UNIT 3 (AHN SEM-III) and its treatment - new.ppt
- 2. Fluid and Electrolyte Imbalance At the end of the unit students will be able to- • Identify the signs & symptoms of shock and electrolyte imbalances. • Develop skills in managing fluid and electrolyte imbalances. • Perform pain assessment and plans for the nursing management.
- 3. Fluid and electrolyte Disturbance Amount and Composition of Body Fluids: - Approximately 60% of a typical adult’s weight consists of fluid (water & electrolyte). - Body fluid is located in two fluid compartments: 1) Intracellular fluids (fluids in the cells) 2/3. 2) Extracelluler fluids :(fluids out side the cells) 1/3. a-Intravascular space (fluids with in blood vessels) contains plasma. b- Interstitial fluids: contain fluids that surround the cell. Eg. Lymph. c- Transcellular space: fluid contained in compartments. eg. Cerebrospinal, Pericardial, Synovial.
- 4. Average daily intake and output in an adult: Intake Output • Oral Liquids :1300ml. Urine :1500ml • Water in foods :1000ml. Stool : 200ml • Water produced Insensible lungs: 300ml • by metabolism : 300ml Skin 600ml 2600ml 2600ml
- 5. Normal Lab Results: - Na→ 135−145mEq/L. - K+ → 3.5−5.5mEq/L. - Ca++→ 8.5−10.5mEq/L. - Cl → 96−106mEq/L. - Mg→ 1.5−2.5mEq/L.
- 6. Fluid Volume Disturbance: I-Hypovolemia (fluids volume deficit): − Contributing Factors: * Loss of water and electrolyte. e.g.( vomiting, diarrhea, burns). * Decreased intake. e.g. (anorexia, nausea, inability to gain access to fluids). * Some diseases. e.g. (D.M, Diabetes Insipidus). − Signs and symptoms: Weight loss, general weakness, dizziness, tachycardia.
- 7. • Assessment Diagnostic evaluation • Health History & Physical examination • Serum BUN & Creatinine • Hematocrit level “great than normal” • Urine specific gravity • Blood osmolarity • Weight loss
- 9. ♣ Management • factors influencing the pt fluid needs should be taken in consideration • In case of severe or acute FVD, IV replacement should be started • Isotonic solutions used to treat hypotension resulted from FVD • Renal function & hemodynamic status should be evaluated. ♣Nursing Management • Monitor I&O as needed. • Monitor Vital signs, skin turgor, mental status & daily weight • Mouth care • Parenteral therapy- TPN
- 10. Fluid Volume Disturbance: II- Hypervolemia (fluid volume excess): − Contributing Factors: * Compromised regulatory mechanism such as renal failure, congestive heart failure, and cirrhosis. * Administration of Na+ containing fluids. * Prolong corticosteroid therapy. * Increase fluid intake. − Signs and Symptoms: • Weight gain • increase blood pressure • Edema • shortness of breathing. • Bounding pulse
- 11. Assessment & Diagnostic Evaluation - Decreased BUN, Creatinine - Decreased Serum osmolality & hematocrit because of plasma dilution & ↓protein intake - Urine sodium is increased if kidneys excrete excess fluid
- 13. Management Direct cause should be treated Symptomatic treatment consist of : - Diuretics - restrict fluid & Na intake - Maintain electrolytes balance -Hemodialysis in case of renal impairment - K+ supplement & specific nutrition Nursing Management: - Assess breathing , weight ,degree of edema regularly - I & O measurement regularly - Semi-fowlers position in case of shortness of breath - Patient education
- 14. Electrolyte imbalance: I- Sodium Deficit (Hyponatremia): −Contributing Factors: * Use of a diuretic. * Loss of GI fluids. * Gain of water. − Signs and Symptoms: • Hypotension • nausea and vomiting • Headache • Lethargy • Confusion • seizures. • Diminished deep tendon reflexes
- 15. Hyponatremia • Treatment: • Fluid restriction, + diuretics • Diet- Sodium rich diet • IV Fluid- Inj. NS 0.9% (Isotonic), Inj. NS 3% (Hypertonic) • Avoid sudden rise- 5 to 8 mEq/L in 24 hours
- 16. Electrolyte imbalance: II- Sodium Excess (Hypernatremia): − Contributing Factors: * Water deprivation in patient. * Hypertonic tube feeding. * Diabetes Insipidus. − Signs and Symptoms: • Hypertension • Thirst • Dry skin • Altered cerebral function • Tachycardia
- 17. Hypernatremia • Treatment: correct underlying disorder • Free water replacement- 150-200ml per Q2H • Slow infusion of D5W -give ½ over first 8 hrs then rest over next 16-24 hrs to avoid cerebral edema. • IV infusion of NS should be stopped • Dilution of drugs in Half saline
- 18. Electrolyte imbalance: III- Potassium Deficit (Hypokalemia): − Contributing factors: * Low intake of potassium from diet * Diarrhea, vomiting, gastric suctions.(increased excretion) * Corticosteroid administration. * Diuretics. − Sign and symptoms: • muscle weakness • Cardiac dysrhythmias • N&V • Deep tendon reflexes become hypoactive • changes in ECG. flat T-waves, ST depression, and U waves
- 19. Hypokalemia, continued • ECG changes in hypokalemia
- 20. Hypokalemia • Treatment: • Check renal function • Treat alkalosis • Potassium rich diet • Oral supplements-Syp Potchlor (max. 15ml at a time) • IV injection of KCl : peripheral 7.5 mEq/hr, central 20 mEq/hr
- 21. Electrolyte imbalance: IV- Potassium Excess (Hyperkalemia): − Contributing Factors: * Renal Failure. * Crush injury, burns. * Blood transfusion. * Administration of IV K+. − Sign and Symptoms: Bradycardia, dysarrythmia, anxiety, irritable. - ECG: peaked T waves then flat P waves, depressed ST segment, widened QRS progressing to sine wave and V fib.
- 22. Hyperkalemia – ECG Changes
- 23. Hyperkalemia, continued Treatment: Remove iatrogenic causes Acute: if > 7.5 mEq/L or EKG changes Ca-gluconate – 1 gm over 2 min IV Sodium bicarbonate – 1 amp, may repeat in 15min D50W (1 ampule = 50 gm) and 10U regular insulin Emergent dialysis Hydration and diuresis kayaxalate (K+ sparing sachet) Nebulization with Salbutamol
- 24. Calcium Hypocalcemia: Decreased intake of Ca Often symptomatic below 8 mEq/dL Check PTH: Vitamin D deficiency, hypoparathyroidism, massive blood transfusion, drugs (e.g. gentamicin) renal insufficiency S/S numbness, tingling, circumoral paresthesia, cramps tetany, increased DTR’s, Chvostek’s sign, Trousseau’s sign EKG has prolonged QT interval & prolonged ST segment
- 26. Calcium • Hypocalcemia cont. • Treatment: • Calcium rich diet • Stop frusemide • Acute: (IV) Calcium Gluconate 10cc of 10% solution • Chronic: (P/O) 0.5-1.25gm CaCO3 = 200-500 mg Ca. • Vit D (calciferol) must have normal serum level • Avoid phosphate rich diet
- 27. Calcium Hypercalcemia Increased intake of Ca rich diet Decreased excretion of Ca- causes are thiazides Acute adrenal insufficiency Hypophosphataemia Hyperparathyroidism Acute crisis is serum Ca > 12mg/dL. Critical at 16-20mg/dL S/S: N/V, anorexia Decreased gastric motility Urinary stones Diminished Deep tendon reflexes Constipation
- 28. Calcium • Treatment: • Hydration with NS • Administer loop diuretic • Phosphate diet increased • Calcitonin
- 29. Magnesium Hypomagnesemia • Decreased intake of magnesium • Burns • Pancreatitis • Parathyroidectomy • Chronic alcoholism • Primary hyperaldosteronism S/S: • weakness, fatigue, Cramps, hyperreflexia, seizure, Chvostek’s sign and Trosseau’s sign Treatment: • IV replacement of 2-4 gm of MgSO4 per day or oral replacement
- 30. Magnesium • Hypermagnesemia • Renal insufficiency • adrenal insufficiency • Hypoparathyroidism • Iatrogenic • Laxatives & Antacids us (that contain Magnseium)- Gelusil S/S: • N/V, muscle weakness, hyporeflexia, paralysis of voluntary muscles. Treatment: • Discontinue source • IV CaGluconate for acute treatment • Dialysis
- 31. Acid−Base Disturbance: Normal Values: PH→ 7.35- 7.45. PCO2→ 35-45mmHg. PO2→ 80-100mmHg. HCO3→ 22-26mEq/L. Respiratory Acidosis: → → → → ↑ PCO2. Respiratory Alkalosis: → → → → ↓ PCO2. Metabolic Acidosis: → → → → ↓ PH, ↓ HCO3. Metabolic Alkalosis: → → → → ↑ PH, ↑ HCO3.
- 32. SHOCK
- 33. TYPES OF SHOCK HYPOVOLE MIC SHOCK CARDIOGENIC SHOCK CIRCULATOR Y SHOCK SEPTIC SHOCK Organizational Chart Back to Agenda Page NEUROGE NIC SHOCK ANAPHY LA-CTIC SHOCK
- 34. • This is the most common type of shock and based on the insufficient circulatory volume. • Primary cause is loss of fluid from circulation from either an internal or external source. • Hypovolemic shock occurs when there is a reduction in intravascular volume by 15% to 30% which represents a loss of 750 ml to 1500 ml of blood in a 70 kg person. HYPOVOLEMIC SHOCK
- 35. RISK FACTORS FOR HYPOVOLEMIC SHOCK 1. EXTERNAL : • Trauma • Surgery • Vomiting • Diarrhoea • Diuretics • Diabetes Insipidus • External bleeding 2. INTERNAL: • Haemorrhage • Burns • Ascites • Peritonitis • Internal bleeding
- 36. Due to etiological factor ↓ Loss of body fluids and bloods ↓ Decrease cardiac output Hypo perfusion Compensatory mechanism ↓ PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK:
- 37. Norepinephrine and Epinephrine Increase heart rate and vascular resistance Renin angiotensin and aldosterone stimulation Intracellular fluid shift to intravascular space ADH release Increase blood volume Increase cardiac output
- 38. Compensatory mechanism fails Decrease cardiac output Decrease blood pressure ↓ Decrease perfusion to the vital organs ↓ Multisystem organ failure
- 39. MEDICAL MANAGEME NT 1. Treatment of the underlying cause 2. Fluid and blood replacement • Crystalloids- 0.9% sodium chloride • Ringer lactate solution • Hypertonic saline • Colloids (Albumin, Dextran) 3. Redistribution of fluid 4. Pharmacologic therapy (Vasoactive agents, Insulin therapy, Desmopressin, Antidiarrhoeal, Antiemetics).
- 40. NURSING MANAGEMENT • Primary prevention of shock is an essential focus of nursing care. 1. Administering blood and fluids safety: • Administration of blood transfusion. • Blood specimens, cross matching of the blood should be done. • Patient should be monitored for cardiovascular overload • Hemodynamic pressure, vital signs, arterial blood gases, serum lactate levels, hematocrit and hemoglobin level need to be monitored.
- 41. • Maintain temperature • Observing jugular venous pressure for distension •The nurse must monitor cardiac and respiratory status 2. Implementing other measures • Oxygen is administered. •Patient may be irritated and apprehensive so frequent explanations about the patient's condition may reduce some of the patient's fear and anxiety.
- 42. CARDIOGENIC SHOCK • Cardiogenic shock occurs when the heart's ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues. • Coronary cardiogenic shock is more common than the non coronary cardiogenic shock. • Non coronary causes of cardiogenic shock are the conditions that stress the myocardium such as severe hypoxemia, acidosis, hypoglycaemia, hypocalcaemia, tension pneumothorax, cardiomyopathies, cardiac temponade, dysrhythmias.
- 43. CLINICAL MANIFESTATION S: • Distended jugular vein due to increased jugular venous pressure. • Absent pulse due to tachyarrhythmia • Anginal pain • Dysrhythmias. • Complain of fatigue • Express feelings of doom • Signs of hemodynamic instability.
- 44. 2. Impaired heart's ability to contract and pump blood. Decrease stroke volume Increase pulmonary pressure Decrease cardiac output pulmonary edema Decrease oxygenation to the tissues. PATHOPHYSIOLOGY 1. Myocardial infarction, arrhythmias, congestive heart failure, cardiac myopathy, cardiac valve problem.
- 45. Hypo-perfusion of tissues Impaired cellular metabolism.
- 46. MEDICAL MANAGEMENT The goals of medical management in cardiogenic shock are to limit further myocardial damage and preserve the healthy myocardium and to improve the cardiac function. 1. Correction of underlying causes. 2. Initiation of first line treatment. • Oxygenation. • Pain control. • Hemodynamic monitoring • Laboratory marker monitoring. • Fluid therapy.
- 47. Pharmacologic treatment :- > Dobutamine. > Nitroglycerine. > Dopamine. > Antiarrhythmic medications. > Other vasoactive medication. > Mechanical assistive devices.
- 48. NURSING MANAGEMENT 1. Preventing cardiogenic shock 2. Monitoring hemodynamic status. 3. Administering medications and intravenous fluids. 4. Maintaining intra-aortic balloon counter pulsation. 5. Enhancing safety and comfort.
- 49. CIRCULATORY SHOCK • Circulatory shock occurs when blood volume pooled in peripheral blood vessels and results in hypovolemia which leads to inadequate tissue perfusion. • Contractility of the heart helps the blood to return to the heart. And the vascular tone is determined by central regulatory mechanism (in BP regulation) and local regulatory mechanism (in tissue demands for oxygen and nutrient) • Thereby circulatory shock can be caused either by a loss of sympathetic tone or by release of biochemical mediators from cells.
- 50. PATHOPHYSIOLOGY :- 1. Precipitating event 2. Vasodilation 3. Activation of inflammatory response 4. Abnormal distribution of blood volume 5. Decreased venous return 6. Decreased cardiac output 7. Decreased tissue perfusion
- 51. CLASSIFICATION OF CIRCULATORY SHOCK: 1. Septic shock 2. Neurogenic shock 3. Anaphylactic shock
- 52. 4. SEPTIC SHOCK • The most common type of circulatory shock, is caused by widespread of infection. • The most common cause of death. • The incidence can be reduced by using strict aseptic technique, thorough hand hygiene techniques. • Interventions include prevention of central line infection, early debriding of wounds to remove the necrotic tissues, carrying out standard precaution, adhering to infection control practices, prompt cleaning and maintaining of equipment.
- 53. PATHOPHYSIOLOGY 1. Severe localized infection of gram negative bacili (E.Coli, Klebsella) 2. Septicemia (invasion of bacteria into the blood stream) 3. Inflammatory response 4. Release of endo-toxin into circulation 5. Immune system releases histamine and other chemical mediators. Massive vasodilation Increase capillary permeability 6. Severe broncho constriction
- 54. 7. Decrease oxygen supply to the tissues 8. Decrease tissue perfusion 9. Shock.
- 55. MEDICAL MANAGEMENT 1. Fluid replacement therapy 2. Pharmacolgic therapy • Broad spectrum antibiotic • Drotrecogin alfa (acts as an anti-inflammatory cytokine, it stimulates fibrinolysis, restoring balance in the coagulation - anticoagulation homeostatic process of the body's inflammatory response to injury and infection 3. Nutritional therapy (should start in first 24 hours after ICU admission
- 56. NURSING MANAGEMENT :- • All invasive procedure must be carried out with aseptic technique. • IV lines, arterial and venous puncture sites, surgical incision, traumatic wounds, urinary catheter and pressure ulcers must be monitored for signs of infection. • Patients with elderly and immunosuppressive, extensive trauma, burns, or diabetes should be given most attention. • Elevated temperature is common in septic shock and increase the metabolic rate so it should not be treated unless it reaches to the dangerous level.
- 57. • The nurse administers prescribed IV fluids and medications including antibiotic agents and vasoactive mediators to restore vascular volume. • Blood levels of BUN, creatinine, WBC, hemoglobin, hematocrit, platelet levels, coagulation studies should be monitored • Fluid intake and output, nutritional status, daily weights should be checked. • Close monitoring of the serum albumin and pre-albumin levels help determine the patients protein requirements.
- 58. NEUROGENIC SHOCK • In neurogenic shock vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation. • Sympathetic stimulation causes vascular smooth muscle to constrict, and parasympathetic stimulation causes vascular smooth muscle to relax or dilate. • In neurogenic shock the sympathetic system not able to respond to the body stressors. Therefore neurogenic shock are signs of parasympathetic stimulation. • Parasympathetic stimulation causes vasodilation that results in hypovolemic state and gradually leads to hypotension and shock.
- 59. ETIOLOGY: • Spinal cord injury • Spinal anesthesia • Nervous system damage. • Depressant action of medication
- 60. PATHOPHYSIOLOGY 1. Spinal cord injury, anaesthesia. 2. Loss of autonomic nervous system and motor function below the level of injury 3. Loss of sympathetic control 4. Arterial or venous pooling 5. Dilatation of blood vessels 6. Hypotension 7. Warm, dry, flushed skin and bradycardia. 8. Decrease tissue perfusion to the vital organ 9. Multisystem organ failure.
- 61. MANAGEMENT :- • Elevate the head of the bed at least 30 degree angle when the patient receives spinal or epidural anaesthesia. Because it helps in the prevention of the spread of anesthetic agent up the spinal cord. • Carefully immobilize the patient in case of patient with spinal cord injury. • Supporting of cardiovascular and neurologic function. • Apply anti-embolism stockings. • Elevate the foot end to prevent the venous pooling of the blood in the legs because it may increase the risk of thrombus formation.
- 62. • The nurse must monitor the lower extremity pain, redness, tenderness and warmth. • Patient should be evaluated for deep vein thrombosis by assessing the calf muscle pain. • Administer heparin or low molecular weight heparin (lovenox) as prescribed. • Passive range of motion of the immobile extremities helps promote circulation. • The nurse must monitor the patient for signs of internal bleeding that could lead to hypovolemic shock.
- 63. ANAPHYLACTIC SHOCK • Anaphylactic shock occurs rapidly and is life threatening. • Anaphylactic shock occurs in patients who has already exposed to an antigen and who have developed antibodies to it. •Caused by an severe anaphylactic reaction to an allergen, antigen, drug, foreign protein causing the release of histamine which causes vasodilation leading to hypotension and increased capillary permeability.
- 64. PATHOPHYSIOLOGY 1. Antigen re-exposure. 2. Hypersensitivity antibody response 3. Activation of mast cells 4. Release of vasoactive substances such as bradykinin, histamine. 5. Arterial vasodilation 6. Increase capillary permeability 7. Severe bronchospasm 8. Decrease oxygen supply and increase demand of oxygen 9. Inadequate tissue perfusion 10. Shock and death.
- 65. MEDICAL MANAGEMENT • Remove the causative antigen • Emergency basic life support. • Epinephrine is given for its vasoactive action • Diphenydramine-to reverse the effects of histamine thereby reducing the capillary permeability. • Nebulized medication such as albutarol to reverse the histamine induced bronchospasm. • CPR in case of cardiac or respiratory arrest. • Endotracheal intubation or tracheostomy to establish the airway.
- 66. NURSING MANAGEMENT • Check the vitals, respiration, BP and Mean arterial pressure. • The nurse must assess for previous reaction of the allergy to medication, blood products, foods, contrast agents. • Observe patient for allergic reaction while administering the medication. • The nurse must identify patients who are at risk for anaphylactic reactions to contrast agents used for diagnostic tests. • This information need to be communicated to the diagnostic testing site. • After recovery from anaphylaxis the patient and family require an explanation of the event.
- 67. PAIN ASSESSMENT
- 68. DEFINITION Pain is an unpleasant sensation and emotional experience that links to tissue damage. - International association for the study of pain (IASP)
- 69. TYPES OF PAIN Acute pain – Short duration , healing process in 30 days. Chronic pain – Its persist for the more than 3-6 month. Physiological pain- it leads to potential tissue damage. Somatic pain – It involves superficial tissues (skin, bone, muscle, joints) Visceral pain- It involves organs (heart, stomach & liver) Neuropathic pain – changes in the nerve cells.
- 70. ASSESSMENT OF PAIN Assessment of pain includes, Subjective data Objective data
- 71. SUBJECTIVE DATA 1. PAIN HISTORY: while taking pain history , nurse must provide an opportunity for clients to express their own words, how they view it and their situation. This is will help the nurse to identify patient pain and how to cope up with it.
- 72. SUBJECTIVE DATA 2. ONSETAND DURA TION OF OCCURRENCE: When did pain begin? How long has it lasted? Does it occur at same time each day? How often does it occurs?
- 73. SUBJECTIVE DATA 3. LOCATION: In which area it is felt? Do the area differ under different circumstances? If several parts of body are painful, do pain occur simultaneously? Is pain unilateral/ bilateral? Ask the individual to point site of discomfort?
- 74. SUBJECTIVE DATA 4. INTENSITY: Use of pain intensity scale is an easy and reliable method of determining the clients pain intensity. Most scales are either 0 to 5 or 0 to 10 Currently used scales are: Numerical scale Descriptive scale Visual analog scale
- 75. TYPES OF PAIN SCALE 1. DESCRIPTIVE SCALE 2 . NUMERICAL SCALE 3 . VISUAL ANALOG SCALE
- 76. PAIN ASSESSMENT SCALE 1. Numerical rating scale: A numerical rating scale with the range of 0 to 10 is a type of pain scale that is used. The word ‘no pain’ appear by “0” and “worst pain possible” is found by “10”. Patient are asked to choose a number from 0 to 10 that best reflects his/her level of pain.
- 78. PAIN SCALE 2. Verbal rating scale: Verbal pain scales as name suggest, use words to describe pain. Word such as no pain, mild pain, moderate pain and severe pain are used to describe pain levels.
- 79. PAIN SCALE 3. Visual analogue scales: ⚫ VAS use a vertical or horizontal line with words that convey “no pain” at one end and “worst pain” at opposite end. ⚫ Patient is asked to place a mark along line that indicates his/her level of pain.
- 81. PAIN SCALE
- 82. NURSING ASSESSMENT Assess the patients risk for pain (Ex. Those undergoing invasive procedures, anxious patients) Assess the patient response to previous pharmacological interventions, especially ability to function. Examine the site of patients pain or discomfort. Assess for physical, behavioral and emotion signs and symptoms of pain: (moaning, decreased activity, abnormal guilt and irritability)
- 83. OBJECTIVE DATA
- 84. OBJECTIVE DATA
- 85. PREPARATION OF EQUIPMENTS 1. Pain scale 2. Privacy screen as per need 3. Patient case sheet
- 86. N URSIN G PROCEDURE
- 87. NURSING PROCED RE S. NO NURSING PROCEDURE ACTION 1. Explain the procedure to the patient. Promotes compliance. 2. Wash hand and wear gloves if needed. To prevent transmission of microorganisms. 3. Provide privacy if needed. To provide comfort. 4. Ensure presence of easy lighting. For easy assessment. 5. Assess the level of pain using a pain scale in the following method: •assess characteristics of pain, using PQRSTU of pain assessment: Provocative/palliative factors- what makes your pain better or worse?
- 88. Quality – tell me what your pain feels like? Region / radiation – show me where your pain is. Where is the pain spreading to? Severity – using a pain intensity scale appropriate to the patient age, developmental level, and comprehension , ask the patient to rate the pain, it has to be related in descriptive and numerical scale for adults and visual analog for children. Timing – ask the patient if pain is continuous, intermittent, constant or a combination. Ask the patient , “ how is the pain affecting you?”
- 89. 6. Ask the remedial non- pharmacological and pharmacological taken at home and in the hospital. To decide the care to be given and the avoid duplication of care. 7. Mark it in the pain assessment form. Serves as an evidence for the care. 8. Perform hand hygiene and discard gloves, if used. Reduces transmission of infections.
- 90. RECORDING & REPORTING Record and report the character of pain before intervention, therapies used and patients response.
- 91. THANKYOU