Summary Nursing, Hypovolemic Shock, Cardiogenic Shock, Septic Shock (complete latest 2021) guide.
Nursing, Hypovolemic Shock, Cardiogenic Shock, Septic Shock SHOCK • Sepsis-Septicemia-Bacteremia-Septic Shock-Whole-body inflammatory process resulting in acute critical illness. Systemic Inflammatory Response Syndrome-SIRS. • SIRS=body’s response to a critical illness that can result from an infectious or noninfectious cause (burns, trauma, pancreatitis), precipitating a whole body inflammatory process. • Sepsis=defined as SIRS resulting from an infection • Severe Sepsis=Sepsis with Acute associated Organ Failure • Septic Shock=defined as a persistently low mean arterial Bp, as a result of overwhelming infection despite adequate fluid resuscitation • Refractory Septic Shock=Persistently low mean arterial Bp, despite vasopressor therapy and adequate fluid resuscitation • Pathophysiology and Etiology -Sepsis is the leading cause of death in noncoronary intensive care units and the 11th leading cause of death in the US. -Many clients with sepsis have comorbidities, and many are 65 -SIRS-precursor to Sepsis-can occur from any infection in the body -SIRS related Infection triggers a systemic inflammatory response that leads to a series of adverse events, including; *Vasodilation *Increased Capillary permeability *Hypercoagulability -SIRS-Also triggers Platelets/Neutrophils/Macrophages/Endothelial cells-to an exaggerated response-uncontrolled release of chemical mediators-sparks a System-wide immune-inflammatory response. -SIRS response is severe Sepsis can develop -DIC-Disseminated intravascular coagulation is a potential risk associated with Sepsis. *DIC is characterized by Simultaneous bleeding and clotting throughout the vasculature. Sepsis injures blood cells, causing platelet aggregation & decreased blood flow-results in blood clots through the microcirculation-Blood clotting slows circulation further while stimulating excess fibrinolysis-Bodies stores of clotting factors are depleted-Generalized bleeding begins Disseminated Intravascular Coagulation Description • In this condition, known to many as DIC, an exaggerated clotting process leads to the formation of clots in the microcirculation. • This thromboembolus formation may result in bleeding and vascular occlusion of the organs. Nursing Considerations • Prevent the complication through early identification of clients at high risk for DIC. • Remove the underlying cause. • Monitor vital signs; assess for bleeding and signs of shock. • Prepare for oxygen therapy, volume replacement, blood component therapy, and possibly heparin therapy. • Administer anticoagulants as prescribed during the early phase of DIC. • Administer cryoprecipitated clotting factors, as prescribed, when DIC progresses and hemorrhage is the primary problem. • Monitor for complications associated with fluid and blood replacement and heparin therapy. • Monitor urine output and maintain at 30 mL/hr (renal failure is a complication of DIC). • Etiology -Sepsis due to infection begins with Septicemia-presence of pathogens and their TOXINS in the blood *Bacteria/Viruses/Fungi/Rickets and certain types of Protozoa may also lead to septic shock *Bacteremia-presence of bacteria and their TOXINS in the blood stream is a common cause of Sepsis -Sepsis is most often the result of; * Gram + bacteria-Staphylococcus & Streptococcus, but may also follow; * Gram – infections-Pseudomonas sp. & E. coli, Klebsiella sp. Incidence of Gram – sepsis has greatly increased *6% of cases are related to fungal infections *Increase of Sepsis in Elderly & non-Caucasian populations/ due to Increase in Invasive procedures/ Immunosuppressive therapy/Antimicrobial resistance -Urinary system-Catheterizations, suprapubic tubes, cystoscopy -Respiratory system-Suctioning/Aspiration/Tracheostomy/Endotracheal tubes/Respiratory therapy/Mechanical ventilators -GI system-Peptic ulcers/Ruptured appendix/Peritonitis -Integumentary System-Surgical wounds/IV/Intra-arterial catheters/Invasive monitoring/Decubitus/Burns/Trauma -Female reproductive system-Abortion/Infections-intrapartal or postpartal periods/Tampon use/STI’s -PNEUMONIA/BLOODSTREAM INFECTIONS/KIDNEY & URINARY TRACT INFECTIONS/ABDOMINAL INFECTIONS • Risk Factors -AT RISK-Clients who are Hospitalized/Debilitating chronic illnesses/Poor Nutritional Status -Risk advanced by Invasive procedures or surgery/Elderly patients/Immunocompromised clients ELDERLY/NB BABY/PREGNANT WOMAN/LONG TERM HEALTH CONDITIONS & COMORBIDITIES/IMMUNOSUPPRESSED/WOUNDS OR INJURIES-BURNS/INVASIVE FOREIGN DEVICES -Immunosuppressed client is vulnerable to overwhelming infection resulting in; *Circulatory failure *Hypo or Hyper-thermia *Tachypnea *Mental changes *Inadequate tissue perfusion *HoTN -Factors contributing to massive infections include; *Inadequate Neutrophil production *Abnormal Granulocytes-not able to be phagocytic *Erosions through normal barriers *Altered Bone Marrow production-caused by chemotherapy/radiation -Toxic Shock Syndrome-virulent form of Septic Shock-bacterial ENDOTOXINS diffuse from the site of infection in the vagina into the circulations. *Manifestations of Toxic Shock Syndrome-Extreme HoTN/Hyperpyrexia/HA/Myalgia/Confusion/Rash/V&D • Prevention -Monitor infants carefully for early signs of sepsis-educate parents -Cancer patients on active treatment-immunosuppressed-Give prophylactic antibiotics because of increased risk -Pneumonia a major cause of Sepsis-Immunizations against organisms-H. Influenza & S. pneumononiae. -IV & Catheter use-ASEPTIC Technique & GOOD HAND WASHING • Clinical Manifestations -Manifestations of Sepsis include; *Fever or Hypothermia *Tachycardia *Tachypnea *Peripheral Vasodilation *Septic Shock *Mental status changes. *REFRACTORY HoTN-low Bp that does not respond to treatment/LETHARGY or CONFUSION/DIFFICULTY BREATING/RAPID HEART RATE/COOL-PALE EXTEMITIES/EXTREME WEAKNESS & LIGHT HEADEDNESS/N&V -Hemodynamic monitoring shows an Increase in Cardiac Output -LABS-show abnormal CBC (Leukocytosis or Leukopenia), Alteration in Clotting Factors (Thrombocytosis or Thrombopenia), and Elevated LIVER ENZYMES, C Reactive Protein, & Creatinine levels. Hypophosphatemia and Positive blood culture are anticipated. -Septic Shock has an early phase and a late phase; *Early phase-Warm phase=Vasodilation resulting in HoTN-due to intense vasodilation and fluid shifts due to increased capillary permeability, Weakness/Warm flushed skin. -Bp normal to HoTN -Pulse-increased & thread -Respirations-rapid & deep -Skin-warm & flushed -Mental status-alert, oriented anxious -Urine output-normal -Other-increased body temp/chills/weakness/NVD/Decreased CVP *Septicemia often causes High fever and Chills *Late phase-Cold phase=Hypovolemia and activity of the compensatory mechanism result in typical shock manifestations including; Cold-Moist Skin/ Oliguria/AMS/ -Bp=HoTN -Pulse=Tachycardia/Arrhythmias -Respirations=Rapid/Shallow/Dyspneic -Skin=Cool/Pale/Edematous -Mental stats=Lethargic to Comatose -Urine output=Oliguria to Anuria -Other=Normal to decreased body temperature/Decreased CVP *Death may result from Respiratory failure/Cardiac failure/Renal failure. • Lifespan and Cultural Considerations -INFANTS-sepsis in infants include; *Temperature Instability *Abdominal distention *Poor feeding *Lethargy *Respiratory distress *Hepatomegaly-Vomiting and or Jaundice -Children under 3 mos. of age with a temp higher than 100.4, Rectally require diagnostic testing to r/o Sepsis, because they are at increased risk due to immature immune systems, and inadequate immune response to infection. -Elderly-Cardiac changes may be included; *Thickened LV wall *Decreased elasticity of Myocardium *Rigid valves *These changes result in a decreased Stroke Volume & Cardiac Output, thus decreasing compensatory responses to Septic Shock. * Decreased arterial wall elasticity & vasomotor tone reduce the older adult’s ability to respond to a decrease in oxygenation. *Decreased elasticity and turgor of the skin make assessments of the skin turgor, and thus dehydration status more difficult. *Decreased immune system response increases the risk of septic shock • Diagnostic Tests -Blood Cultures are performed to ID the infectious agent -CBC w/ Diff-especially to check WBC & Platelets. WBC may increase or decrease as the body attempts to fight the infection, the WBC‘s will decrease as an increasing # of WBC’s are destroyed. * Elevation of Neutrophils indicate acute infection. *Increased Monocytes indicate a bacterial infection *Increased Eosinophils indicate an allergic response -Lactic Acid-measure amount of lactic acid in the body-elevated in Late stages of Septic shock as capillaries of the liver are damaged. Also may demonstrate a severe infection. -PT/PTT/INR-test blood clotting factors -AST/ALT & Serum bilirubin-test liver function -BUN/Creat-test kidney function-Renal function declines as reduced perfusion and microclotting damage the small renal arterioles. BUN/Creat/Specific gravity and osmolality Increase as Renal Perfusion Decreases. -Blood gas-test for impaired oxygenation-Septic shock and the body’s compensatory mechanisms cause a decrease in the pH (indicated acidosis), decrease in PaO2-total oxygen saturation, and an Increase in Carbon Dioxide-PaCO2. -Hgb & Hct-changes to Hct concentrations usually occur in clients with Septic shock as fluid leaks from intravascular to extravascular spaces. Reflect the body’s response to endotoxins. In septic shock resulting from intravascular fluid loss Hgb &Hct concentrations are Higher than normal -Electrolytes-measured to monitor the severity and progression of Septic shock. Glucose levels decrease/Sodium levels decrease/Potassium level Increases -Microbiology tests: Wound/Urine/Respiratory culture -X-rays for pneumonias/CT for abscesses or infections in the body/US to visualize organs/MRI for soft tissue infections. • Vital signs and Labs that may suggest Organ failure -A temperature greater than 100.4, or less than 96.8 -HR greater than 90 bpm at rest -Respiratory rate greater than 20 breaths per minute at rest -WBC count greater than 12,000 or less than 4,000 -Oxygen saturation 90% or below -A Systolic Bp less than 90, or a MAP less than 65 -Urine output of less than 0.5ml/kg/Hr, or a Creatinine greater than 0.5 from baseline -A lactate level greater than or equal to 4 -A platelet level less than100, 000, or an INR greater than 1.5, unless the client is on Coumadin therapy • Pharmacologic Therapy -Antimicrobials are a primary pharmacologic treatment if the infection is caused by bacteria or fungi. -IV Antibiotics which begin immediately-even before the infectious agent is ID. Initially a broad-spectrum antibiotic, will be given -The client may be placed on several antibiotics to ensure adequate coverage of the pathogen until culture and sensitivity results return in 72 hours. -As antibiotics take effect, the client’s condition may worsen initially as increasing numbers of toxins are released into the circulating bloodstream because of pathogen destruction, further activating the immune response. -Inotropes agents and Vasopressors could also be used: These medications can cause blood vessels to narrow increasing the Bp & Blood flow around the body. Facilitating Myocardial contractility and dilating coronary arteries to increase perfusion of the myocardium. This will allow proper perfusion to vital organs. These agents will also increase the Cardiac Contractility. Dopamine/Dobutamine/Epinephrine -Other medications can include-Corticosteroids for inflammation and Insulin to help maintain stable blood Glucose. -Oxygen therapy-Establishing and maintaining a client’s airway and ensuring adequate oxygenation are critical interventions in reversing septic shock. Non rebreather 10ml-to maintain PaO2 greater than 80mmHg during the first 4-6 hours of care. If the client cannot maintain 80 ventilator assistance may be needed. -Fluid replacement-Most effective treatment for the client in Septic shock is the administration of IV fluids or blood. *Whole blood or blood products increase the oxygen-carrying capacity of the blood and thus increase oxygenation of cells. *Crystalloid & Colloid solutions increase circulating blood volume and tissue perfusion *fluid replacements are administered in massive amounts through 2 large bore IV lines, or a central line. & • As the nurse receives the laboratory results of clients admitted for sepsis, which of the following values needs to be reported to the physician immediately? a. Neutrophils 50%, Platelet Count 200,000/cu/mm, D-dimer 0.0ug/mL b. INR 1.0, Prothrombin Time 11 secs, Partial Thromboplastin Time (activated) 25 secs c. Platelet Count 400,000/cu/mm, Prothrombin Time 9.5 secs, Neutrophils 70% d. INR 3.5, D-dimer 1.0ug/mL, Platelet Count 95,000/cu/mm, WBC’s 19,000 Answer is D, represents hematologic dysfunction. WBC’s are elevated, Platelets are low, and INR is elevated, and a positive d-dimer • Nursing Process • Assessment; Nursing assessment is critical in reducing the complications associated with sepsis. -Continuous monitoring of Vitals -Continuous monitoring of Hemodynamic status-CVP/PA /Swan-Ganz catheter -Monitor adequacy of ventilation, perfusion, and Renal function -As septic shock progresses, blood pressure decreases and pulse becomes rapid, weak, and thready -As perfusion to the lungs decreases, crackles, wheezes, and dyspnea are commonly present. -Capillary refill is prolonged, and peripheral pulses are weak or nonpalpable. -Flattened neck veins that cannot be seen when the client is in the supine position indicate decreased intravascular volume -Normal CVP ranges from 2-8mmHg, CVP will be decreased in clients experiencing septic shock • Diagnosis; priority RN dx include the following. -Risk for Shock -Impaired Gas Exchange -Risk for ineffective Renal perfusion -Ineffective Peripheral tissue perfusion -Risk for imbalanced Fluid Volume • Planning-Care for the client with sepsis is very fluid, because the client’s condition and needs can change very quickly. Potential outcomes appropriate for the client with sepsis include; -The client will maintain oxygen saturation greater than 90% and PaO2 within normal limits -The client will maintain adequate renal perfusion to produce a minimum of 30mL of urine per hr. -The client will respond to fluid resuscitation with MAP that returns to normal range • Implementation-Diminished tissue perfusion causes ischemia and hypoxia of major organ systems, with potential for significant impact on the kidneys, brain, heart, lungs, and GI tract. RN working with clients who have sepsis should do the following; -Monitor client’s skin color, temp, turgor and moisture. Decreased tissue perfusion is evidenced by the skin becoming pale, cool, and moist; as hemoglobin concentrations decrease, cyanosis occurs. -Monitor the client’s cardiopulmonary function by assessing/monitoring the following-Bp/Rate & Depth of Resp/Lung sounds/Pulse OX/Peripheral pulses-utilize Doppler/Monitor client’s JVD/Take CVP measurements/Monitor Temp/Monitor Urinary output/Monitor mental status • Evaluation-Sepsis patients need continuous reevaluation sometimes every few minutes, because their condition can change quickly. • Shock • Shock-clinical syndrome characterized by a decrease in blood flow resulting in inadequate oxygenation • Imbalance results in a state of inadequate blood flow to body organs and tissues, causing life-threatening cellular dysfunction • To maintain cellular metabolism, the cells of all body organs and tissues require a regular and consistent supply of oxygen and removal of metabolic wastes. • This homeostatic regulation is maintained primarily by the cardiovascular system and depends on four physiological components -Cardiac output sufficient to meet bodily demands -Uncompromised vascular system, in which the vessels have a diameter sufficient to allow unimpeded blood flow and have good tone. -Volume of blood sufficient to fill the circulatory system, and a Bp adequate to maintain blood flow -Tissues that are able to extract and use the oxygen delivered though the capillaries *CO/UVF&T/BVBP/OX • Stroke Volume-SV-amount of blood pumped into the Aorta with each contraction of the LV • Cardia Output-CO-amount of blood pumped per minute into the aorta by the LV. SV x HR=CO • Mean Arterial Pressure-MAP-average pressure in the arterial circulation throughout the cardiac cycle. CO X SVR=MAP. - When CO & SVR or total blood volume rises-MAP & tissue perfusion increase. -When CO & SVR or total blood volume falls, MAP & tissue perfusion Decrease • Sympathetic Nervous System-SNS-maintains SMC surrounding the arteries and arterioles in a state of partial contraction called Sympathetic tone. -Increased sympathetic stimulation increases vasoconstriction & SVR -Decreased sympathetic stimulation allows vasodilation & decreases SVR • Pulse Pressure-Difference between systolic and diastolic Bp. Early indicator of shock. -Narrowing pulse pressure is consistent with Hypovolemic & Cardiogenic shock-due to reduced CO -Widening pulse pressure is indicative of Septic shock. Pathophysiology • When one or more cardiovascular components do not function properly, the body’s hemodynamic properties are altered. -Tissue perfusion may be inadequate to sustain normal cellular metabolism=SHOCK -Manifestation of shock result from the body’s attempts to maintain vital organs, and to preserve life following a drop in cellular perfusion. -If injury or condition triggering shock is severe/long enough duration, then cellular hypoxia and cell death occur -SHOCK is Triggered by a Sustained drop in MAP. • Stage 1: Early, Reversible, and Compensatory Shock -Initial stage of shock begins when baroreceptors in the aortic arch and the carotid sinus detect a sustained drop in MAP of less than 10mmHg from normal levels. -Body reacts to the decrease in MAP. -SNS increases HR & Force of cardiac contraction, thus increasing CO -SNS also, causes peripheral vasoconstriction-increasing SVR & rise in Arterial Pressure -Net result is that perfusion of cells, tissues and organs is maintained. -Symptoms almost imperceptible during the early stage of shock. *Pulse slightly elevated *Arterial pressure usually maintained -Compensatory shock in adults begins after MAP falls 10-15mmHg below normal levels. *Circulating BV is reduced by 23%-35% (1000ml or more) *Compensatory mechanisms are able to maintain Bp & tissue perfusion to vital organs. *Pediatric clients can often maintain their Bp until they are in profound shock. HoTN in a child is often a late finding of shock *Compensatory mechanisms of shock: -SNS release of epinephrine from the adrenal medulla and the release of norepinephrine from the adrenal medulla and the sympathetic fibers. *Both hormones rapidly stimulate the alpha- and beta- adrenergic fibers. *Stimulated alpha-adrenergic fibers cause vasoconstriction in the blood vessels supplying the skin and most of the abdominal viscera. Perfusion in these areas decrease *Stimulated beta-adrenergic fibers cause vasodilation in vessels supplying the heart and skeletal muscles, and increase the HR and Force of cardiac contraction. *Thus, stimulation of the SNS results in increased cardiac output and oxygenation of these tissues. -Renin-angiotensin response occurs as the blood flow to the kidneys decreases. *Renin is released from the kidneys-converts a plasma protein to angiotensin II-which causes vasoconstriction & stimulates the adrenal cortex to release Aldosterone *Aldosterone causes the kidneys to absorb water and sodium and to lose K. The absorption of water maintains circulating blood volume while increased vasoconstriction increases SVR, maintaining central vascular volume and raising Bp. ....................Continued
Written for
- Institution
- Mercer County Community College
- Course
- NRS225 (NRS225)
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- Uploaded on
- February 15, 2021
- Number of pages
- 69
- Written in
- 2020/2021
- Type
- SUMMARY
Subjects
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nrs 225
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nursing
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hypovolemic shock
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cardiogenic shock
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septic shock
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• sepsis septicemia bacteremia septic shock whole body inflammatory process resulting in acute critical illness systemic inflammato
