liver Enzymes
· Pulse oximetry Electrolytes
· AGD
· Creatinine
· Albumin / serum transforin
· HSD
3. Distributive Syock
a. Definition
Distributive or vasogenic shock occurs when abnormal blood volume displaced in the vasculature such as when blood collects in the peripheral vasculature.
b. Etiology
Distributive shock may be caused either by loss of sympathetic tone or by the release of chemical mediators of cell-to cell. Kondosi-conditions that put patients at risk of distributive shock, namely (1) neurogenic shock such as spinal cord injury, spinal anesthesia, (2) anaphylactic shock such as sensitivity to penicillin, transfusion reactions, bee sting allergy (3) septic shock such as immunosuppressive, age extremes of> 1 year and> 65 years, malnutrition
Various mechanisms leading to early vasodiltasi in distributive shock shock classification further divides these into 3 types:
1) Syock Neurogenic
a) Definition
Neurogenic shock is also called spinal shock is a form of distributive shock, neurogenic shock caused by the failure of the vasomotor center due to the loss of vascular tone throughout tubuh.Sehingga sudden hypotension and blood accumulation in vessel capacity (capacitance vessels). Result of changes in systemic vascular resistance is caused by injury to the nervous system (such as head trauma, spinal injury, or general anesthesia in).
Neurogenic shock is also called syncope. Neurogenic shock occurs due to excessive vasovagal reaction that results in vasodilation splangnikus so thorough in the area of blood flow to the brain is reduced. Vasovagal reactions are generally caused by hot ambient temperatures, shock, fear, or severe pain. Patients usually feel dizzy and fainted. After the patient was laid, generally turn into good condition again spontaneously.
Isolated head trauma that will not cause shock. Presence of shock in trauma head to look for other causes. Trauma to the spinal cord will cause hypotension due to loss of sympathetic tone. Classical picture of neurogenic shock is hypotension without tachycardia or peripheral vasoconstriction.
b) Etiology
· Spinal cord injuries with quadriplegia or paraplegia (spinal shock).
· Stimulation great fun as a less severe pain at the bone fracture.
· Stimulation of the spinal cord such as drug use spinal anesthesia / lumbar.
· Head trauma (located in the central autonomic disturbances).
· The ambient temperature is hot, shocked, scared.
c) Clinical Manifestations
Almost the same as the shock in general but there are marks on neurogenic shock drop in blood pressure, rapid pulse does not increase, even more can be slow (bradycardia), sometimes accompanied by neurological deficits such as quadriplegia or paraplegia. While the situation further, after the patient becomes unconscious, then pulse quickened. Because the collection of blood in the arterioles, capillaries and veins, the skin feels a bit warm and reddish fast.
2) anaphylactic Syock
a) Definition
Anaphylaxis (Greek, Ana = away from and phylaxis = protection). Eliminating anaphylaxis means of protection. Anaphylaxis is an allergic reaction common with effects on multiple organ systems, especially the cardiovascular, respiratory, cutaneous and gastro intestinal immunological reactions that are preceded by exposure to allergens that have previously been sensitized. Anaphylactic shock (= shock anafilactic) is anaphylactic reactions are accompanied hypotension with or without loss of consciousness. Anaphylactoid reaction is an anaphylactic reaction that occurs without involving antigen-antibody complexes. Because of the similarity of symptoms and signs are usually treated as anaphylaxis.
Anaphylactic Syock caused by an allergic reaction when a patient who previously had formed antibodies against foreign substances (anti-gene) had a reaction anti-anti-body systemic gene
b) Pathophysiology
By Coombs and Gell (1963), grouped into anaphylactic hypersensitivity reaction type 1 or tipesegera (Immediate type reaction). Anaphylactic mechanism through several phases:
· Sensitization phase ie the time required for the formation of IgE bound up by specific receptors on the surface of mast cells and basophils. Allergens that enter through the skin, mucosa, respiratory tract or the food channel arrested by macrophages.
Macrophages soon mempresen-tate these antigens to T lymphocytes, where it would secrete cytokines (IL-4, IL-13) that induces B lymphocytes to proliferate into plasma cells (Plasmosit).
Plasma cells produce immunoglobulin E (IgE) specific for the antigen. IgE is then bound to the cell surface receptor Mast (Mast cells) and basophils.
· Phase Activation was time for the re-exposure to the same antigen. Mast cells and basophils to release their contents in the form of granules that cause a reaction on repeated exposure. On another occasion the same allergens enter the body. The same allergen was going to be bound by specific IgE and trigger immediate reactions that release of vasoactive mediators such as histamine, serotonin, bradykinin and other vasoactive some material from the granules called by the term Preformed mediators.
Stimulate antigen-antibody bond degradation of arachidonic acid from the cell membrane to produce leukotrienes (LT) and prostaglandin (PG) which occurred some time after degranulation called Newly formed mediators. Effector phase is the time of occurrence of a complex response (anaphylaxis) as a mediator of the effects of the removable mast cells or basophils with pharmacologic activity in a particular organ organ. Effects of histamine bronchoconstriction, increased capillary permeability which will cause edema, mucus secretion and vasodilation. Serotonin Bradykinin increases vascular permeability and causes smooth muscle contraction. Platelet activating factor (PAF) effect bronchospasm and increased vascular permeability, platelet aggregation and activation. Several chemotactic factors attract eosinophils and neutrophils. Prostaglandins are produced to cause bronchokonstriksi, as well as leukotrienes.
3) Septic Shock
a) Definition
Septic shock is the most common form and is caused by the shock distributuf widespread infection. The incidence of septic shock can be reduced by performing infection control practices, conduct a careful aseptic teknijk, do debriden ntuk throw jarinan necrotic wounds, maintenance and cleaning of equipment appropriately and wash hands thoroughly
b) Etiology
Microorganisms that cause septic shock is gram-negative bacteria. When microorganisms invade the body tissue, the patient will exhibit an immune response. The immune response evokes activation of various chemical mediators that have a variety of effects that lead to shock. Increased capillary permeability, which engarah on fluid permeability of capillaries and vasodilation are two effects.
c) Signs and Symptoms
Sepsis is a systemic response to bacteremia. At the time of bacteremia caused a change in the circulation lead to decreased tissue perfusion and shock sepsis occurred. Approximately 40% of patients with sepsis caused by gram-positive microorganisms and 60% due to gram-negative microorganisms. In adult urinary tract infection is a major source of infection. In the hospital was the likely source of infection and wound catheter or intravenous catheter. The most common organisms causing sepsis are Staphylococcus aureus and Pseudomonas sp
Patients with sepsis and septic shock is an acute illness. Assessment and treatment are needed. The patient may die of sepsis. Common symptoms are:
· Fever
· Sweating
· Headache
· Muscle pain
G. Management Syock
Main target, syock management is the provision of sufficient oxygen by the blood to the heart (oxygen deliverip)
1. Adequate oxygenation, avoid hyroksemia.
The main objective increase arterial oxygen content (CaO2) to maintain oxygen saturation (SaO2) 98-100% by way of:
a. Airway.
b. Adequate oxygenation, keep in> 65 = 7 mmHg.
c. Reduce pain & auxietas.
2. Cadiovaskuler suport system.
a. Fluid therapy to increase the preload
· Pairs of vascular access as soon as possible.
· Initial resuscitation volume is given 10-30 ml / kg bw kastolord liquid or kalois quickly (<20 minutes). can be repeated 2-3 times until blood pressure and good peripheral perfusion.
According to the consensus Asia Africa I (1997).
Ø more kaloid fluid therapy is recommended as recommended intiab kaloid or kristoloid.
Ø dopaadv therapy based on clinical response, peripheral perfusion, cup, according MEP elements.
b. Inetropik drugs to treat disretmia, heart kontraklitas improvement without increasing myocardial oxygen consumption.
· Dopevin (10 Kg / Kg / mut) increase vasokmstrokuta.
· Epinoprin: Increased myocardial perfusion pressure.
· Novepheriphin: mengkatkan myocardial perfusion pressure.
· Dobtanine: cardiak increase output.
· Amiodarone: increased myocardial kontraklitas, expansive heart, lowers systemic vascular pressure.
CHAPTER III
NURSING CONCEPTS
A. Assessment
The data can be found at the time of the assessment include:
a. Restlessness, anxiety, blood pressure decreased
b. Systolic blood pressure <90 mm Hg (hypotension)
c. Left ventricular pressure increased left ventricular end-diastolic pressure, left atrial pressure, pulmonary artery wedge pressure (PCWP)
d. Cardiac output 2.2 l / min, decreased ejection fraction, cardiac index decreased
e. Increased central venous pressure dyne/dtk/cm-5 1600
f. Increase in right ventricular filling pressure jugular venous distension, increased CVP (pressure> 15 cm H2O, increased reflexes hepatojugular
g. Tachycardia smooth radial pulse, pulse absent or diminished peripheral
h. Hear a gallop S3, S4 or murmurs
i. Respiratory distress tachypnea, orthopnea, hypoxia
j. Changes in the level of awareness of apathy, lethargy, semicoma, coma
k. Changes in skin pale, cool, moist, cyanosis
l. Subnormal body temperature changes, increased
m. Very thirsty
n. Nausea, vomiting
o. Status kidney urine output less than 20 ml / hr, increased serum creatinine, serum urea nitrogen increased
p. Changes in ischemic ECG changes, dysrhythmias, ventricular fibrillation
q. Leisure chest pain, abdominal pain
2. Nursing diagnoses
a. Changes in tissue perfusion (cerebral, cardiopulmonary, peripheral) associated with decreased cardiac output.
b. Decrease in cardiac output associated with mechanical factors (preload, afterload and myocardial contractility)
c. Damage to gas exchange associated with increased pulmonary capillary permeability
d. Asietas / fear of dealing with the threat of actual or potential biological
3. Nursing Interventions
a. Changes in tissue perfusion (cerebral, cardiopulmonary, peripheral) associated with decreased cardiac output
1) Purpose:
Tissue perfusion is maintained with the following criteria:
o blood pressure within normal limits
o Urine output normal
o Skin warm and dry
o Nadi peripheral> 2 times the body temperature
2) Plan of action
o Assess signs and symptoms indicating impaired tissue perfusion
o Maintain full bed rest (total bedrest) to facilitate the circulation of extremity position
o Maintain appropriate parenteral therapy with therapy programs, such as complete blood count, plasmanat, additional volume
o Measure intake and output per hour
o Connect the catheter to gravity drainage system closed and reported physician if urine output less than 30 ml / hour
o Give the medicine according to the program and examine the effects of drug therapy as well as signs of toxicity
o Keep clients warm and dry
b. Decrease in cardiac output associated with mechanical factors (preload, afterload and myocardial contractility)
1) Purpose
Clients showed an increase in cardiac output with the following criteria:
o Vital signs are within normal limits
o Cardiac output in normal limits
o Improved mental
2) Plan of action
o Maintain the best position to improve the optimum ventilation by elevating the head of bed 30-60 degrees
o Maintain full bed rest (total bedrest)
o Monitor ECG continuously
o Maintain appropriate parenteral fluid therapy program
o Monitor vital signs every hour and report when there is a drastic change
o Provide oxygen according to therapy
o Provide medication therapy in accordance with
o Keep clients warm and dry
o Auscultation of heart sounds every 2 to 4 hours
o Limit and planned activities; provide rest periods between procedures
o Avoid constipation, straining or rectal stimulation
c. Damage to gas exchange associated with increased pulmonary capillary permeability
1) Purpose
Clients showed an increase in ventilation with the following criteria:
o Client breathe without difficulty
o Clean Lungs
o PO2 and PCO2 levels within normal limits
2) Plan of action
o Assess breathing pattern, note the frequency and depth of breathing
o Auscultation of the lungs every 1-2 hours once
o Monitor series Agda
o Provide oxygen according to client's requirements
o Perform suction when indicated
o Assist and teach clients effective coughing and deep breathing
d. Asietas / fear of dealing with the threat of actual or potential biological
1) Purpose
Anxiety / fear-controlled client criteria:
o The client revealed a decrease in anxiety
o Client calm and relaxed
o Clients can rest in peace
2) Plan of action
o Determine the sources of anxiety or fear clients
o Explain all procedures and treatment and provide a concise explanation of when the client does not understand
o When anxiety is ongoing, accompany clients
o Anticipate client needs
o Maintain a quiet environment and not filled with stress
o Let your family and those closest to remain with the client if the client's condition allows
o Advise to express needs and fear of death
o Maintain poise and convincing
Chapter IV
cover
A. Conclusion
1. Success or failure depends on the shock response of the ability to know the symptoms of shock, knowing and anticipating the cause shock and the effectiveness and efficiency of our work in the first saat-saat/menit-menit patients in shock.
2. Shock is a disorder of the circulatory system in which the cardiovascular system (heart and blood vessels) are not able to carry blood through the body in adequate amounts which cause inadequate tissue perfusion and oxygenation. Shock occurs due to various circumstances that cause a reduction in blood flow, including cardiac abnormalities (eg, heart attack or heart failure), low blood volume (due to severe bleeding or dehydration) or changes in the blood vessels (eg due to an allergic reaction or infection)
B. Suggestion
1. By studying these materials nursing student who later became a professional nurse to be more sensitive to the signs and symptoms when encountering patients with syock that can help immediately.
2. Students can undertake emergency measures to help quickly to patients who experience syock.
REFERENCES
Alexander R H, H J. Proctor Shock. In the book: Advanced Trauma Life Support Course for Physicians. USA, 1993; 75-94
Atkinson R, S, Hamblin J J, Wright J E C. Shock. In the book: Hand book of Intensive Care. London: Chapman and Hall, 1981; 18-29.
Bartholomeusz L, Shock, in the book: Safe Anaesthesia, 1996; 408-413
Franklin C M, Darovic G O, and B B. Monitoring the Patient in Shock. In the book: Darovic GO, ed, Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application. USA: EB. Saunders Co.. 1995; 441-499.
Haupt M T, Carlson R W. Reactions Anaphylactic and anaphylactoid reactions. In the book: Shoemaker WC, Ayres S, Grenvik A eds, texbook of Critical Care. Philadelphia, 1989; 993-1002.
Thijs L G. The Heart in Shock (With Emphasis on Septic Shock). In a collection of papers: Indonesian Symposium On Shock & Critical Care. Jakarta-Indonesia, August 30 - September 1, 1996; 1-4.
Wilson R F, ed. Shock. In the book: Critical Care Manual. 1981, c :1-42.
Zimmerman JL, Taylor RW, Dellinger RP, Farmer JC, Diagnosis and Management of Shock, in the book: Fundamental Critical Support. Society of Critical Care Medicine, 1997.
CHAPTER I
INTRODUCTION
A. Background
Shock refers to a condition in circumstances where there is loss of body fluids quickly so that the occurrence of multiple organ failure due to inadequate perfusion. Shock occurs most often occur after heavy bleeding (hemorrhagic shock). Acute external bleeding caused by penetrating trauma and severe bleeding due to gastrointestinal kelianan 2 causes hemorrhagic shock is most often found. Hemorrhagic shock can also result from acute internal bleeding into the thoracic cavity and the abdominal cavity. Internal bleeding is the leading cause of trauma on organs and rupture of abdominal aortic aneurysm. Shock may result from loss of body fluids other than blood in significant amounts. Examples of hypovolemic shock caused by the loss of other fluids are refraktrer gastroenteritis and severe burns. Overall objective of this journal is focused to hypovolemic shock caused by bleeding and the many controversies that arise around how to handle.
Most trauma merbahaya when the war around 1900 has given the impression that a significant detriment to the development of the principles of treatment of hemorrhagic shock resuscitation. When World War I, W.B. Cannon recommends fluid resuscitation to slow so the main cause of shock addressed surgically. Giving blood kristalloid and used extensively during World War II to deal with patients with unstable conditions. Can experience in wartime against Korea and Vietnam showed bahawa fluid resuscitation and early surgical intervention is an important step to save trauma patients with hemorrhagic shock causing. This and some other principle helps in the development of guidelines for the treatment of hemorrhagic shock face of opposition from trauma. However, most researchers have questioned these guidelines, and today it has raised many controversies about how to handle the most optimal hemorrhagic shock.
B. Destination
1. General Purpose
Students can learn nursing care to patients syock
2. Special Purpose
Students can learn: understanding syock, cause shock, syock pathophysiology, signs and symptoms syock, manifestations kllinis syock, syock types, management syock
Chapter II
review theory
Nursing care in patients with SHOCK
A. Definition
A state / tissue perfusion disorder syndrome that is not optimal, complete metabolic networks. (Rupii, 2005)
Critical state due to failure of the circulatory system in sufficient nutrients and oxygen in terms of both supply and use for cellular metabolism of body tissue, causing an acute deficiency of oxygen in acute secular level. (Tash Ervien S, 2005)
A form of dynamic syndrome caused by tissue damage because ultimately be necessary substrate for aerobic metabolism at the microcellular level removed at a pace that does not adekuatoleh very little blood flow or flow maldistribusi (Candido, 1996)
Weight form of lack of oxygen supply compared to the needs. This situation is caused by a decrease in tissue oxygenation or changes in the capillary circulation. Lack of oxygen will be in touch with lactate acidosis, which is an indicator of body lactat levels of severity level syock
Shock resistance in the peripheral blood circulation leading to tissue perfusion is not sufficient to meet the nutrient needs of the cell and threw the rest metabolism (Theodore, 93), or a less than perfect tissue perfusion.
The first step is to be able to overcome the shock should be able to recognize the symptoms of shock. There is no laboratory test that can diagnose shock immediately. Diagnosis is made based on an inadequate understanding of clinical organ perfusion and tissue oxygenation.
The second step in tackling the shock is trying to find out possible causes of shock. In patients with trauma, shock is directly related to the introduction of the mechanism of trauma. All types of shock can occur in trauma patients and the most common is of hypovolemic shock due to bleeding. Cardiogenic shock can also occur in patients who experience trauma in the diaphragm and neurogenic shock can be caused by trauma to the central nervous system and spinal cord. Septic shock should also be considered in trauma patients who arrive too late to get help.
B. Stadium Syock
Compensation
Body composition by increasing reflex syarpatis ie increased systemic resistance which occurs only in the selective detruksi vital organs. TD sistokis normal, dioshalik systemic arterial resistance is increased due to an increase in addition TN skresi vaseprsin and activation of RAA system. special menitestasi talekicad, rowdy restless, pale skin, kapir retail> 2 docks.
Decompensation
Composition mechanisms begin to fail, made strong sulfuric cadiac worsen tissue perfusion, anaerobic metabolism occurs. because lactic acid accumulates there asidisif who gain weight with intracellular formation of carbonate asan. It inhibits the heart kontraklilitas already on the mechanism of Na + K Pompo energy at the cellular level. At syock also occur due to histamine release smesvar but when syock continues to aggravate the situation, which occurs disfori vasodilation and increased capillary permeability so volumevenous retwn reduced incidence of depression that occurs muocard. Clinical Maniftrasi: TD decreased, porfsi bad teriter olyserci, acidosis, kusmail napus.
3. Irreversible
Compensation failed terlanjut with cell death and multiorgan system dysfunction, ATP reserves in keper and heart out (new synthesis 2 hours). recent death of circulation can be recovered even if the clinical manifestations: TD taktenkur, no palpable pulse, consciousness (coma), anuria.
C. Occurrence of Shock Pathophysiology
D. Signs And Symptoms
1. Cardiovascular System
· Impaired peripheral circulation - pale, cold extremities. Lack of peripheral venous more meaningful than a decrease in blood pressure.
· Rapid pulse and smooth.
· Low blood pressure. It can not be hold, due to compensatory mechanisms occur losing one third of the volume of circulating blood.
· Peripheral veins collapse. Neck veins are best judgment.
· Low CVP.
2. Respiratory System
Breathing fast and shallow.
3. Central nervous system
Mental changes vary widely shock patients. If low blood pressure causes hypoxia to the brain, the patient became agitated until unconscious. Sedative and analgesic drugs should not be given to believe that the patient is restless because of the pain.
4. Digestive System
Nausea and vomiting can occur.
5. Urethral System
Reduced urine production. Normal urine production average adult patient was 60 ml / hour (1/5-1 ml / kg / hour).
E. Clinical Manifestations
In general, the clinical manifestations syock that arise include: pale, confused, tachicardy coma, cyanosis, congestive heart failure Arithnia, sweating, tachypnea, temperature changes, pulmonary edema, Restlessness, disorientation. Other clinical manifestations being that can arise
1. Decline in glomerular filtration
2. decreased urine output
3. keeping the increased blood
4. metabolic acidosis
5. hyperglikemi
F. Shock Type
1. Shock Hypovolemik
Circumstances hypovolemic shock refers to a condition in which there is loss of body fluids quickly so that the occurrence of multiple organ failure due to inadequate perfusion. Hypovolemic shock is most often happen after a severe bleeding (hemorrhagic shock). Acute external bleeding caused by penetrating trauma and severe bleeding due to gastrointestinal kelianan 2 causes hemorrhagic shock is most often found. Hemorrhagic shock can also result from acute internal bleeding into the thoracic cavity and the abdominal cavity
a. Causes
In general, hypovolemic shock due to bleeding, while other causes are extreme discharge of salt (NaCl). Such as occurs in shock: long-bone fracture, rupture spleen, hematothorak, arterial dissection, pangkreatitis weight. Being due to hypovolemic shock secondary to the gathering of fluid in the interstitial space due to: increased capillary permeability due to heat injury, allergic reactions, toxins bekteri.
Internal bleeding is the leading cause of trauma on organs and rupture of abdominal aortic aneurysm. Hypovolemic shock may result from loss of body fluids other than blood in significant amounts. Examples of hypovolemic shock caused by the loss of other fluids are refraktrer gastroenteritis and severe burns. Overall objective of this journal is focused to hypovolemic shock caused by bleeding and the many controversies that arise around how to handle.
Most trauma merbahaya when the war around 1900 has given the impression that a significant detriment to the development of the principles of treatment of hemorrhagic shock resuscitation.
When World War I, W.B. Cannon recommends fluid resuscitation to slow so the main cause of shock addressed surgically. Giving blood kristalloid and used extensively during World War II to deal with patients with unstable conditions. Can experience in wartime against Korea and Vietnam showed bahawa fluid resuscitation and early surgical intervention is an important step to save trauma patients with hemorrhagic shock causing. This and some other principle helps in the development of guidelines for the treatment of hemorrhagic shock face of opposition from trauma. However, most researchers have questioned these guidelines, and today it has raised many controversies about how to handle the most optimal hemorrhagic shock.
b. Pathophysiology
The human body responds to acute hemorrhage by activating the body's physiology 4 major systems: the hematologic, cardiovascular system, renal system and hematologic neuroendokrin.system system responds to severe bleeding which occurred acutely by activating the blood clotting cascade and mengkonstriksikan blood vessels (with release of thromboxane Local A2) and form a blockage immatur the source of bleeding. The damaged vessel will expose the collagen layer, which will subsequently lead to fibrin deposition and stabilization of subatan formed. About 24 hours required for the formation of fibrin obstruction perfect and mature formations.
Cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, myocardial contractility raised, and mengkonstriksikan heart blood vessels. This response arises due to the elevation of the release of norepinephrine and decreased vagal tone (which is regulated by the arch baroreceptors located in the carotid, aortic arch, left atrium and pulmonary veins. Cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys, and carries blood from the skin, muscle, and GI.
Urogenital system (kidneys) responds to stimulation that increases the release of renin from justaglomerular apparatus. Of renin release then proceed then the formation of angiotensin II, which has two main effects memvasokontriksikan blood vessels and stimulates the secretion of aldosterone in the adrenal cortex. Adrenal responsible for the reabsorption of sodium and water conservation perpetually active.
Neuroendocrine system responds to hemorrhagic shock by increasing the secretion of ADH. ADH is released from the posterior hipothalmus responds to a decrease in blood pressure and a decrease in sodium concentration. Reabsorsi ADH directly improve water and salt (NaCl) in the distal tubule. Colletivus ductus and the loop of Henle.
Patofisiology of hypovolemic shock more than what has been mentioned. for mengexplore more about patofisiology, bibliographic references on a reference bias. Mechanisms that have been described sufficiently effective to maintain perfusion of vital organs due to heavy blood loss. Without the blood and fluid resuscitation and correction of the cause of hemorrhagic shock, cardiac perfusion usually fail and multiple organ failure
c. Hypovolemic Shock stage
1) Phase I:
· Occurs bika 0-10% blood loss (approx 500ml)
· Compensation which occurs usually Cardiak output and blood pressure can still be maintained
2) Phase II:
· Occurs when blood kehilanagan 15-20%
· Drop in blood pressure, PO2 down, tachycardia, tachypnea, diaforetik, restless, pale.
3) Phase III
· If there is blood kehilengan more than 25%
· Decline: blood pressure, Cardiak output, PO2, perfusion rapid network
· Occurs in the ischemic organ
· Fluid extravasation occurs
2. Cardiogenic Shock
a. Definition
Cardiogenic shock caused by the failure of the pump function of the heart resulting in cardiac output to be reduced or stopped altogether.
Cardiogenic shock is defined as the presence of tissue hypoperfusion signs of heart failure caused by low preload corrected. There is no clear definition of hemodynamic parameters, but cardiogenic shock is usually characterized by a decrease in blood pressure (systolic less than 90 mmHg, or a decrease in mean arterial pressure over 30 mmHg) and or a decrease in urine output (less than 0.5 ml / kg / hour) with a pulse rate of more than 60 times per minute with or without the presence of organ congestion. There is no clear boundary between the low cardiac output syndrome with shock kerdiogenik. (Www.fkuii.org)
Cardiogenic shock is an end-stage left ventricular dysfunction or congestive heart failure, occurs when the left ventricle suffered extensive damage. Contractility of heart muscle loses strength, causing a decrease in cardiac output with inadequate tissue perfusion to vital organs (heart, brain, kidneys). Comparable degree of shock with left ventricular dysfunction. Although cardiogenic shock usually occurs as a complication of MI often, but can also terajdi on temponade cardiac, pulmonary embolism, cardiomyopathy and dysrhythmias. (Brunner & Suddarth, 2001)
Cardiogenic shock is shock caused adekua cardiac function, as in myocardial infarction or mechanical obstruction of the heart; manifestations include hypovolemia, hypotension, cold skin, weak pulse, mental confusion, and anxiety. (Dorland's Medical Dictionary, 1998)
b. Etiology
Cause of cardiogenic shock have a coronary and non-coronary etiology. Coronary, caused by myocardial infarction, while non-cardiomyopathy caused by coronary, valve damage, cardiac tamponade, and dysrhythmias.
Lab / SMF Anesthesiology FKUA / Hospital Dr. M. Djamil, Padang classify the cause of cardiogenic shock following:
· Ischemic heart disease (IHD)
· Drugs that depress the heart
· Heart Rhythm Disorders.
c. Clinical Manifestations
Cardiogenic shock is characterized by impaired left ventricular function resulting in impaired resulting in impaired function of the left ventricular lead to severe impairment of tissue perfusion and oxygen delivery to the tissues that are characteristic of cardiogenic shock due to acute myocardial infarction was 40% or more loss of muscle tissue in the left ventricle and necrosis of vocal throughout the ventricle because of the imbalance between myocardial oxygen demand and supply. Gmbaran clinical left heart failure:
· Shortness of breath dyspnea on effert, paroxymal nocturnal dyspnea
· Breathing cheyne stokes
· Cough-cough
· Cyanosis
· Hoarseness
· Ronchi wet, smooth is not loud in the lung basal hydrothorax
· Abnormalities of the heart such as cardiac enlargement, gallop rhythm, tachycardia
· BMR may rise
· Abnormalities in X-rays
d. Pathophysiology
Signs and symptoms of cardiogenic shock reflects the nature of the circulatory pathophysiology of heart failure. Damage to the heart resulting in decreased cardiac output, which in turn lowers blood pressure arteries to vital organs. Blood flow to the coronary arteries is reduced, so that the intake of oxygen to the heart decreases, which in turn increases ischemia and further decreased the heart's ability to pump, finally there was a vicious circle. Cardiogenic shock is a classic sign of low blood pressure, rapid and weak pulse, brain hypoxia manifested by the confusion and agitation, decreased output of urine, and the skin cool and moist.
Dysrhythmias often occur due to decreased oxygen to jantung.seperti in heart failure, the use of a pulmonary artery catheter to measure left ventricular pressure and cardiac output are very important to assess the severity of the problem and evaluate the management has done. Increased left ventricular diastolic tekananakhir sustainable (LVEDP = Left Ventricular End Diastolic Pressure) showed that the heart fails to function as an effective pump.
e. Diagnostic Examination
Trigger factors of diagnostic test include:
· Electrocardiogram (ECG)
· Sonogram
· Scan heart
· Cardiac catheterization
· Roentgen chest
· Liver Enzymes
· Pulse oximetry Electrolytes
· AGD
· Creatinine
· Albumin / serum transforin
· HSD
3. Distributive Syock
a. Definition
Distributive or vasogenic shock occurs when abnormal blood volume displaced in the vasculature such as when blood collects in the peripheral vasculature.
b. Etiology
Distributive shock may be caused either by loss of sympathetic tone or by the release of chemical mediators of cell-to cell. Kondosi-conditions that put patients at risk of distributive shock, namely (1) neurogenic shock such as spinal cord injury, spinal anesthesia, (2) anaphylactic shock such as sensitivity to penicillin, transfusion reactions, bee sting allergy (3) septic shock such as immunosuppressive, age extremes of> 1 year and> 65 years, malnutrition
Various mechanisms leading to early vasodiltasi in distributive shock shock classification further divides these into 3 types:
1) Syock Neurogenic
a) Definition
Neurogenic shock is also called spinal shock is a form of distributive shock, neurogenic shock caused by the failure of the vasomotor center due to the loss of vascular tone throughout tubuh.Sehingga sudden hypotension and blood accumulation in vessel capacity (capacitance vessels). Result of changes in systemic vascular resistance is caused by injury to the nervous system (such as head trauma, spinal injury, or general anesthesia in).
Neurogenic shock is also called syncope. Neurogenic shock occurs due to excessive vasovagal reaction that results in vasodilation splangnikus so thorough in the area of blood flow to the brain is reduced. Vasovagal reactions are generally caused by hot ambient temperatures, shock, fear, or severe pain. Patients usually feel dizzy and fainted. After the patient was laid, generally turn into good condition again spontaneously.
Isolated head trauma that will not cause shock. Presence of shock in trauma head to look for other causes. Trauma to the spinal cord will cause hypotension due to loss of sympathetic tone. Classical picture of neurogenic shock is hypotension without tachycardia or peripheral vasoconstriction.
b) Etiology
· Spinal cord injuries with quadriplegia or paraplegia (spinal shock).
· Stimulation great fun as a less severe pain at the bone fracture.
· Stimulation of the spinal cord such as drug use spinal anesthesia / lumbar.
· Head trauma (located in the central autonomic disturbances).
· The ambient temperature is hot, shocked, scared.
c) Clinical Manifestations
Almost the same as the shock in general but there are marks on neurogenic shock drop in blood pressure, rapid pulse does not increase, even more can be slow (bradycardia), sometimes accompanied by neurological deficits such as quadriplegia or paraplegia. While the situation further, after the patient becomes unconscious, then pulse quickened. Because the collection of blood in the arterioles, capillaries and veins, the skin feels a bit warm and reddish fast.
2) anaphylactic Syock
a) Definition
Anaphylaxis (Greek, Ana = away from and phylaxis = protection). Eliminating anaphylaxis means of protection. Anaphylaxis is an allergic reaction common with effects on multiple organ systems, especially the cardiovascular, respiratory, cutaneous and gastro intestinal immunological reactions that are preceded by exposure to allergens that have previously been sensitized. Anaphylactic shock (= shock anafilactic) is anaphylactic reactions are accompanied hypotension with or without loss of consciousness. Anaphylactoid reaction is an anaphylactic reaction that occurs without involving antigen-antibody complexes. Because of the similarity of symptoms and signs are usually treated as anaphylaxis.
Anaphylactic Syock caused by an allergic reaction when a patient who previously had formed antibodies against foreign substances (anti-gene) had a reaction anti-anti-body systemic gene
b) Pathophysiology
By Coombs and Gell (1963), grouped into anaphylactic hypersensitivity reaction type 1 or tipesegera (Immediate type reaction). Anaphylactic mechanism through several phases:
· Sensitization phase ie the time required for the formation of IgE bound up by specific receptors on the surface of mast cells and basophils. Allergens that enter through the skin, mucosa, respiratory tract or the food channel arrested by macrophages.
Macrophages soon mempresen-tate these antigens to T lymphocytes, where it would secrete cytokines (IL-4, IL-13) that induces B lymphocytes to proliferate into plasma cells (Plasmosit).
Plasma cells produce immunoglobulin E (IgE) specific for the antigen. IgE is then bound to the cell surface receptor Mast (Mast cells) and basophils.
· Phase Activation was time for the re-exposure to the same antigen. Mast cells and basophils to release their contents in the form of granules that cause a reaction on repeated exposure. On another occasion the same allergens enter the body. The same allergen was going to be bound by specific IgE and trigger immediate reactions that release of vasoactive mediators such as histamine, serotonin, bradykinin and other vasoactive some material from the granules called by the term Preformed mediators.
Stimulate antigen-antibody bond degradation of arachidonic acid from the cell membrane to produce leukotrienes (LT) and prostaglandin (PG) which occurred some time after degranulation called Newly formed mediators. Effector phase is the time of occurrence of a complex response (anaphylaxis) as a mediator of the effects of the removable mast cells or basophils with pharmacologic activity in a particular organ organ. Effects of histamine bronchoconstriction, increased capillary permeability which will cause edema, mucus secretion and vasodilation. Serotonin Bradykinin increases vascular permeability and causes smooth muscle contraction. Platelet activating factor (PAF) effect bronchospasm and increased vascular permeability, platelet aggregation and activation. Several chemotactic factors attract eosinophils and neutrophils. Prostaglandins are produced to cause bronchokonstriksi, as well as leukotrienes.
3) Septic Shock
a) Definition
Septic shock is the most common form and is caused by the shock distributuf widespread infection. The incidence of septic shock can be reduced by performing infection control practices, conduct a careful aseptic teknijk, do debriden ntuk throw jarinan necrotic wounds, maintenance and cleaning of equipment appropriately and wash hands thoroughly
b) Etiology
Microorganisms that cause septic shock is gram-negative bacteria. When microorganisms invade the body tissue, the patient will exhibit an immune response. The immune response evokes activation of various chemical mediators that have a variety of effects that lead to shock. Increased capillary permeability, which engarah on fluid permeability of capillaries and vasodilation are two effects.
c) Signs and Symptoms
Sepsis is a systemic response to bacteremia. At the time of bacteremia caused a change in the circulation lead to decreased tissue perfusion and shock sepsis occurred. Approximately 40% of patients with sepsis caused by gram-positive microorganisms and 60% due to gram-negative microorganisms. In adult urinary tract infection is a major source of infection. In the hospital was the likely source of infection and wound catheter or intravenous catheter. The most common organisms causing sepsis are Staphylococcus aureus and Pseudomonas sp
Patients with sepsis and septic shock is an acute illness. Assessment and treatment are needed. The patient may die of sepsis. Common symptoms are:
· Fever
· Sweating
· Headache
· Muscle pain
G. Management Syock
Main target, syock management is the provision of sufficient oxygen by the blood to the heart (oxygen deliverip)
1. Adequate oxygenation, avoid hyroksemia.
The main objective increase arterial oxygen content (CaO2) to maintain oxygen saturation (SaO2) 98-100% by way of:
a. Airway.
b. Adequate oxygenation, keep in> 65 = 7 mmHg.
c. Reduce pain & auxietas.
2. Cadiovaskuler suport system.
a. Fluid therapy to increase the preload
· Pairs of vascular access as soon as possible.
· Initial resuscitation volume is given 10-30 ml / kg bw kastolord liquid or kalois quickly (<20 minutes). can be repeated 2-3 times until blood pressure and good peripheral perfusion.
According to the consensus Asia Africa I (1997).
Ø more kaloid fluid therapy is recommended as recommended intiab kaloid or kristoloid.
Ø dopaadv therapy based on clinical response, peripheral perfusion, cup, according MEP elements.
b. Inetropik drugs to treat disretmia, heart kontraklitas improvement without increasing myocardial oxygen consumption.
· Dopevin (10 Kg / Kg / mut) increase vasokmstrokuta.
· Epinoprin: Increased myocardial perfusion pressure.
· Novepheriphin: mengkatkan myocardial perfusion pressure.
· Dobtanine: cardiak increase output.
· Amiodarone: increased myocardial kontraklitas, expansive heart, lowers systemic vascular pressure.
CHAPTER III
NURSING CONCEPTS
A. Assessment
The data can be found at the time of the assessment include:
a. Restlessness, anxiety, blood pressure decreased
b. Systolic blood pressure <90 mm Hg (hypotension)
c. Left ventricular pressure increased left ventricular end-diastolic pressure, left atrial pressure, pulmonary artery wedge pressure (PCWP)
d. Cardiac output 2.2 l / min, decreased ejection fraction, cardiac index decreased
e. Increased central venous pressure dyne/dtk/cm-5 1600
f. Increase in right ventricular filling pressure jugular venous distension, increased CVP (pressure> 15 cm H2O, increased reflexes hepatojugular
g. Tachycardia smooth radial pulse, pulse absent or diminished peripheral
h. Hear a gallop S3, S4 or murmurs
i. Respiratory distress tachypnea, orthopnea, hypoxia
j. Changes in the level of awareness of apathy, lethargy, semicoma, coma
k. Changes in skin pale, cool, moist, cyanosis
l. Subnormal body temperature changes, increased
m. Very thirsty
n. Nausea, vomiting
o. Status kidney urine output less than 20 ml / hr, increased serum creatinine, serum urea nitrogen increased
p. Changes in ischemic ECG changes, dysrhythmias, ventricular fibrillation
q. Leisure chest pain, abdominal pain
2. Nursing diagnoses
a. Changes in tissue perfusion (cerebral, cardiopulmonary, peripheral) associated with decreased cardiac output.
b. Decrease in cardiac output associated with mechanical factors (preload, afterload and myocardial contractility)
c. Damage to gas exchange associated with increased pulmonary capillary permeability
d. Asietas / fear of dealing with the threat of actual or potential biological
3. Nursing Interventions
a. Changes in tissue perfusion (cerebral, cardiopulmonary, peripheral) associated with decreased cardiac output
1) Purpose:
Tissue perfusion is maintained with the following criteria:
o blood pressure within normal limits
o Urine output normal
o Skin warm and dry
o Nadi peripheral> 2 times the body temperature
2) Plan of action
o Assess signs and symptoms indicating impaired tissue perfusion
o Maintain full bed rest (total bedrest) to facilitate the circulation of extremity position
o Maintain appropriate parenteral therapy with therapy programs, such as complete blood count, plasmanat, additional volume
o Measure intake and output per hour
o Connect the catheter to gravity drainage system closed and reported physician if urine output less than 30 ml / hour
o Give the medicine according to the program and examine the effects of drug therapy as well as signs of toxicity
o Keep clients warm and dry
b. Decrease in cardiac output associated with mechanical factors (preload, afterload and myocardial contractility)
1) Purpose
Clients showed an increase in cardiac output with the following criteria:
o Vital signs are within normal limits
o Cardiac output in normal limits
o Improved mental
2) Plan of action
o Maintain the best position to improve the optimum ventilation by elevating the head of bed 30-60 degrees
o Maintain full bed rest (total bedrest)
o Monitor ECG continuously
o Maintain appropriate parenteral fluid therapy program
o Monitor vital signs every hour and report when there is a drastic change
o Provide oxygen according to therapy
o Provide medication therapy in accordance with
o Keep clients warm and dry
o Auscultation of heart sounds every 2 to 4 hours
o Limit and planned activities; provide rest periods between procedures
o Avoid constipation, straining or rectal stimulation
c. Damage to gas exchange associated with increased pulmonary capillary permeability
1) Purpose
Clients showed an increase in ventilation with the following criteria:
o Client breathe without difficulty
o Clean Lungs
o PO2 and PCO2 levels within normal limits
2) Plan of action
o Assess breathing pattern, note the frequency and depth of breathing
o Auscultation of the lungs every 1-2 hours once
o Monitor series Agda
o Provide oxygen according to client's requirements
o Perform suction when indicated
o Assist and teach clients effective coughing and deep breathing
d. Asietas / fear of dealing with the threat of actual or potential biological
1) Purpose
Anxiety / fear-controlled client criteria:
o The client revealed a decrease in anxiety
o Client calm and relaxed
o Clients can rest in peace
2) Plan of action
o Determine the sources of anxiety or fear clients
o Explain all procedures and treatment and provide a concise explanation of when the client does not understand
o When anxiety is ongoing, accompany clients
o Anticipate client needs
o Maintain a quiet environment and not filled with stress
o Let your family and those closest to remain with the client if the client's condition allows
o Advise to express needs and fear of death
o Maintain poise and convincing
Chapter IV
cover
A. Conclusion
1. Success or failure depends on the shock response of the ability to know the symptoms of shock, knowing and anticipating the cause shock and the effectiveness and efficiency of our work in the first saat-saat/menit-menit patients in shock.
2. Shock is a disorder of the circulatory system in which the cardiovascular system (heart and blood vessels) are not able to carry blood through the body in adequate amounts which cause inadequate tissue perfusion and oxygenation. Shock occurs due to various circumstances that cause a reduction in blood flow, including cardiac abnormalities (eg, heart attack or heart failure), low blood volume (due to severe bleeding or dehydration) or changes in the blood vessels (eg due to an allergic reaction or infection)
B. Suggestion
1. By studying these materials nursing student who later became a professional nurse to be more sensitive to the signs and symptoms when encountering patients with syock that can help immediately.
2. Students can undertake emergency measures to help quickly to patients who experience syock.
REFERENCES
Alexander R H, H J. Proctor Shock. In the book: Advanced Trauma Life Support Course for Physicians. USA, 1993; 75-94
Atkinson R, S, Hamblin J J, Wright J E C. Shock. In the book: Hand book of Intensive Care. London: Chapman and Hall, 1981; 18-29.
Bartholomeusz L, Shock, in the book: Safe Anaesthesia, 1996; 408-413
Franklin C M, Darovic G O, and B B. Monitoring the Patient in Shock. In the book: Darovic GO, ed, Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application. USA: EB. Saunders Co.. 1995; 441-499.
Haupt M T, Carlson R W. Reactions Anaphylactic and anaphylactoid reactions. In the book: Shoemaker WC, Ayres S, Grenvik A eds, texbook of Critical Care. Philadelphia, 1989; 993-1002.
Thijs L G. The Heart in Shock (With Emphasis on Septic Shock). In a collection of papers: Indonesian Symposium On Shock & Critical Care. Jakarta-Indonesia, August 30 - September 1, 1996; 1-4.
Wilson R F, ed. Shock. In the book: Critical Care Manual. 1981, c :1-42.
Zimmerman JL, Taylor RW, Dellinger RP, Farmer JC, Diagnosis and Management of Shock, in the book: Fundamental Critical Support. Society of Critical Care Medicine, 1997.
