Shock
Progressive stage of shock
-All organ systems suffer from hypoperfusion -Lungs fail decreased pulmonary blood flow -Cardiac Pump fails (heart is overworked body is unable to meet O2 demands- ischemia) -Biochemical mediators cause myocardial depression- edema, dysrhythmia, MI -Microcirculation fails response to the numerous biochemical mediators increased capillary permeability occurs -Fluid leaks from the capillaries resulting in interstitial edema and decreased return to the heart -Acute Renal Failure may occur, GFR can not be maintained MAP falls below 60 -Disseminated intravascular coagulation (DIC) may occur as a complication of shock
Neurological effects of progressive shock
-Blood Flow to the brain impaired -Mental status deteriorates -Changes in mental status occur with decreased cerebral perfusion and hypoxia -Initially may demonstrate subtle changes in behavior or agitation and confusion -Lethargy increases and pt begins to lose consciousness
Blood pressure regulation
-When BP decreases, catecholamines (epi and norepinephrine) release from the adrenal medulla to increase HR (causes vasoconstriction to restore BP) -Kidneys regulate BP by releasing renin and this converts angiotension I to angiotension II (potent vasoconstrictor). -Leads to the release of aldosterone which promotes the retention of Na and H2O (hypernatremia). -Hypernatremia stimulates the release of ADH which causes the kidneys to retain H2O to raise blood volume and BP.
What is shock?
A clinical syndrome that results from inadequate tissue perfusion creating an imbalance between the delivery of and requirement for oxygen and nutrients that support cellular function.
What is renin?
A proteolytic enzyme that is released into the circulation by the kidneys. Its release is stimulated by: -Sympathetic nerve activation (acting through β1-adrenoceptors) -Renal artery hypotension (caused by systemic hypotension or renal artery stenosis) -Decreased sodium delivery to the distal tubules of the kidney
Anaerobic energy production in cell (without oxygen)
ATP stores are quickly used up due to decreased circulatory volume and decreased circulating oxygen. Anaerobic metabolism - toxic end product which yields lesser amounts of glucose. The cell cannot operate the sodium-potassium pump. Causes buildup of sodium in the cell and potassium is forced out. Water is drawn into the cell. Metabolic Acidosis occurs= Lactic Acid production. Cells have less ability to carry oxygen. This decreases vascular blood volume "third spacing"
Administration of vasoactive medications
Administered through a Central Venous Pressure Line (CVP) -Medication can cause tissue necrosis occurs in smaller vessels. -Line may also be in the superior vena cava Titrated by the nurse based on prescribed dose and target parameters (ex keep MAP at 60 mm Hg) Vital signs every 15 minutes MAP, Heart rate Dosage must be titrated by the nurse to the outcome parameter (BP, Heart rate). Adjusted to the MAP Never stop abruptly because this could cause severe hemodynamic instability, perpetuating the shock state.
Multiple organ dysfunction syndrome (MODS)
Altered function of two or more organs that requires medical intervention to support continued organ function Can be primary or secondary Can be a complication of any type of shock- most common in severe sepsis Presentation is insidious- tissues become hypoperfused at a microcellular and macrocellular level Organ failure usually begins in the lungs and cardiovascular instability -progressive dyspnea and respiratory faiure
Hypovolemic shock causes
External fluid losses Trauma Severe dehydration Severe edema Ascites Burns
Gastrointestinal effects of progressive stage of shock
GI ischemia may cause stress ulcers in the stomach Increased risk of GI bleed Intestinal mucosal may slough off in the small intestine causing bloody diarrhea Bacterial toxins enter the bloodstream Paralytic ileus, bowel ischemia bowel infarction
Cellular effects of shock
Na-K pump becomes impaired and mitochondria are damaged and death of the cell results. The cell swells and the cell membrane becomes more permeable Fluids and electrolytes seep from and into the cell. Mitochondria and lysosomes and damaged and this results in cell death. With decreased circulatory volume and subsequent decreased circulating oxygen the cell shifts from aerobic to anaerobic metabolism. ATP stores are used up. Without ATP, the cell cannot operate the sodium potassium pump. Causes build up of sodium in the cell. Potassium forced out. Water drawn into cell.
Progressive stage of shock
Shock mechanisms that regulate BP can no longer compensate MAP falls below normal limits- pt clinically hypotensive (systolic BP below 90 or a decrease in systolic BP of 40 mm from baseline) Demonstrates signs of declining mental status
Hypovolemic shock
Shock state resulting from decreased intravascular volume due to fluid loss.
Cardiogenic shock
Shock state resulting from impairment or failure of myocardium
Neurogenic shock
Shock state resulting from loss of sympathetic tone causing relative hypovolemia.
Medical management of progressive stage of shock Which finding is the best indicator that the fluid resuscitation for a patient with hypovolemic shock has been effective? a. Hemoglobin is within normal limits. b. Urine output is 60 mL over the last hour. c. Central venous pressure (CVP) is normal. d. Mean arterial pressure (MAP) is 72 mm Hg.
Specific medical management in the progressive stage of shock depends on: -The type of shock -Underlying cause -Degree of decompensation in the organ systems Use of appropriate IV fluids and medications to restore tissue perfusion by the following methods: -Support the respiratory system -Optimize the intravascular system -Support the pumping system of the heart -Improve the competence of the vascular system
General management of irreversible shock
Support the respiratory system with supplemental O2 Fluid replacement to restore intravascular volume Vasoactive medications to restore vasomotor tone and improve cardiac function Nutritional support to address metabolic requirements
Stages of shock
The earlier that interventions are initiated along the continuum the greater the pts chance of survival. Research is demonstrating an inc survival rate if aggressive therapy begins within 6 hrs of identifying a shock state. -Shock Progresses along a continuum and can be identified as early or late -The stage depends on signs and symptoms and the severity or degree of organ dysfunction
Cardiovascular effects of progressive stage of shock
-Dysrhythmias and ischemia are caused from a lack of blood supply -Heart rate is rapid- may be over 150 -Chest pain or MI may occur -Cardiac Enzyme levels and biomarkers increase (CK-MB, and cardiac troponin (cTn-I) -Myocardial depression and ventricular dilation may impair the hearts ability to pump blood to the tissues to meet O2 requirements.
Respiratory effects of progressive stage of shock
-Lungs are affected and further decompensated -Respirations are rapid and shallow -Crackles are heard across lung fields -Decreased pulmonary blood flow causes arterial O2 levels to decrease and CO2 levels to increase -Alveoli are hyperperfused stop producing surfactant and collapse -Pulmonary capillaries leak causing pulmonary edema and shunting Acute Lung Injury (ALI) -As ALI continues interstitial inflammation and fibrosis occur leading to Acute R--Respiratory Distress Syndrome (ARDS) -May need mechanical ventilation
Renal effects of progressive stage of shock
-When the MAP decreases below 65 mm Hg the glomerular filtration rate of the kidneys is not maintained. -Acute kidney injury occurs (AKI)- inc BUN and creatinine -Fluid and electrolytes shift, acid base imbalance occurs loss of renal-hormonal regulation of BP -Urine output decreases to less than 0.5 mL/kg per hour (30ml/hr)
TPN formulas mixed by pharmacy
A total of 1 to 3 L of solution is administered over a 24-hour period The label of the solution is verified with the prescription Intravenous fat emulsions (IVFEs) may be infused simultaneously with PN through a Y connector close to the infusion site and should not be filtered TPN solutions are initiated slowly and advanced gradually each day to the desired rate PN may be administered through either peripheral or central IV lines, depending on the patient's condition and the anticipated length of therapy. An infusion pump is always used for administration of PN
A 78-kg patient with septic shock has a urine output of 30 mL/hr for the past 3 hours. The pulse rate is 120/minute and the central venous pressure and pulmonary artery wedge pressure are low. Which order by the health care provider will the nurse question? a. Give PRN furosemide (Lasix) 40 mg IV. b. Increase normal saline infusion to 250 mL/hr. c. Administer hydrocortisone (Solu-Cortef) 100 mg IV. d. Titrate norepinephrine (Levophed) to keep systolic BP >90 mm Hg.
ANS: A Furosemide will lower the filling pressures and renal perfusion further for the patient with septic shock. The other orders are appropriate.
A patient with septic shock has a BP of 70/46 mm Hg, pulse 136, respirations 32, temperature 104° F, and blood glucose 246 mg/dL. Which intervention ordered by the health care provider should the nurse implement first? a. Give normal saline IV at 500 mL/hr. b. Give acetaminophen (Tylenol) 650 mg rectally. c. Start insulin drip to maintain blood glucose at 110 to 150 mg/dL. d. Start norepinephrine (Levophed) to keep systolic blood pressure >90 mm Hg.
Ans: A Because of the low systemic vascular resistance (SVR) associated with septic shock, fluid resuscitation is the initial therapy. The other actions also are appropriate, and should be initiated quickly as well.
Which data collected by the nurse caring for a patient who has cardiogenic shock indicate that the patient may be developing multiple organ dysfunction syndrome (MODS)? a. The patient's serum creatinine level is elevated. b. The patient complains of intermittent chest pressure. c. The patient's extremities are cool and pulses are weak. d. The patient has bilateral crackles throughout lung fields
Ans: A The elevated serum creatinine level indicates that the patient has renal failure as well as heart failure. The crackles, chest pressure, and cool extremities are all consistent with the patient's diagnosis of cardiogenic shock.
A patient is admitted to the emergency department (ED) for shock of unknown etiology. The first action by the nurse should be to a. administer oxygen. b.obtain a 12-lead electrocardiogram (ECG). c. obtain the blood pressure. d. check the level of consciousness.
Ans: A The initial actions of the nurse are focused on the ABCs—airway, breathing, and circulation—and administration of oxygen should be done first. The other actions should be accomplished as rapidly as possible after oxygen administration.
A nurse is caring for a patient with shock of unknown etiology whose hemodynamic monitoring indicates BP 92/54, pulse 64, and an elevated pulmonary artery wedge pressure. Which collaborative intervention ordered by the health care provider should the nurse question? a. Infuse normal saline at 250 mL/hr. b. Keep head of bed elevated to 30 degrees. c. Hold nitroprusside (Nipride) if systolic BP <90 mm Hg. d. Titrate dobutamine (Dobutrex) to keep systolic BP >90 mm Hg.
Ans: A The patient's elevated pulmonary artery wedge pressure indicates volume excess. A saline infusion at 250 mL/hr will exacerbate the volume excess. The other actions are appropriate for the patient.
After change-of-shift report in the progressive care unit, who should the nurse care for first? a. Patient who had an inferior myocardial infarction 2 days ago and has crackles in the lung bases b. Patient with suspected urosepsis who has new orders for urine and blood cultures and antibiotics c. Patient who had a T5 spinal cord injury 1 week ago and currently has a heart rate of 54 beats/minute d. Patient admitted with anaphylaxis 3 hours ago who now has clear lung sounds and a blood pressure of 108/58 mm Hg
Ans: B Antibiotics should be administered within the first hour for patients who have sepsis or suspected sepsis in order to prevent progression to systemic inflammatory response syndrome (SIRS) and septic shock. The data on the other patients indicate that they are more stable. Crackles heard only at the lung bases do not require immediate intervention in a patient who has had a myocardial infarction. Mild bradycardia does not usually require atropine in patients who have a spinal cord injury. The findings for the patient admitted with anaphylaxis indicate resolution of bronchospasm and hypotension.
Which finding is the best indicator that the fluid resuscitation for a patient with hypovolemic shock has been effective? a. Hemoglobin is within normal limits. b. Urine output is 60 mL over the last hour. c. Central venous pressure (CVP) is normal. d. Mean arterial pressure (MAP) is 72 mm Hg.
Ans: B Assessment of end organ perfusion, such as an adequate urine output, is the best indicator that fluid resuscitation has been successful. The hemoglobin level, CVP, and MAP are useful in determining the effects of fluid administration, but they are not as useful as data indicating good organ perfusion.
he nurse is caring for a patient who has septic shock. Which assessment finding is most important for the nurse to report to the health care provider? a. Blood pressure (BP) 92/56 mm Hg b. Skin cool and clammy c. Oxygen saturation 92% d. Heart rate 118 beats/minute
Ans: B Because patients in the early stage of septic shock have warm and dry skin, the patient's cool and clammy skin indicates that shock is progressing. The other information will also be reported, but does not indicate deterioration of the patient's status.
After receiving 2 L of normal saline, the central venous pressure for a patient who has septic shock is 10 mm Hg, but the blood pressure is still 82/40 mm Hg. The nurse will anticipate an order for a. nitroglycerine (Tridil). b. norepinephrine (Levophed). c. sodium nitroprusside (Nipride). d. methylprednisolone (Solu-Medrol).
Ans: B When fluid resuscitation is unsuccessful, vasopressor drugs are administered to increase the systemic vascular resistance (SVR) and blood pressure, and improve tissue perfusion. Nitroglycerin would decrease the preload and further drop cardiac output and BP. Methylprednisolone (Solu-Medrol) is considered if blood pressure does not respond first to fluids and vasopressors. Nitroprusside is an arterial vasodilator and would further decrease SVR.
3. A 19-year-old patient with massive trauma and possible spinal cord injury is admitted to the emergency department (ED). Which assessment finding by the nurse will help confirm a diagnosis of neurogenic shock? a. Inspiratory crackles. b. Cool, clammy extremities. c. Apical heart rate 45 beats/min. d. Temperature 101.2° F (38.4° C).
Ans: C Neurogenic shock is characterized by hypotension and bradycardia. The other findings would be more consistent with other types of shock.
After reviewing the information shown in the accompanying figure for a patient with pneumonia and sepsis, which information is most important to report to the health care provider? a. Temperature and IV site appearance b. Oxygen saturation and breath sounds c. Platelet count and presence of petechiae d. Blood pressure, pulse rate, respiratory rate.
Ans: C The low platelet count and presence of petechiae suggest that the patient may have disseminated intravascular coagulation and that multiple organ dysfunction syndrome (MODS) is developing. The other information will also be discussed with the health care provider but does not indicate that the patient's condition is deteriorating or that a change in therapy is needed immediately.
Vascular responses
Auto-regulation occurs and stimulates vasodilation or vasoconstriction in response to biochemical mediators. Diameter of the artery changes in response to chemical messengers such as SNS - flight or flight- (SNS-epinephrine and nor-epinephrine). BP elevates, HR increases Renal system activates renin-angiotension Adrenal medulla activates aldosterone Pituitary activates ADH (Anti-Diuretic Hormone) - with fluid volume deficit Blood is shunted from non-essential organs (skin, kidney GI) to essential organs (brain, heart, and lungs)
Signs and symptoms of irreversible stage of shock
BP remains low despite treatment Renal and Liver dysfunction occurs Necrotic tissue toxins are released Severe metabolic acidosis Anaerobic metabolism contributes to lactic acidosis Reserves of ATP are depleted Multi-organ system failure occurs- mottling and cyanosis occur Death occurs in minutes to hours Be clear with significant others, discuss pt wishes Organs probably not considered harvest material due to profound ischemia
Blood pressure regulation
Blood Volume Cardiac Pump Vasculature must respond to -Neural -Chemical -Hormonal feedback systems to maintain blood pressure and perfuse body tissues
Pathophysiology of shock
Cells switch from aerobic to anaerobic metabolism because they lack an adequate blood supply. Cell function ceases & swells. Lactic acid is produced and must be removed from the cell and transported to the liver for conversion into glucose and glycogen. Membrane becomes more permeable. Electrolytes and fluids seep in and out of cell. Na & K pump impaired. Mitochondria damage and cell death occurs.
Hypovolemia
Characterized by decreased intravascular volume. Loss of 15-25% of volume (approx 1000 ml of blood) Often due to injury and massive blood loss Can also have nontraumatic causes Gastrointestinal bleed Ruptured ectopic pregnancy. third-spacing from burn injuries dehydration from frequent vomiting or diarrhea
Septic shock
Circulatory shock state resulting from overwhelming infection causing relative hypovolemia.
Anaphylactic shock
Circulatory shock state resulting from severe allergic reaction producing overwhelming systemic vasodilation, relative hypovolemia.
Hematologic effects of progressive stage of shock
Clotting cascade is activated in shock states causing deposition of microthrombi in multiple areas of the body and consumption of clotting factors DIC (Disseminated intravascular coagulation may occur as a cause or as a complication of shock Widespread clotting and bleeding occur simultaneously Bruises (ecchymosis) and bleeding (petechia) may appear on the skin
Fluid Replacement to Expand Intravascular Volume
Crystalloids: 0.9% normal saline, lactated Ringer's solution, hypertonic solutions (3% hypertonic saline) Colloids: albumin, dextran (dextran may interfere with platelet aggregation) Blood components for hypovolemic shock Complications of fluid replacement include fluid overload, pulmonary edema
Hepatic effects of progressive stage of shock
Decreased blood flow to the liver impairs the ability of liver cells to perform metabolic and phagocytic functions Less likely to metabolize medications and waste products (ammonia and lactic acid) Gluconeogenesis and glycogenolysis are impaired Increased susceptible to infection as the liver fails to filter bacteria from blood All liver enzymes become elevated (AST, ALT, LDH, bilirubin) Pt becomes jaundiced
Inotropic Agents
Dobutamine Dopamine (Intropin) Epinephrine (Aderenaline) Milrlone Desired action in shock: improve contractility, increase stroke volume, increase cardiac output Disadvantages: Increase oxygen demand on the heart
Q-SOFA score
Early detection is Key to survival GCS < or equal to 13 or altered mental state Systolic BP < 100 mm HG Respiratory rate > 22 breaths minute Patients with suspected infection and score of 2 or greater have greater than 10% chance of mortality.
What does adequate blood flow to the tissues and cells require?
Effective cardiac pump, adequate vasculature or circulatory system, sufficient blood volume. If one of these components is impaired, perfusion to the tissues is threatened or compromised.
Aerobic energy production in cell (with oxygen)
Energy metabolism occurs within the cell nutrients are chemically broken down and stored in the form of Adenosine Triphosphate (ATP) Aerobic metabolism yields far greater amounts of ATP per mole of glucose Cells use the stored energy to perform necessary functions (active transport, muscle contraction, biochemical synthesis and conduction of electronic impulses)
Nursing management of progressive shock
Expertise assessment Significance of changes in assessment data Closely monitor patient ECG, arterial blood gases, serum electrolyte levels, physical and mental status changes Rapid and frequent administration of various prescribed medications and fluids Careful documentation- VS at least every 15 minutes Promote safety- always use aseptic technique Reduce the risk of Ventilator-associated pneumonia (VAP) Frequent oral care, elevate head of bed 30 degrees to prevent aspiration Position and reposition to promote comfort and maintain skin integrity Support patient and family emotionally - family members may be reluctant to ask questions- keep the family informed frequently
Nursing management of hypovolemic shock
Frequent Assessment Closely monitor patients who are at risk for fluid deficit Safely administer fluids Proper positioning- modified Trendelenburg Administer blood and fluids safely
Key points
Goal is to increase awareness and additional assessment of patients with sepsis risk Focus is on organ dysfunction Early diagnosis of sepsis and organ dysfunction are key to reducing morbidity and mortality in patients with sepsis. USE SOFA score without waiting for lab values in suspected infections. A SOFA score of 2 or greater over baseline leads to over 10% mortality risk. Follow institutions sepsis pathway. Norepinephrine is first choice vasopressor in septic shock. Fluid resuscitation with sepsis or vasopressors with septic shock.
Pathophysiology of septic shock
Gram-negative bacteria most common Gram positive is increasing Viral infections Fungal infections Up to 30% no identifiable site
Medical management of septic shock
Identification and elimination of infection source (6hrs) Culture specimens- use broad spectrum antibiotics until causative organism is known -Blood -Sputum -Urine -Wound drainage -Tips of invasive catheters -Remove IV lines and reinsert at alternative sites -Drain abscesses, debride necrotic areas Fluid replacement and vasopressor agents -Norepinephrine is the first vasopressor choice (Surviving sepsis campaign, 2017) Induced coma to reduce metabolic demands DVT prophylaxis Stress ulcer prophylaxis Nutritional therapy - aggressive within 24 to 48 hours of ICU admission
Compensatory stage- medical management
Identify the cause of shock Correct the underlying disorder so shock does not progress Support the processes that have responded to the threat Initial fluid resuscitation- IV access (crystalloids- NS, LR, and colloids-albumin, hespan, hetastarch) see page 297 Medication therapy to maintain BP and tissue perfusion Vasoactive Agents- (Dopamine, Levophed)
Fluid replacement (fluid resuscitation) in shock
Improve cardiac and tissue oxygenation Fluids used may include: -Crystalloids: NS, LR, hypertonic solution, plasmalyte -Colloids: albumin, dextran, blood, hydroxyethyl starch Close monitoring is required to identify side effects and complications, cardiovascular overload and pulmonary edema
Vasoactive medication therapy in shock
Improve the hemodynamic stability when fluids alone don't work to maintain the MAP Medications are selected for their action on receptors of the Sympathetic Nervous System: -Alpha-Adrenergic receptors -Beta-Adrenergic receptors -Further classified as beta-1 and beta-2 adrenergic receptors The medications used consist of various combinations of vasoactive medications to maximize tissue perfusion
Nutrional support
Increased metabolic rates during shock increase energy requirements and therefore caloric requirements (more than 3000 cals per day) Glycogen stores are depleted in 8 to 10 hrs due to the release of catecholamines early in shock -Lean body mass is broken down Parenteral or enteral support should be initiated as soon as possible -Enteral is prefered -Promotes GI function via direct exposure of nutrients and limiting infection complications
Total Parental Nutrition
Indications include: -Inability to ingest adequate oral food or fluids within a 7 to 10 day timeframe -Enteral nutrition should be considered before parenteral support because it assists in maintaining gut mucosal integrity and improved immune function and is typically associated with fewer complications
Key to nursing management in compensatory stage
Key: Early intervention: key to improving the patient's prognosis Assess: Systematically assess" patient at risk for shock, recognize subtle clinical signs before the BP drops Identify: cause of shock: administer intravenous fluids and oxygen Obtain: Obtain necessary lab tests: rule out, treat metabolic imbalances or infection (e.g. Na and Blood glucose levels are elevated)
Calculating MAP
MAP = SBP + 2 (DBP)/3 MAP = 83 +2 (50)/ 3 MAP = 83 +100/3 MAP = 183/3 MAP = 61 mm HG
Medical management of hypovolemic shock
Main: correct underlying cause Oxygenation- Sat needs to be above 90% Pain Control- Chest Pain-IV Morphine, Decreases Anxiety Hemodynamic Monitoring- Assesses response to treatment (Arterial line, Pulmonary line) Laboratory Marker Monitoring Cardiac Enzymes 12 lead EKG Fluid replacement to restore intravascular volume Vasoactive medications to restore vasomotor tone, improve cardiac function Nutritional support to address metabolic requirements
Clinical manifestations of MODS
May remain hemodynamically stable but may require increased IV fluids and vasoactive agents to support BP and CO Usually a precipitating event which is associated with resultant HYPOTENSION: 1. Patient is resuscitated 2. The cause is treated 3. Patient appears to do well for a few days • SEQUENCE OF EVENTS OFTEN DEVELOPS **Most likely- Patient experiences SIRS before MODS develops** Signs of a hypermetabolic State: -Hyperglycemia -Hyperlacticacidemia -Increased BUN -Loss of skeletal muscle mass
Mean Arterial Pressure (MAP)
Mean arterial BP= Cardiac output x Peripheral resistance (mean arterial pressure must exceed 65 mm Hg for cells to receive the O2 and nutrients needed to metabolize energy to sustain life) To calculate a mean arterial pressure, double the diastolic blood pressure and add the sum to the systolic blood pressure. Then divide by 3. For example, if a patient's blood pressure is 83 mm Hg/50 mm Hg, his MAP would be 61 mm Hg.
Nursing management in compensatory stage
Monitor tissue perfusion: Observe for changes in LOC Observe for changes in VS (pulse, BP, RR, urinary Op, skin and lab values) Na and Blood glucose (65-110)levels are elevated (CBC, wbc's, lytes-Na (135-145), K (3.5-5.0), Cl (95-105), BUN (7-21), CR (0.5-1.4), CK-MB (0-3), Promptly report changes to the primary care provider (The nurse should report a systolic BP lower than 90 mm or a drop in systolic of 40 mm from baseline or a MAP less than 65) Observe for narrowing pulse pressure Reduce anxiety: provide brief explanations about the diagnostic and treatment procedures, speak in a calm reassuring voice Promote safety: monitor closely, frequent orientation (prevent falls)
Vasodilators
Nitroglycerin (Tridil) Nitroprusside (Nipride) Desired action in shock: Reduce preload and afterload, reduce oxygen demand of the heart Disadvantages: hypotension
Vasopressor agents
Norepinephrin (Levophed) Dopamine (Intropine) Phenulephrine (Neosynephrine) Vasopressin (Pitressin) Desired action in shock: Increase blood pressure by vasoconstriction Disadvantages: Increase afterload, thereby increasing cardiac workload compromise perfusion to skin, kidneys, lungs and GI tract
Compensatory stage- clinical manifestations
Normal BP HR> 100 bpm RR >20 PaCO2 <32mm Hg Skin- cold clammy pale Urinary output decrease Bowel sounds are hypoactive Mentation- Confusion or agitation, restlessness Acid Base Balance-Metabolic Acidosis (may compensate with respiratory alkalosis) (Patients display the fight or flight response from the stimulation of the sympathetic nervous system and the release of catecholamines norepinephrine and epinephrine)
Insulin support and TPN
Overall, management of hyperglycemia is most important Patients receive both IV insulin (added) and subcutaneous intermediate or short-acting insulins Blood glucose level is monitored and insulin administered at regular intervals Insulin assists with Management of hyperglycemia, protein accretion (anabolism)Anti-inflammatory activity Practice varies widely among patient populations, disciplines and individual clinicians
Irreversible stage of shock (refractory)
Represents the point along the shock continuum when organ damage is so severe that the pt does not respond to treatment and cannot survive.
If shock is not reversed during progressive stage what occurs?
Sequence of compensatory responses to the decrease in tissue perfusion perpetuates the shock state Chances of survival depend of the underlying health of the patient prior to the shock state and the amount of time it takes to restore tissue perfusion.
Nursing management of septic shock
Strict aseptic technique during invasive procedures/Strict handwashing Obtain appropriate specimens for culture and sensitivity Hyperthermia-administer acetaminophen or apply hyperthermia blanket if temp more than 40C (104) Monitor closely for shivering Administer IV fluids and vasoactive medications to restore vascular volume Daily weights, careful I and O, coagulation studies Monitor lactate levels- guide to resuscitation Monitor procalcitonin- detects bacterial vs nonbacterial- Initial IV Fluid bolus sepsis patient : 30ml/kg 0.9NS solution (Surviving sepsis campaign) within first 3 hours. -Why ? Fluids expand the intravascular volume. Goal is perfusion. Treat the vasodilation.
Septic shock
The most common type of circulatory shock Caused by widespread infection or sepsis Sepsis occurs in stages that may progress from uncomplicated sepsis to septic shock Leading cause of death in noncoronary ICU patients
