DEFINITION. Imbalance in supply/demand for O2 and nutrients

Transcription

1 NURS 452 SHOCK

2 Outcome Relate the pathophysiology to the clinical manifestations of the different types of shock: cardiogenic, hypovolemic, distributive, and obstructive Compare the collaborative care, drug therapy, and nursing management of the patients experiencing different types of shock

3 DEFINITION Profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs Decreased tissue perfusion and impaired cellular metabolism Imbalance in supply/demand for O2 and nutrients

4 Shock U1GiQ&feature=related Another good video that is more detailed mh0g&feature=related

5 Classification of Shock Cardiogenic Hypovolemic Neurogenic Anaphylaxis Septic

6 Precipitating Factors Cardiogenic Shock (pump failure or SV) Systolic or diastolic dysfunction Compromised cardiac output (CO) Causes: Myocardial Infarction Cardiomyopathy Pulmonary Hypertension Dysrhythmias Valvular stenosis or regurgitation

7 Pathophysiology of Cardiogenic Shock Fig Relationship of shock, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. CNS, Central nervous system. Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 7

8 Cardiogenic Shock Clinical Manifestations Early manifestations Tachycardia Hypotension SBP <90, MAP <60 Narrowed pulse pressure myocardial O2 consumption

9 Cardiogenic Shock Clinical Manifestations Physical examination Tachypnea, pulmonary congestion Pallor; cool, clammy skin Decreased capillary refill time Anxiety, confusion, agitation in pulmonary artery wedge pressure Decreased renal perfusion and UO

10 Precipitating Factors Hypovolemic Shock ( preload) Absolute hypovolemia: loss of intravascular fluid volume Causes: Acute hemorrhage Vomiting/Diarrhea Diabetes insipidus Hyperglycemia Relative hypovolemia Bowel obstruction Dehydration Burns Severe pancreatitis

11 Pathophysiology of Hypovolemic Shock Fig The pathophysiology of hypovolemic shock. Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 11

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13 Clinical manifestations Anxiety Tachypnea Hypovolemic Shock Clinical Manifestations Increase in CO, heart rate Decrease in stroke volume, PAWP, urinary output If loss is >30%, blood volume is replaced.

14 Precipitating Factors Neurogenic ( SVR) Normal SVR Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks

15 Pathophysiology of Neurogenic Shock Fig The pathophysiology of neurogenic shock. BP, Blood pressure. Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 15

16 Neurogenic Shock Clinical Manifestations Clinical manifestations Hypotension Bradycardia-What will you do? Temperature dysregulation (resulting in heat loss) Hypothermia, or Hyperthermia?? Dry skin Poikilothermia (taking on the temperature of the environment)

17 Precipitating Factors Anaphylactic Acute, life-threatening hypersensitivity reaction Causes: Blood transfusion Contrast media Insect bites Clinical manifestations Anxiety, confusion, dizziness Sense of impending doom Chest pain Incontinence Swelling of the lips and tongue, angioedema Wheezing, stridor Flushing, pruritus, urticaria Respiratory distress and circulatory failure

18 Precipitating Factors Septic systemic inflammatory response to documented or suspected infection Severe sepsis = Sepsis + Organ dysfunction Septic shock = Presence of sepsis with hypotension despite fluid resuscitation Presence of tissue perfusion abnormalities Clinical manifestations coagulation and inflammation fibrinolysis Formation of microthrombi Obstruction of microvasculature Hyperdynamic state: increased CO and decreased SVR Tachypnea/hyperventilation Temperature dysregulation (warm shock/cold chock) urine output Altered neurologic status GI dysfunction Respiratory failure is common

19 Septic Shock Meningococcal and Pneumococcal Septic Shock Must have vaccines after splenectomy

20 Pathophysiology of Septic Shock Fig The pathophysiology of septic shock. CNS, Central nervous system. Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 20

21 Precipitating Factors Obstructive Shock Develops when physical obstruction to blood flow occurs with decreased CO Cardiac tamponade Tension pneumothorax Abdominal compartment syndrome Pulmonary embolism Clinical manifestations Decreased CO Increased afterload Variable left ventricular filling pressures Jugular vein distention Pulsus paradoxus Rapid assessment and immediate treatment are important.

22 Stages of Shock Initial Stage Usually not clinically apparent Metabolism changes from aerobic to anaerobic. Lactic acid (Lactic acidosis) accumulates and must be removed by blood and broken down by liver. Process requires unavailable O2.

23 Stages of Shock Compensatory Stage Clinically apparent Neural Hormonal Biochemical compensatory mechanisms Attempts are aimed at overcoming consequences of anaerobic metabolism and maintaining homeostasis Baroreceptors in carotid and aortic bodies activate SNS in response to BP blood to kidneys activates renin angiotensin system If perfusion deficit corrected, patient recovers with no residual sequelae If deficit not corrected, patient enters progressive stage

24 Compensatory Stage of Shock Fig Compensatory stage: reversible stage during which compensatory mechanisms are effective and homeostasis is maintained. Copyright 2011, 2007 by Mosby, Inc., an 24

25 Stages of Shock Progressive Stage Begins when compensatory mechanisms fail Aggressive interventions to prevent multiple organ dysfunction syndrome Hallmarks of cellular perfusion and altered capillary permeability Anasarca Movement of fluid from pulmonary vasculature to interstitium Fluid moves into alveoli CO begins to fall Myocardial dysfunction results in Dysrhythmias Ischemia Myocardial infarction End result: complete deterioration of cardiovascular system Mucosal barrier of GI system becomes ischemic Liver fails to metabolize drugs and waste

26 Progressive Stage of Shock Fig Progressive stage: compensatory mechanisms are becoming ineffective and fail to maintain perfusion to vital organs. Copyright 2011, 2007 by Mosby, Inc., an affiliate 26 of Elsevier Inc.

27 Stages of Shock Irreversible Stage Exacerbation of anaerobic metabolism Accumulation of lactic acid capillary permeability Profound hypotension and hypoxemia Tachycardia worsens. Failure of one organ system affects others. Recovery unlikely

28 Irreversible Stage of Shock Fig Irreversible or refractory stage: compensatory mechanisms are not functioning or are totally ineffective, leading to multiple organ dysfunction syndrome. Copyright 2011, 2007 by Mosby, Inc., an 28

29 Diagnostic Studies Thorough history and physical examination No single study to determine shock Blood studies Elevation of lactate Base deficit 12-lead ECG Chest x-ray Hemodynamic monitoring

30 Collaborative Care Successful management includes Identification of patients at risk for shock Integration of the patient s history, physical examination, and clinical findings to establish a diagnosis Interventions to control or eliminate the cause of decreased perfusion Protection of target and distal organs from dysfunction Provision of multisystem supportive care

31 Collaborative Care General management strategies Ensure patent airway Maximize oxygen delivery Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = Volume expansion Volume expansion If the patient does not respond to 2 to 3 L of crystalloids, blood administration and central venous monitoring may be instituted. Complications of fluid resuscitation Hypothermia Coagulopathy

32 Collaborative Care Primary goal of drug therapy = Correction of decreased tissue perfusion Vasopressor drugs (e.g., norepinephrine) Achieve/maintain MAP >60 to 65 mm Hg. Reserved for patients unresponsive to fluid resuscitation Vasodilator therapy (e.g., nitroglycerin, nitroprusside) Achieve/maintain MAP >65 mm Hg.

33 Collaborative Care Nutrition is vital to decreasing morbidity from shock. Initiate enteral nutrition within the first 24 hours Nutrition is vital to decreasing morbidity from shock Early enteral feedings enhance the perfusion of the GI tract and help maintain the integrity of the gut mucosa

34 Collaborative Care Cardiogenic Shock Restore blood flow to the myocardium by restoring the balance between O2 supply and demand. Thrombolytic therapy Angioplasty with stenting Emergency revascularization Valve replacement Hemodynamic monitoring (swan ganz catheter) Drug therapy (e.g., diuretics to reduce preload) Circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device)

35 Swan-Ganz Catheter

36 Swan Ganz Catheter Left end-diastolic pressure

37 Swan-Ganz Interpretation Etiology CO PCWP SVR cardiogenic decreased increased increased hypovolemic decreased decreased increased distributive increased decreased decreased obstructive decreased Increased increased

38 Intra-Aortic Balloon Pump

39 Collaborative Care Hypovolemic Shock Management focuses on stopping the loss of fluid and restoring the circulating volume. Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss).

40 Collaborative Care Septic Shock Fluid replacement to restore perfusion Hemodynamic monitoring Vasopressor drug therapy Vasopressin for patients refractory to vasopressor therapy IV corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP Antibiotics after cultures are obtained (e.g., blood, wound exudate, urine, stool, sputum) Drotrecogin alfa (Xigris) Major side effect: bleeding

41 Collaborative Care Septic Shock (cont) Glucose levels <150 mg/dl Stress ulcer prophylaxis with histamine (H2)-receptor blockers Deep vein thrombosis prophylaxis with low-dose unfractionated heparin or lowmolecular-weight heparin

42 Collaborative Care Neurogenic Shock In spinal cord injury: spinal stability Treatment of the hypotension and bradycardia with vasopressors and atropine Fluids used cautiously as hypotension generally is not related to fluid loss Monitor for hypothermia.

43 Collaborative Care Anaphylactic Shock Epinephrine, diphenhydramine Maintaining a patent airway Nebulized bronchodilators Endotracheal intubation or cricothyroidotomy may be necessary. Aggressive fluid replacement Intravenous corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive therapy

44 Collaborative Care Obstructive Shock Early recognition and treatment is primary strategy. Mechanical decompression Radiation or removal of mass Decompressive laparotomy

45 Nursing Assessment ABC s Focused assessment of tissue perfusion Vital signs Peripheral pulses Level of consciousness Capillary refill Skin (e.g., temperature, color, moisture) Urine output

46 Nursing Diagnoses Ineffective tissue perfusion: renal, cerebral, cardiopulmonary, gastrointestinal, hepatic, and peripheral Fear Potential complication: organ ischemia/dysfunction

47 Nursing Implementation Neurologic status: orientation and level of consciousness Cardiac status Continuous ECG VS, capillary refill Hemodynamic parameters: central venous pressure, PA pressures, CO, PAWP Heart sounds: murmurs, S3, S4 Respiratory status Respiratory rate and rhythm Breath sounds Continuous pulse oximetry Arterial blood gases Most patients will be intubated and mechanically ventilated.

48 Nursing Implementation Urine output Hourly core temperature Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection Bowel sounds, check q 4 hrs and watch for distention Nasogastric drainage/stools for occult blood I&O, fluid and electrolyte balance Oral care/hygiene based on O2 requirements (oral chlorhexadine) Passive/active range of motion Assess level of anxiety and fear

49 Case Study 55yo male otherwise healthy who is fresh postop from a colon resection for CA Pt has tachycardia, hypotension, altered mental status, hypothermia, and abd distension On exam: pale, dry mucous membranes, disoriented, abdomen is tender and tense UOP is 15mL over past hour What else do you want to know? What is the most likely diagnosis? What is the collaborative management?