Hypovolemic, Neurogenic, and Anaphylactic Shock *Read your modules for cross reference SHOCK © Asyndrome characterized by decreased tissue perfusion and impaired cellular metabolism. This results in an imbalance between the supply of and demand for oxygen and nutrients. The exchange of oxygen and nutrients at the cellular level is essential to life. When cells experience hypoperfusion, the demand for oxygen and nutrients exceeds the supply at the microcirculatory level. + There are four main categories of shock: cardiogenic, hypovolemi and obstructive. distributive,SHOCK The stages of shock Thitial stage Compensatory stage Progressive stage Refractory stage » Body switches from > Sympathetic nervous » Electrolyte imbalance > Irreversible cellular aerobic taraerobie system stimaated |} etal acest and organ damage > Elevated lactic acid * cardiac contractility > Respiratory acidosis” ‘Impending death ra) ' > Peripheral oedema > Hinrvtrstea mmpomse | » treoer » Subtle cangms in|? Ncceetcton are ood |” tciyentythnias Simei wowtlouans” | » teem y > Pallor > Aldosterone released urine output (<30mV/hr) > Cool and clammy skin ’ > Altered level of > t Heart rate consciousness y > Glucose levels 01 HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK Reduced intravascular blood volume causing circulatory dysfunction and inadequate tissue perfusion. Vascular fluid volume loss causing extreme tissue hypoperfusion. The volume is inadequate to fil the vascular space. There two types: Relative and Absolute. Relative hypovolemia, fluid volume moves out of the vascular space into the extravascular space (eg, intracavitary space). Absolute results when fluid is lost through hemorrhage, gastrointestinal (Gi) loss (e.g., voriting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. Causes: Internal fluid loss, external fluid loss and inadequate vascular volume. HYPOVOLEMIC SHOCK Hypovolemic Shock Absolute Hypovolemia PATHOPHYSIOLOGY MAP. Relative Absolute hypovolemia JM hypovolemia Circulating volume a aaa T Venous return f T Stoke volume Cardiac output {Celular oxygen supply Impaired collar metabolism FIG, 67-3 The pathophysiology of hypovoleic shock * External loss of whole Hemorthage from trauma, surgery, Gl blood bleeding © Loss of other body fluids Vomiting, diarrhea, excessive diuresis, diabetes insipidus, diabetes mellitus Relative Hypovolemia Pooling of blood or fluids. Bowel obstruction Fluid shifts Burn injuries, ascites Internal bleeding Fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis Massive vasodilation SepsisPATHOPHYSIOLOGY MAP Ges eae) 4 Circulating volume ear Teeny | 4 Venous return ¥ 1 Stroke volume 1 4 Cardiac output ¥ 4 Cellular oxygen supply Cee eee ered FIG. 67-3 The pethophysicloay of hypovolemic shock HYPOVOLEMIC SHOCK Clinical Manifestations Cardiovascular: | Preload | Stroke volume | Capillary refill Pulmonary: Tachypnea —» bradypnea (late) Renal: | Urine output Integumentary: Pallor Cool, clammy rol | Cerebral perfusion: + Anxiety * Confusion + Agitation Gastrointestinal: Absent bowel sounds Diagnostic findings: | Hematocrit | Hemoglobin 1 Lactate 1 Urine specific gravity Changes in electrolytes NOTE: } Lactate - Usually increases once significant hypoperfusion and impaired oxygen utilization at the cellular level have occurred. By-product of anaerobic metabolism. | Hematocrit & Hemoglobin - Hemorrhagic shock after fluid resuscitation when fluids other than blood are used.HYPOVOLEMIC SHOCK Prevention Medical Management Early detection Volume expansion Accurate 1&0 Pneumatic antishock garment Treat underiying cause Complications Redistribution of fluid (modified Trendelenburg Acute respiratory distress syndrome position) Acute tubular necrosis Disseminated intravascular coagulation Pharmacologic Therapy Multiple organ dysfunction syndrome Vasoactive drugs Desmopressin (DDAVP) Assessment and Diagnostic Findings ‘Antidlarrhesl drugs Antiemetics Laboratory findings Urine characteristics Blood considerations HYPOVOLEMIC SHOCK Nursing Management [ins aca coed aardana Ende Nursing Assessment Petecnss rape eran telnmasnte eer ee History Fiche “Ghicttaiteariane’ “earn nnn Vital signs aaa Senon rasrtehesteechee ‘erinete ieee a so he Nursing Interventions st ‘Snelormesiarmaa "| Spoon” china pera Sarg ann Safe administration of blood | sey - a —— Safe administration of fluids | Putesmstsce "fasts taosess ecenes O-eryeg AEtees ot shck Sar pcan ay Heed erston Monitor weight rash totw sora Ragas Compton con cen Monitor vital signs om ‘nooner Oxygen administration CIE etm ee Wpwcaete pet Limes ene ot ean abe Sein ee er ae en02 NEUROGENIC SHOCK vevroce SHOCK {Loss of sympathetic tone Vasodilation occurs as a result of a loss of balance 1 between parasympathetic and sympathetic Vers anda stimulation. © Caused by the sudden loss of signals from the sympathetic nervous system that maintain the uaa normal muscle tone in blood vessel walls * a hemodynamic phenomenon that can occur SS within 30 minutes of a spinal cord injury at the a fifth thoracic (T5) vertebra or above; it can last Sue volume up to 6 weeks. = © Spinal anesthesia can block transmission of cardiac oat impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (¢¢., Teeter aaa opioids, benzodiazepines) also can decrease the vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock FIG. 67-4 The pethophysology of neurogenic shock. —NEUROGENIC SHOCK Distributive Shock Neurogenic Shock Hemodynamic consequence of spinal cord injury and/or disease at or above T5 ¢ Spinal anesthesia * Vasomotor center depression NEUROGENIC SHOCK Clinical Manifestations Cardiovascular: Neurologic: TBP Flaccid paralysis below the \/t Temperature level of the lesion Bradycardia Loss of reflex activity Pulmonary: Gastrointestinal: Dysfunction related to level Bowel dysfunction of injury Renal: Bladder dysfunction Integumentary: 1 Skin perfusion Cool or warm Dry Severe pain, drugs, hypoglycemia, injury NOTE: ‘The most important clinical manifestations in neurogenic shock are hypotension (from the ‘massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation).NEUROGENIC SHOCK Assessment and Diagnostic Findings NOTE: Computerized tomography (CT) scan Hypotension, which occurs as a result of a loss of X-rays sympathetic tone, is associated with peripheral vasodilation Magnetic resonance imaging (MRI) and decreased venous return. Treatment involves the use of vasopressors (e.g., phenylephrine) to maintain BP and, Medical Management organ periusion. Restoring sympathetic tone (stabilization) Immobilization Bradycardia may be treated with atropine (AtroPen). Pinas Infuse fluids cautiously as the cause of the hypotension is not related to fluid loss, Pharmacologic Therapy Inotropic agents Methylprednisolone (Solu-Medrol) is used for patients with Atropine a spinal cord injury to prevent secondary spinal cord Steroids damage caused by the release of chemical mediators. Heparin NEUROGENIC SHOCK Nursing Management Nursi i lursing Interventions Nursing Assesment Elevate head of bed BS eee acral Lower extremity interventions (anti- Neurologic assessment embolism stockings) Exercise (Passive ROM) Oxygen Activities BP monitoring Reduce anxiety Neurogenic Shock ‘© Maintain patent airway * Cautious administration of fluids» Vasopressors(e.g., phenylephrine) ‘+ Provide supplemental O; ‘Atropine (for bradycardia) “Intubation and mechanical ventilation lf necessary) © Minimize spinal cord treuma with stabilization * Monitor temperature03 ANAPHYLACTIC SHOCK ANAPHYLACTIC SHOCK moomoo Re-exposure to allergic substances > © Asystemic, type L hypersensitivity reaction that often has fatal consequences. * Anaphylaxis causes the immune system to release a flood of chemicals that can cause a person to go into shock. © Anacute, life threatening hypersensitivity (allergic) reaction to a sensitizing substance (eg, drug, chemical, vaccine, food, insect venom) © Already produced antibodies to a foreign substance (antigen) develop a systemic antigen- antibody reaction; specifically, an Massive vasodilation Release of vasoactive mediators Increase in capillary permeability Fluid leaks from vascular spaces to the interstitial spaces Respiratory distress'd/t laryngeal edema or bronchospasm Circulatory failure d/t massive vasodilation Anephylactic Shock ‘+ Hypersensitivity (allergic) Contrast media, blood or blood products, reaction to a sensitizing drugs, insect bites, anesthetic agents, ‘substance food or food additives, vaccines, environmental agents, latexMediators of Injury Histamine Mast cells Leukotrienes Prostaglandins Examples Allergic rhinitis Asthma Skin Test ‘Wheel and flare Clinical Manifestations Cardiovascular: Renal: Chest pain incontinence Third spacing of fluids peo Pulmonary: Anxiety Shortness of breath Feeling of impending doom Edema of larynx and Confusion epiglottis LOC Wheezing Metallic taste Stridor Rhinitis Gastrointestinal: Cramping Integumentary Abdominal pain Flushing Nausea Pruritus Vomiting Urticaria Diarrhea Angioedema 6.166 swore ne tage acon © upavcri SHOCK FG, 147 Cincal manflesatns oa system anaphyateeacton Sudden onset History of allergies Exposure to contrast media NOTE: Pitting edema test is used to assess third spacing of fluids. 22222 Nope aaa© worsen SHOCK Prevention Medical Management Avoid exposure to allergens Remove antigen Desensitization Administer medications Monitoring CPR a ET insertion & IV therapy Complications Respiratory obstruction Pharmacologic Therapy Systemic vascular collapse Epinephrine (1:1000 or 0.1 to 0.5mL repeated every 5 to 20 mins. Assessment and Diagnostic Fi Diphenhydramine (Benadryl) Histamine & Tryptase assessment ‘Albuterol S-hydroxyindoleacetic acid levels Colloids (fluid resuscitation) Allergy test (Full panel) wor ncri SHOCK Nursing Management Nursing Assessment Nursing Interventions Assess any kind of allergy Monitor client’ airway Assess patient's knowledge Monitor the oxygenation status New allergies Focus breathing Positioning Activity. Hemodynamic parameters Monitor urine output Emergency medications Precipitating factors ‘Anaphylactic Shock ‘© Maintain patent airway © Aggressive fluid resuscitation with ® Epinephrine (IM or IV) © Identity and remove '* Optimize oxygenation colloids '* Antihistamines (e.g., diphenhydramine) offending cause ‘with supplemental O, '* Histamine (H,-receptor blockers (e.g., '* Prevent via avoidance of '® Intubation and mechanical famotidine [Pepcid] known allergens ‘ventilation, if necessary. ' Bronchodilators: nebulized (e.g., '* Premedicate with history of albuterol) prior sensitivity (e.9., ‘© Corticosteroids if hypotension persists) contrast media)