week 13

TTP meds

-Antiplatelet medications (aspirin, alprostadil, plicamycin) -Immunosuppressive therapy decreases the intensity of complications.

risk factors hit

-Female sex -Receiving heparin longer than 1 week -Exposure to unfractionated heparin -Postsurgical thromboprophylaxis (prevention of thromboembolic disease)

DIC meds

Anticoagulants (heparin) can be used to decrease microclots from forming and using up clotting factors.

risk factors ITP

Female sex (ages 20 to 50 years), Secondary conditions (medications, viruses [HIV, hepatitis C]), Other autoimmune disorders, Recent virus (children only)

distributive shock

Neurogenic shock: a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury and last up to 6 weeks. Neurogenic shock related to spinal cord injuries is generally associated with a cervical or high thoracic injury. The injury results in a massive vasodilation without compensation because of the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and impaired cellular metabolism. --In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) can decrease the vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock. --The classic manifestations are hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation). The patient may not be able to regulate body temperature. Combined with massive vasodilation, the inability to regulate temperature promotes heat loss. At first, the patient's skin is warm due to the massive vasodilation. As the heat disperses, the patient is at risk for hypothermia. Later, the patient's skin may be cool or warm depending on the ambient temperature (poikilothermia, taking on the temperature of the environment). In either case, the skin is usually dry. --Although spinal shock and neurogenic shock often occur in the same patient, they are not the same disorder. Spinal shock is a transient condition that is present after an acute spinal cord injury. The patient with spinal shock has an absence of all voluntary and reflex neurologic activity below the level of the injury. Anaphylactic shock: an acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom). The reaction quickly causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space. --Anaphylactic shock can lead to respiratory distress due to laryngeal edema or severe bronchospasm and circulatory failure from the massive vasodilation. The patient has a sudden onset of symptoms, including dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, and stridor. Skin changes include flushing, pruritus, urticaria, and angioedema. The patient may be anxious and confused and have a sense of impending doom. --A patient can have a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion, or injection with an antigen (allergen) to which the person has previously been sensitized. IV administration of the antigen (allergen) is the route most likely to cause anaphylaxis. However, oral, topical, and inhalation routes can cause anaphylactic reactions. Quick and decisive action is critical to prevent an allergic reaction from progressing to anaphylactic shock. Septic shock: Sepsis is a life-threatening syndrome in response to an infection. It is characterized by a dysregulated patient response along with new organ dysfunction related to the infection. In as many as 30% of patients with sepsis, the causative organism is not identified. Sepsis and septic shock have a high incidence worldwide, with a mortality rate of 25% or higher. --Septic shock is a subset of sepsis. It has an increased mortality risk due to profound circulatory, cellular, and metabolic abnormalities. Septic shock is characterized by persistent hypotension, despite adequate fluid resuscitation, and inadequate tissue perfusion that results in tissue hypoxia. The main organisms that cause sepsis are gram-negative and gram-positive bacteria. Parasites, fungi, and viruses can also cause sepsis and septic shock. --When a microorganism enters the body, the normal immune or inflammatory responses are triggered. However, in sepsis and septic shock the body's response to the microorganism is exaggerated. Both proinflammatory and antiinflammatory responses are activated, coagulation increases, and fibrinolysis decreases. Endotoxins from the microorganism cell wall stimulate the release of cytokines. These include tumor necrosis factor (TNF), interleukin-1 (IL-1), and other proinflammatory mediators that act through secondary mediators, such as platelet-activating factor, IL-6, and IL-8. The release of platelet-activating factor results in the formation of microthrombi and obstruction of the microvasculature. The combined effects of the mediators result in damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium. --Septic shock has 3 major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. Patients may be euvolemic, but because of acute vasodilation and shifting of fluids out of the intravascular space, relative hypovolemia and hypotension occur. Blood flow in the microcirculation is decreased, causing poor O2 delivery and tissue hypoxia. We think the combination of TNF and IL-1 has a role in sepsis-induced myocardial dysfunction. The ejection fraction (EF) is decreased for the first few days after the initial insult. Because of a decreased EF, the ventricles dilate to maintain the SV. The EF typically improves, and ventricular dilation resolves over 7 to 10 days. Persistent high CO and a low SVR beyond 24 hours is an ominous finding. It is often associated with an increased development of hypotension. Coronary artery perfusion and myocardial O2 metabolism are not primarily altered in septic shock. --Respiratory failure is common. The patient initially hyperventilates as a compensatory mechanism, causing respiratory alkalosis. Once the patient can no longer compensate, respiratory acidosis develops. Respiratory failure develops in 85% of patients with sepsis, and 40% develop acute respiratory distress syndrome (ARDS). These patients may need to be intubated and mechanically ventilated. --Other signs of septic shock include changes in neurologic status, decreased urine output, and GI dysfunction, such as GI bleeding and paralytic ileus.

risk factors ttp

autoimmune disorders

laboratory tests

-Hemoglobin (decreased with DIC and ITP): Expected reference range males, 14 to 18 g/dL; females, 12 to 16 g/dL -Platelet levels (thrombocytopenia; decreased with DIC, TTP, and ITP): Expected reference range 150,000 to 400,000 mm -Fibrinogen levels (decreased with DIC): Expected reference range 200 to 400 mg/dL -Prothrombin time (increased with DIC): Expected reference range 11.0 to 12.5 seconds -Partial thromboplastin (increased with DIC): Expected reference range aPTT, 30 to 40 seconds; PTT, 60 to 70 seconds -Thrombin time (increased with DIC): 8 to 11 seconds -Fibrin split product levels/fibrin degradation products (increased with DIC): Expected reference range less than 10 mcg/mL -D-dimer (increased with DIC): Expected reference range less than 0.4 mcg/mL -Blood typing and cross-match

DIC interventions

-Monitor for manifestations of microemboli (cyanotic nail beds, pain). -Regularly assess vital signs and hemodynamic status. -Monitor for manifestations of organ failure or intracranial bleed (oliguria, decreased level of consciousness). -Monitor laboratory values for clotting factors. -Administer fluid volume replacement. -Transfuse blood, platelets, and other clotting products. -Monitor for complications from the administration of blood and blood products. -Avoid use of NSAIDs. -Administer supplemental oxygen. -Provide protection from injury. -Instruct client to avoid Valsalva maneuver (could cause cerebral hemorrhage). -Implement bleeding precautions (avoid use of needles).

expected findings coag disorders

-Unusual spontaneous bleeding from the gums and nose (epistaxis) -Oozing, trickling, or flow of blood from incisions or lacerations -Petechiae and ecchymoses -Hematuria -Excessive bleeding from venipuncture, injection sites, or slight traumas -Tachycardia, hypotension, and diaphoresis -Organ failure secondary to microemboli -Respiratory distress -Redness, pain, warmth and swelling of lower extremities (HIT)

sepsis

A life-threatening, life-altering emergency, sepsis can have catastrophic effects. When the condition progresses undetected, it can lead to multiple organ dysfunction syndrome and death. Mortality ranges from 9% to 35% and rises sharply with each passing hour that sepsis goes unidentified. In the United States alone, an estimated 20,000 to 40,000 children are diagnosed with septic shock annually—and the number is increasing. Prompt recognition and treatment can improve survival odds. Unfortunately, sepsis is harder to recognize in children than adults. Although most children with sepsis don't arrive at the hospital in full septic shock, they can deteriorate quickly as the condition progresses. Sepsis can develop in both the community and the hospital. So all nurses—not just those working in emergency departments, intensive care units, and transport teams—must know how to assess for and identify early warning signs of sepsis in children.

assessment findings of shock

anxiety, chills, confusion, cool clammy skin (warm in early of septic and neurogenic), cyanosis, decreased LOC/O2, dysrhythmias, extreme thirst, impending doom, low BP, narrow pulse pressure, n/v, obvious hemorrhage, injury, pale, rapid/weak/thready pulse, restless, tachypnea, dyspnea, shallow/irregular resp, temp dysreg, weak

ongoing monitoring shock

ABC, LOC, vitals, pulse ox, peripheral pulses, cap refill, skin color, temp), respiratory status, HR and rhythm, urine output

HIT meds

Anticoagulants with direct thrombin inhibitor (argatroban, lepirudin, bivalirudin)

Sodium Nitroprusside

arterial and venous vasodilator, decreased preload, afterload, CVP, PAWP, and BP fluctuating CO wrap bottle with opaque covering, D5W with only, monitor cyanide levels (toxic: met acid, tachycardia, altered LOC, seizure, coma, almond smell on breath)

Physical finding associated with DIC:

epistaxis- unexpected bleeding of gums and nose, hypotension, tachycardia

cardiogenic shock

Cardiogenic shock occurs when either systolic or diastolic dysfunction of the heart's pumping action results in reduced cardiac output (CO), stroke volume (SV), and BP. These changes compromise myocardial perfusion, further depress myocardial function, and decrease CO and perfusion. Mortality rates for patients with cardiogenic shock are around 50%. It is the leading cause of death from acute myocardial infarction (MI). -The heart's inability to pump the blood forward is called systolic dysfunction. This inability results in a low CO (less than 4 L/min) and cardiac index (less than 2.5 L/min/m2). Systolic dysfunction primarily affects the left ventricle since systolic pressure is greater on the left side of the heart. The most common cause of systolic dysfunction is acute MI. When systolic dysfunction affects the right side of the heart, blood flow through the pulmonary circulation is reduced. Decreased filling of the heart results in decreased SV. -Whether the first event is myocardial ischemia, a structural problem (e.g., valvular disorder, ventricular septal rupture), or dysrhythmias, the physiologic responses are similar. The patient has impaired tissue perfusion and cellular metabolism. -The early presentation of a patient with cardiogenic shock is similar to that of a patient with acute decompensated heart failure (HF). The patient may have tachycardia and hypotension. Pulse pressure may be narrowed due to the heart's inability to pump blood forward during systole and increased volume during diastole. An increase in systemic vascular resistance (SVR) increases the workload of the heart. This increases myocardial O2 consumption. -On assessment, the patient is tachypneic and has crackles on auscultation of breath sounds because of pulmonary congestion. The hemodynamic profile shows an increase in the pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV), and pulmonary vascular resistance. -Signs of peripheral hypoperfusion (e.g., cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill) occur. Decreased renal blood flow results in sodium and water retention and decreased urine output. Anxiety, confusion, and agitation may develop with impaired cerebral perfusion.

coag disorders

Coagulation disorders occur secondary to an alteration in platelets, clotting factors, or both. Coagulopathy is the term for any condition that affects an individual's ability to coagulate. Coagulopathies are suspected when the usual measures used to stop bleeding fail. Coagulopathy can occur secondary to an autoimmune disorder or extensive blood loss in which platelets and clotting factors are lost. In some cases, the development of microemboli in the circulatory system paradoxically uses up the clotting factors that cause hemorrhages to occur at the same time intravascular clotting occurs.

meds ITP

Corticosteroids and immunosuppressants

interprofessional care shock

Critical factors in the successful management of a patient in shock relate to the early recognition and treatment of the shock state. Prompt intervention in the early stages of shock may prevent the decline to the progressive or irreversible stage. Successful management of the patient in shock includes (1) identification of patients at risk for the development of shock; (2) integration of the patient's history, physical examination, and clinical findings to establish a diagnosis; (3) interventions to control or eliminate the cause of the decreased perfusion; (4) protecting target and distal organs from dysfunction; and (5) providing multisystem supportive care. General management strategies begin with ensuring that the patient is responsive and has a patent airway. Once the airway is established, either naturally or with an endotracheal tube, O2 delivery must be optimized. Supplemental O2 and mechanical ventilation may be needed to maintain an arterial O2 saturation of 90% or more (PaO2 greater than 60 mm Hg) to avoid hypoxemia. The mean arterial pressure (MAP) and circulating blood volume are optimized with fluid replacement and drug therapy.

shock

a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism. This results in an imbalance between the supply of and demand for O2 and nutrients. The exchange of O2 and nutrients at the cellular level is essential to life. When cells are hypoperfused, the demand for O2 and nutrients exceeds the supply at the microcirculatory level. Ischemia can occur, leading to cell injury and death. Thus shock of any cause is life-threatening.

stages of shock

In addition to understanding the underlying pathogenesis of the type of shock the patient has, management is guided by knowing where the patient is on the shock "continuum." We categorize shock into 4 overlapping stages: (1) initial stage, (2) compensatory stage, (3) progressive stage, and (4) refractory stage.

cardiogenic shock measures

For a patient in cardiogenic shock, the overall goal is to restore heart function and the balance between O2 supply and demand in the myocardium. Cardiac catheterization is done as soon as possible after the initial insult. Specific measures to restore blood flow include angioplasty with stenting, emergency revascularization, and valve replacement. Until these interventions are done, we must support the heart to optimize SV and CO to achieve optimal perfusion. -Hemodynamic management of a patient in cardiogenic shock aims to reduce the workload of the heart through drug therapy and/or mechanical interventions. Drug choice is based on the clinical goal and a thorough understanding of each drug's mechanism of action. Drugs can be used to decrease the workload of the heart by dilating coronary arteries (e.g., nitrates), reducing preload (e.g., diuretics), afterload (e.g., vasodilators), and heart rate and contractility (e.g., β-adrenergic blockers). -The patient may benefit from a circulatory assist device (e.g., intraaortic balloon pump, ventricular assist device [VAD]). The goals of this intervention are to decrease SVR and left ventricular workload so that the heart can heal. A VAD may be used as a temporary measure for the patient in cardiogenic shock who is awaiting heart transplantation. Heart transplantation is an option for a small, select group of patients with cardiogenic shock.

anaphylactic shock causes

Hypersensitivity/allergic reaction to a sensitizing substance which causes massive vasodilation and increased capillary permeability - so fluid leaks out of the vascular space to the interstitial space -contrast media, blood or blood products, insect bites, drugs, anesthetic agents, food/food additives, vaccines, environmental agents, latex

risk factors for sepsis

In children, sepsis risk factors include: • infancy (less than 8 weeks old) • compromised immune system • concurrent illness • wounds or injuries (including burns) • invasive medical devices (including indwelling catheters) • hemoglobin SS disease (the most common type of sickle cell disease), which carries a 400-fold higher risk of sepsis • congenital heart disease • current hospitalization. To help identify sepsis risk factors, obtain a concise history from family members, including the patient's symptoms and their onset and severity. Also find out if the patient recently was exposed to sick family members or classmates.

management of sepsis

If you suspect your patient has sepsis, immediately notify the attending practitioner and request available nurses to assist with this critical condition. The clock starts when sepsis is identified. Many hospital guidelines require clinicians to complete certain time-sensitive interventions at first recognition of sepsis. Use of the American Heart Association Pediatric Advanced Life Support's sepsis shock algorithm and hospital-dependent bundles and guidelines for treating sepsis has improved outcomes and decreased hospital stays for patients with sepsis. As ordered, begin oxygen administration via nonrebreather face mask at 15 L/minute, regardless of the patient's blood oxygen saturation. Some patients may require high-flow nasal cannula, nasopharyngeal continuous positive airway pressure, or early intubation and mechanical ventilation. Place the patient on a cardiac monitor with continuous pulse oximetry. As ordered, insert two large-bore I.V. lines (as large as the patient's vein will support). After two failed I.V. insertion attempts, prepare for intraosseous access. In some cases, a central line may be placed. Expect the practitioner to order rapid resuscitation fluids (isotonic crystalloids—specifically Lactated Ringer's or normal saline solution) administered by I.V. push at a rate of 20 mL/kg. As ordered, repeat boluses up to four times unless respiratory distress, crackles, or hepatomegaly develops. Fluid resuscitation should continue with vasopressors until blood pressure and peripheral perfusion improve. The type of shock (normotensive, warm, or cold) determines which drug is ordered. Strict fluid intake and output documentation is crucial, so anticipate inserting an indwelling urinary catheter. As ordered, administer glucose to correct hypoglycemia and calcium chloride or calcium gluconate to correct hypocalcemia. For febrile patients, expect to give antipyretics as well. Draw samples for a complete blood count with differential, arterial blood gasses, blood cultures, serum glucose (or glucose finger stick), ionized calcium, and serum lactate. Notify the practitioner of critical laboratory values, and obtain blood culture specimens before antibiotic therapy begins. However, know that broad-spectrum antibiotics must be given within 1 hour of sepsis recognition and must not be delayed if blood specimens can't be obtained. Continue to monitor the patient's vital signs frequently. Check for signs of fluid overload every 5 to 15 minutes; these include increased work of breathing, crackles on lung auscultation, an irregular gallop rhythm on heart auscultation, and an enlarged liver on palpation. The patient may need to be monitored in the pediatric intensive care unit (PICU). If your facility lacks PICU services, the patient may require transfer to a tertiary care center.

sepsis terminology update

In 2016, a task force of the Society of Critical Care Medicine and the European Society of Intensive Care Medicine issued new consensus definitions and criteria (called Sepsis-3) for sepsis and septic shock. Sepsis-3 updated the terminology for sepsis and related conditions and moved away from the model of sepsis as a continuum. Defines sepsis as a life-threatening organ dysfunction caused by a dysregulated host response to infection and defines septic shock as a subset of sepsis with profound circulatory, cellular, and metabolic dysfunction linked to a higher mortality risk than sepsis alone. In addition, Sepsis-3 concluded that criteria for systemic inflammatory response systems (SIRS) lack the sensitivity and specificity to detect sepsis in its early stages. (Nonetheless, the SIRS criteria may still be useful in helping clinicians determine if the patient has an ongoing infectious process.) Sepsis-3 recommends use of a secondary screening tool, the quick Sepsis-Related Organ Failure Assessment (qSOFA), in patients with an identified or suspected infection to evaluate risk for clinical deterioration. In adults, two of three qSOFA elements—altered mental status, respiratory rate of 22 breaths/minute or higher, or systolic pressure of 100mm Hg or lower—predict poor clinical odds. These patients should be evaluated for possible organ dysfunction. Although the Sepsis-3 task force focused on adults, it recognized the need for research to adapt qSOFA criteria for use in pediatric patients. Currently, Sepsis-3 doesn't consider pediatric pathophysiology and age-dependent vital signs, and it lacks supporting evidence in the pediatric population. In children, increased respiratory and heart rates alone aren't clinically definitive for sepsis. Also, not only do children's compensatory mechanisms differ from those of adults, but children with sepsis may have adequate blood pressure, with hypotension developing only as a late sign of septic shock. Without an evidence-based (EB) adaptive screening tool specifically for children, clinicians must be extra vigilant in assessing patients to recognize subtle changes.

refractory stage

In the last stage of shock, the refractory stage, decreased perfusion from peripheral vasoconstriction and decreased CO worsen anaerobic metabolism. The accumulation of lactic acid contributes to increased capillary permeability and dilation. Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in the capillary beds due to the constricted venules and dilated arterioles. The loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow. Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO. Cerebral blood flow cannot be maintained and cerebral ischemia results. -The patient in this stage of shock has profound hypotension and hypoxemia. The failure of the liver, lungs, and kidneys results in an accumulation of waste products, such as lactate, urea, ammonia, and CO2. The failure of 1 organ system affects several other organ systems. Recovery is unlikely in this stage. The organs are in failure and the body's compensatory mechanisms are overwhelmed.

Epinephrine (adrenaline)

Low dose: beta adrenergic agonist (cardia stim, bronchodilation, peripheral vasodilation), increased HR, contractility, CO, decreased SVR cardiogenic shock, anaphylactic shock, septic shock (norepi is first) monitor HR over 110, dyspnea, pulmonary embolism, chest pain, dysrhythmias from increased MVO2, monitor for renal failure due to ischemia high doses used for cardiac arrest, vfib, pulseless v tach, asystole: alpha adrenergic agonist (peripheral vasoconstriction): increased SV, SVR, CVP, PAWP, increased SBP, decreased DBP, widened pulse pressure

flaws in EHR peds sepsis

Many hospitals use electronic health records (EHRs) to create order set sepsis bundles. Technology can extrapolate pertinent data entered into the EHR, such as vital signs and laboratory values, to generate sepsis-warning and best-practice notifications. If the patient meets sepsis criteria, a warning is generated, signaling the nurse to notify the attending practitioner. Practitioners receive similar notifications to initiate the order set. This system lets practitioners use their best clinical judgment; in some cases, the practitioner may conclude that although a particular patient appears to meet sepsis criteria, a different underlying cause explains the presence of these criteria. Unfortunately, some EHRs lack age-specific vital signs and laboratory values to capture true sepsis in pediatric patients. As a result, false-positive warnings may occur, which can lead to warning fatigue and cause clinicians to ignore valid warnings. EHRs must be fine-tuned to detect sepsis early in children. Along with continual education on pediatric sepsis for all healthcare providers, EHR improvements are crucial for saving the lives of children with sepsis.

sympathomimetic drugs

Many of the drugs used in the treatment of shock influence the SNS. Drugs that mimic the action of the SNS are called sympathomimetic. The effects of these drugs are mediated through their binding to α- or β-adrenergic receptors. The various drugs differ in their relative α- and β-adrenergic effects. Many of these drugs cause peripheral vasoconstriction and are called vasopressor drugs (e.g., norepinephrine, dopamine, phenylephrine). These drugs can cause severe peripheral vasoconstriction and an increase in SVR, further risking tissue perfusion. The increased SVR increases the workload of the heart and myocardial O2 demand. It can harm a patient in cardiogenic shock by causing further myocardial damage and increasing the risk for dysrhythmias. Use of vasopressor drugs is limited to patients who do not respond to fluid resuscitation. Adequate fluid resuscitation must be achieved before starting vasopressors because the vasoconstrictor effects in patients with low blood volume will cause further reduction in tissue perfusion. Typically, if the patient has persistent hypotension after adequate fluid resuscitation, a vasopressor (e.g., norepinephrine, dopamine) and/or an inotrope (e.g., dobutamine) is given. The goal of vasopressor therapy is to achieve and maintain a MAP of greater than 65 mm Hg. Continuously monitor end-organ perfusion (e.g., urine output, level of consciousness) and serum lactate levels (e.g., every 3 hours for the first 6 hours) to ensure that tissue perfusion is adequate.

nursing care bleeding disorders

Nursing interventions for DIC initially focus on assessing for and correcting the underlying cause (sepsis, malignancy, hemorrhage). Focus then turns to preventing organ damage secondary to microemboli and replacing the blood's clotting components. -Monitor for manifestations of microemboli (cyanotic nail beds, pain). DIC, HIT, ITP, and TTP -Regularly assess vital signs and hemodynamic status. -Monitor for manifestations of organ failure or intracranial bleed (oliguria, decreased level of consciousness). -Monitor laboratory values for clotting factors. -Administer fluid volume replacement. -Transfuse blood, platelets, and other clotting products. -Monitor for complications from administration of blood and blood products. -Avoid use of NSAIDs. -Administer supplemental oxygen. -Provide protection from injury. -Instruct client to avoid Valsalva maneuver (could cause cerebral hemorrhage). -Implement bleeding precautions (avoid use of needles).

oxygenation and ventilation shock

O2 delivery depends on CO, available hemoglobin, and arterial O2 saturation (SaO2). Methods to optimize O2 delivery are directed at increasing supply and decreasing demand. Supply is increased by (1) optimizing the CO with fluid replacement and/or drug therapy, (2) increasing the hemoglobin through transfusion of whole blood or packed red blood cells (RBCs), and/or (3) increasing the arterial O2 saturation with supplemental O2 and mechanical ventilation. Plan care to avoid disrupting the balance of O2 supply and demand. Space activities that increase O2 consumption (e.g., endotracheal suctioning, position changes) appropriately for O2 conservation. Intermittent or continuous monitoring of ScvO2 by a central venous catheter or mixed venous O2 saturation (SvO2) may be helpful. Both reflect the dynamic balance between O2 supply and demand. Assess these values along with related hemodynamic measures (e.g., arterial pressure-based cardiac output [APCO], O2 consumption, hemoglobin) to evaluate the patient's response to treatments and activities.

hypovolemic shock causes

absolute hypovolemia- external loss of whole blood, loss of other body fluids: hemorrhage from trauma, surgery, GI bleeding loss of body fluids- vomit, diarrhea, diuresis excessive, DI, diabetes relative hypovolemia- fluid shifts (burn injuries, ascites), internal bleeding (fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis), massive vasodilation (sepsis), pooling of blood or fluids (bowel obstruction

vasodilator drugs

Patients in cardiogenic shock have decreased myocardial contractility, and vasodilators may be needed to decrease afterload. This reduces myocardial workload and O2 requirements. Although generalized sympathetic vasoconstriction is a useful compensatory mechanism for maintaining BP, excessive constriction can reduce tissue blood flow and increase the workload of the heart. The reason for using vasodilator therapy for a patient in shock is to break the harmful cycle of widespread vasoconstriction causing a decrease in CO and BP, resulting in further sympathetic-induced vasoconstriction. The goal of vasodilator therapy, as in vasopressor therapy, is to maintain the MAP greater than 65 mm Hg. Monitor hemodynamic parameters (e.g., CVP, CO, ScvO2/SvO2, SV, PA pressures) and assessment findings so that fluids can be increased or vasodilator therapy decreased if a serious fall in CO or BP occurs. The vasodilator agent most often used for the patient in cardiogenic shock is nitroglycerin. Vasodilation may be enhanced with nitroprusside or nitroglycerin in noncardiogenic shock.

septic shock measures

Patients in septic shock need large amounts of fluid replacement. The overall goal of fluid resuscitation is to restore the intravascular volume and organ perfusion. Initial volume resuscitation is achieved by giving 30 mL/kg of an isotonic crystalloid solution. Albumin 4% to 5% may be added when patients need substantial volumes. -A fluid challenge technique (e.g., a minimum of 30 mL/kg of crystalloids) may be used and repeated until hemodynamic improvement (e.g., increase in MAP and/or CVP, change in SVV) is seen. One of these methods is a passive leg raise (PLR) challenge along with hemodynamic measures to monitor response. A PLR challenge provides a transient increase in fluid volume of 150 to 500 mL by placing the patient supine and raising the legs to 45 degrees. Response is monitored within 1 to 2 minutes by measuring CO, CI, SV, SVV, or other parameters for improvement. If the response is positive, the patient is fluid responsive and should receive more fluids. To optimize and evaluate large-volume fluid resuscitation, hemodynamic monitoring with various noninvasive or invasive monitors is needed. -If the patient is hypotensive after initial volume resuscitation and no longer fluid responsive, vasopressors may be added. The first drug of choice is norepinephrine. Vasodilation and low CO, or vasodilation alone, can cause low BP despite adequate fluid resuscitation. Vasopressin may be added for those who are refractory to initial vasopressor therapy. Exogenous vasopressin can replace the stores of physiologic vasopressin that are often depleted in septic shock. -Vasopressor drugs may increase BP but can decrease SV. An inotropic agent (e.g., dobutamine) may be added to offset the decrease in SV and increase tissue perfusion. IV corticosteroids may be considered for patients in septic shock who cannot maintain an adequate BP despite vasopressor therapy and fluid resuscitation. -To try to meet the increasing tissue demands coupled with a low SVR, the patient initially has a normal or high CO. If the patient is unable to achieve and maintain an adequate CO and has unmet tissue O2 demands, CO may have to be increased using drug therapy (e.g., dopamine). ScvO2 or SvO2 monitoring is used to assess the balance between O2 delivery and consumption, and the adequacy of the CO. If balance is maintained, the tissue demands will be met. -Broad-spectrum antibiotics are an important and early part of therapy. They should be started within the first hour of sepsis or septic shock. Obtain cultures (e.g., blood, wound, urine, stool, sputum) before antibiotics are started. However, this should not delay the start of antibiotics within the first hour. Specific antibiotics may be ordered once the organism has been identified. -Glucose levels should be maintained below 180 mg/dL (10.0 mmol/L) for patients in shock. Monitor glucose levels in all patients in septic shock according to agency policy. Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole) and VTE prophylaxis (e.g., heparin, enoxaparin [Lovenox]) are recommended.

blood or blood product (platelet, FFP, pRBCs)

all types of shock, replace blood loss, increase O2 carrying capacity, replace coag factors, helps control bleeding caused by thrombocytopenia

phenylephrine

alpha adrenergic agonist (peripheral vasoconstriction), renal mesenteric, splanchnic, cutaneous, and pulmonary blood vessel constriction, CO fluctuates, increased HR, BP, SVR neurogenic shock monitor for reflex bradycardia, headache, restlessness, monitor for renal failure from decreased renal blood flow, give central line (infiltration leads to tissue sloughing)

nutritional therapy shock

Protein-calorie malnutrition is common because of hypermetabolism. Nutrition is vital to reducing mortality. Enteral nutrition (EN) should be started within the first 24 hours. However, full calorie replacement is not recommended for previously well-nourished adults early in a critical illness. Start the patient on a trophic feeding. This is a small amount of EN (e.g., 10 mL/hr). Early EN enhances the perfusion of the GI tract and helps maintain the integrity of the gut mucosa. Advance feedings as tolerated and as prescribed. Parenteral nutrition (PN) is used only if EN is contraindicated. Weigh the patient daily on the same scale (usually the bed scale) at the same time of day. If the patient has a significant weight loss, rule out dehydration before adding more calories. Large weight gains are common because of third spacing of fluids. Therefore daily weights serve as a better indicator of fluid status than caloric needs. Serum protein, total albumin, prealbumin, BUN, serum glucose, and serum electrolytes are all used to assess nutritional status.

dic risk factors

Septicemia, Cardiopulmonary arrest, Trauma (hemorrhage, burns, crush injuries), Obstetric complications (toxemia, amniotic fluid embolism, placental abruption), Cancer, Allergic reaction

Hydrocortisone

Solu-Cortef decreased inflammation, reverses increased BP, HR, cap permeability septic shock requiring pressor (despite fluid), anaphylactic shock if hypotensive after therapy monitor low K, high BG, use continuous?

ITP interventions

Splenectomy can be performed if the client does not respond to medical management.

septic shock symptoms

Tachycardia, fluctuating temp, myocardial dysfunction, decreased EEF, biventricular dilation, hyperventilation, crackles, resp alk to acid, hypoxic, ARDS, resp failure, pulmonary hypertension, decreased urine, warm and flushed to cool/mottled (late), change in mental state, confused, agitated, coma (late), GI bleed, paralytic ileus, WBC off, decreased platelets, urine NA, increased lactate/BG/procal/urine specific gravity, positive blood cultures

shock classifications

The 4 main categories of shock are cardiogenic, hypovolemic, distributive, and obstructive. Although the cause, initial presentation, and management vary for each type, the physiologic responses of the cells to hypoperfusion are similar.

initial stage

The continuum begins with the initial stage of shock that occurs at a cellular level. This stage is usually not clinically apparent. Metabolism changes at the cellular level from aerobic to anaerobic, causing lactic acid buildup. Lactic acid is a waste product that is removed by the liver. However, this process requires O2, which is unavailable because of the decrease in tissue perfusion.

Fluid resuscitation shock

The cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion with administration of the appropriate fluid. Fluid resuscitation should start using 1 or 2 large-bore (e.g., 14- to 16-gauge) IV catheters, an intraosseous (IO) access device, or a central venous catheter. The choice of resuscitation fluid is based on the type and volume of fluid lost and the patient's clinical status. The ideal choice of fluid is controversial. Currently, normal saline is most often used in the initial resuscitation of shock. Large-volume resuscitation with normal saline can lead to hyperchloremic metabolic acidosis. Lactated Ringer's solution can cause serum lactate levels to increase because the failing liver cannot convert lactate to bicarbonate. Transfusions of RBCs may be given to treat hypovolemic shock due to bleeding. Colloids (4% to 5%) have not been shown to improve patient outcomes. Fluid responsiveness is determined by clinical assessment. This includes vital signs, cerebral and abdominal perfusion pressures, capillary refill, skin temperature, and urine output. Hemodynamic parameters, such as SVV or CO, are also used. Monitor trends in BP with an automatic BP cuff or an arterial catheter to assess the patient's response. Use an indwelling urinary catheter to monitor urine output during resuscitation. The goal for fluid resuscitation is to restore tissue perfusion. Although BP helps determine whether the patient's CO is adequate, an assessment of end-organ perfusion (e.g., urine output, neurologic function, peripheral pulses) provides more relevant data.

hypovolemic shock measures

The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume. We often calculate the initial fluid resuscitation using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss).

hit

an immunity-mediated clotting disorder that causes unexplained low blood platelet count as a result of treatment with heparin.

vasopressin

antidiuretic hormone, nonadrenergic vasoconstrictor, increase MAP and urine, shock states (septic more likely refractory to other pressors), give with norepi and in low doses, don't titrate, monitor hemodynamic pressure and urine output

anaphylactic shock measures

The first strategy in managing patients at risk for anaphylactic shock is prevention. A thorough history is key to avoiding risk factors for anaphylaxis. The clinical presentation of anaphylactic shock is dramatic, and immediate intervention is required. Epinephrine is the first drug of choice to treat anaphylactic shock. It causes peripheral vasoconstriction and bronchodilation and opposes the effect of histamine. Diphenhydramine and histamine receptor blockers (e.g., famotidine) are given as adjunctive therapies to block the ongoing release of histamine from the allergic reaction. Maintaining a patent airway is important because the patient can quickly develop airway compromise from laryngeal edema or bronchoconstriction. Nebulized bronchodilators are highly effective. Aerosolized epinephrine can reduce treat laryngeal edema. Endotracheal intubation may be needed to secure and maintain a patent airway. -Hypotension results from leakage of fluid out of the intravascular space into the interstitial space because of increased vascular permeability and vasodilation. Aggressive fluid resuscitation, usually with crystalloids, is needed. IV corticosteroids may be helpful in anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy

drugs shock

The goal of drug therapy for shock is to correct decreased tissue perfusion. Decisions on which drug to use should be based on the physiologic goal. Drugs used to improve perfusion in shock are given IV via an infusion pump and central venous line. Many of these drugs have vasoconstrictor properties that are harmful if the drug leaks into the tissues while being infused peripherally.

obstructive shock measures

The main strategy in treating obstructive shock is early recognition and treatment to relieve or manage the obstruction. Mechanical decompression for pericardial tamponade, tension pneumothorax, and hemopneumothorax may be done by needle or tube insertion. Obstructive shock from a pulmonary embolism requires immediate anticoagulation therapy or pulmonary embolectomy. Superior vena cava syndrome, a compression or obstruction of the outflow tract of the mediastinum, may be treated by radiation, debulking, or removal of the mass or cause. A decompressive laparotomy may be done for abdominal compartment syndrome for patients with high intraabdominal pressures and hemodynamic instability.

diagnosis shock

There is no single diagnostic study to determine whether a patient is in shock. The diagnosis starts with a history and physical examination. Obtaining a thorough medical and surgical history and a history of recent events (e.g., surgery, chest pain, trauma) gives valuable data. Decreased tissue perfusion in shock leads to an increased lactate with a base deficit (the amount needed to bring the pH back to normal). These laboratory changes reflect an increase in anaerobic metabolism. Other diagnostic studies include a 12-lead electrocardiogram (ECG), continuous ECG monitoring, chest x-ray, continuous pulse oximetry, and invasive and noninvasive hemodynamic monitoring.

neurogenic shock measures

The specific treatment of neurogenic shock is based on the cause. If the cause is spinal cord injury, general measures to promote spinal stability (e.g., spinal precautions, cervical stabilization with a collar) are initially used. Once the spine is stabilized, treatment of the hypotension and bradycardia is essential to prevent further spinal cord damage. Treatment involves the use of vasopressors (e.g., phenylephrine) to maintain BP and organ perfusion. Bradycardia may be treated with atropine. Infuse fluids cautiously as the cause of the hypotension is not related to fluid loss. The patient with a spinal cord injury is monitored for hypothermia caused by hypothalamic dysfunction

applying the evidence pediatric sepsis

To improve early sepsis recognition, clinicians need to take active roles in creating policies and EB protocols specific to pediatric sepsis. Too often, we view pediatric care through the lens of adult care even when specialty care is crucial. Many state health departments, hospital associations, and policy makers have banded together to create legislation, regulations, and initiatives with common goals—to implement EB policies and processes and to educate staff to rapidly recognize and treat sepsis, collect data, identify gaps, and share sepsis prevention and best practices. The Surviving Sepsis Campaign encourages hospitals to initiate sepsis intervention bundles. Hospitals can customize these bundles to maximize benefits as long as they uphold the same standards.

TTP

a coagulopathy in which platelets abnormally clump together in capillaries due to an autoimmune reaction from platelet aggregation, resulting in an insufficient from platelet aggregation, resulting in an insufficient quantity in circulation. Inappropriate clotting occurs, and clotting fails to occur with trauma. This can lead to kidney failure, myocardial infarction, and stroke, and can be fatal within 3 months if untreated.

ITP

a coagulopathy that is an autoimmune disorder in which the life span of platelets is decreased by antiplatelet antibodies although platelet production is normal. This can result in severe hemorrhage following a cesarean birth or lacerations.

dic

a life-threatening coagulopathy in which clotting and anticlotting mechanisms occur at the same time. A client who has DIC is at risk for both internal and external bleeding, as well as damage to organs resulting from ischemia caused by microclots.

initial interventions shock

assess CAB if unresponsive, if responsive ABC, stabilize cervical spine, control bleeding with pressure externally, give high flow (100%) O2 by nonrebreather or bag-valve mask (anticipate need for intubate and mech vent), IV access 2 large bore 14-16 gauge or IO, fluid resuscitation with crystalloids (30mL/kg until improvement in hemodynamic status seen), draw blood for lab studies (WBC, lactate, culture), assess for life threatening injuries (cardiac tamponade, liver lac, tension pneumothorax), consider vasopressor therapy if hypotension persists after fluid resuscitation, insert ng tube and indwelling cath, start abx if sepsis is suspected, 12 lead ecg/treat dysrhythmias

Norepinephrine (Levophed)

b1 adrenergic agonist (cardiac stim), alpha adrenergic agonist (peripheral vasoconstriction), renal and splanchnic vasoconstriction, increased BP, MAP, CVP, PAWP, SVR, increased/decreased CO cardiogenic shock after MI, first drug for septic shock unresponsive to fluids give centrally (infiltration leads to tissue slough), monitor for dysrhythmias due to increased MVO2

progressive stage

begins as compensatory mechanisms fail. Changes in the patient's mental status are important findings in this stage. Patients must be moved to the intensive care unit (ICU), if not already there, for advanced monitoring and treatment. -The cardiovascular system is profoundly affected in the progressive stage of shock. CO begins to fall, resulting in a decrease in BP and coronary artery, cerebral, and peripheral perfusion. Continued decreased cellular perfusion and resulting altered capillary permeability are the distinguishing features of this stage. Altered capillary permeability allows fluid and protein to leak out of the vascular space into the surrounding interstitial space. In addition to the decrease in circulating volume, there is an increase in systemic interstitial edema. The patient may have anasarca (diffuse profound edema). Fluid leakage from the vascular space affects the solid organs (e.g., liver, spleen, GI tract, lungs) and peripheral tissues by further decreasing perfusion. -Sustained hypoperfusion results in weak peripheral pulses, and ischemia of the distal extremities eventually occurs. Myocardial dysfunction from decreased perfusion results in dysrhythmias, myocardial ischemia, and possibly MI. The result is a complete deterioration of the cardiovascular system. -The pulmonary system is often the first system to display signs of critical dysfunction. During the compensatory stage, blood flow to the lungs is already reduced. In response to the decreased blood flow and SNS stimulation, the pulmonary arterioles constrict, resulting in increased pulmonary artery (PA) pressure. As the pressure within the pulmonary vasculature increases, blood flow to the pulmonary capillaries decreases and ventilation-perfusion mismatch worsens. -Another key response in the lungs is the movement of fluid from the pulmonary vasculature into the interstitial space. As capillary permeability increases, the movement of fluid to the interstitial spaces results in interstitial edema, bronchoconstriction, and a decrease in functional residual capacity. With further increases in capillary permeability, fluid moves into the alveoli, causing alveolar edema and a decrease in surfactant production. The combined effects of pulmonary vasoconstriction and bronchoconstriction are impaired gas exchange, decreased compliance, and worsening ventilation-perfusion mismatch. Clinically, the patient has tachypnea, crackles, and an overall increased work of breathing. -The GI system is affected by prolonged decreased tissue perfusion. As the blood supply to the GI tract is decreased, the normally protective mucosal barrier becomes ischemic. This ischemia predisposes the patient to ulcers and GI bleeding. It increases the risk for bacterial migration from the GI tract to the blood and lungs. The decreased perfusion to the GI tract leads to a decreased ability to absorb nutrients. -The effect of prolonged hypoperfusion on the kidneys is renal tubular ischemia. The resulting acute tubular necrosis may lead to acute kidney injury (AKI). This can be worsened by nephrotoxic drugs (e.g., certain antibiotics, anesthetics, diuretics). The patient has decreased urine output and increased blood urea nitrogen (BUN) and serum creatinine. Metabolic acidosis occurs from the kidneys' inability to excrete acids (especially lactic acid) and reabsorb bicarbonate. -The sustained hypoperfusion in the progressive stage of shock greatly affects other organs. The loss of the functional ability of the liver leads to a failure of the liver to metabolize drugs and waste products (e.g., lactate, ammonia). Jaundice results from an accumulation of bilirubin. As the liver cells die, liver enzymes increase. The liver loses its ability to function as an immune organ. Kupffer cells no longer destroy bacteria from the GI tract. Instead, they are released into the bloodstream, increasing the possibility of bacteremia. -Dysfunction of the hematologic system adds to the complexity of the clinical picture. The patient is at risk for disseminated intravascular coagulation (DIC). The consumption of the platelets and clotting factors with secondary fibrinolysis results in clinically significant bleeding from many orifices. These include the GI tract, lungs, and puncture sites.

neurogenic shock symptoms

bradycardia, decreased BP, CO, CVP, SVR, fluctuating temp, resp dysfunction + bowel and bladder, cool or warm, dry, decreased perfusion, flaccid paralysis below lesion, loss of reflexes,

symptoms of progressive stage of shock

decreased cerebral perfusion pressure and blood flow, delirium, decreased responsiveness to stimuli, increase cap permeability-systemic interstitial edema, decreased CO +BP, increased HR, MAP under 60, decreased coronary perfusion - dysrhythmias, MI, myocardial ischemia, decreased peripheral perfusion- ischemia of distal extremities, decreased pulses and cap refill, cold and clammy, hypo or hyperthermia, DIC (thrombin clots in microcirculation, consumption of platelets and clotting factors), failure to metabolize drugs/waste products, increased liver enzymes with cell death, jaundice (can't clear bili), increased ammonia and lactate, increased urine sodium, decreased urine osmolality/specific gravity/potassium, met acid, decreased urine, increased bun-creatinine ratio, acute tubular necrosis (ischemic), vasoconstriction and decreased perfusion (ischemic gut), erosive ulcers, GI bleed, translocation of GI bacteria, impaired nutrient absorption, increased cap permeability, ARDS, pulmonary vasoconstriction and interstitial edema, alveolar edema, diffuse infiltrates, tachypnea, decreased compliance, moist crackles

obstructive shock

develops when a physical obstruction to blood flow occurs with a decreased CO. This can be caused by restricted diastolic filling of the right ventricle from compression (e.g., cardiac tamponade, tension pneumothorax, superior vena cava syndrome). Other causes include abdominal compartment syndrome, in which increased abdominal pressures compress the inferior vena cava. This decreases venous return to the heart. Pulmonary embolism and right ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through the pulmonary artery. This leads to decreased blood flow to the lungs and decreased blood return to the left atrium. -Patients have a decreased CO, increased afterload, and variable left ventricular filling pressures depending on the obstruction. Other signs include jugular venous distention and pulsus paradoxus. Rapid assessment and treatment are important to prevent further hemodynamic compromise and possible cardiac arrest

Treatment modalities for the management of cardiogenic shock include (select all that apply)

dobutamine to increase myocardial contractility, circulatory assist devices such as an intraaortic balloon pump

IO access

emergency resuscitation when IV access can't be obtained, insert into sternum, proximal or distal tibia, and proximal and distal humerus, remove within 24 hrs of insertion (asap when peripheral or central is there), monitor complications (extravasation of drugs and fluids into soft tissue/fractures caused during insertion, osteomyelitis)

isotonic fluid (LR, 0.9NS)

fluid primarily stays in intravascular space (increased), mostly initial replacement for shock monitor for circulatory overload. Don't use LR in liver failure. use LR if hyperchloremic acidosis from NS

Hypertonic (1.8, 3, 5 NaCl %)

fluid stays in intravascular space, increase serum osmolarity, shifts fluid from intra to extracellular to intravascular space initial volume expansion for hypovolemic shock monitor for hypernatremia (disorientated, seizures). central line preferred over 3% (damage veins)

diagnostic criteria for sepsis

general: altered mental state, fever 100.9+, HR over 90, high BG over 140 without diabetes, hypothermia under 97, SBP over 100, edema or positive fluid balance over 20 mL/kg in 24hrs, RR over 22 inflammatory variables- WBC below 4000 or above 12000 or normal with more than 10% bands, high crp/procal arterial hypotension SBP under 90, MAP under 70, decrease in SBP over 40 hyperlactatemia (over 1), mottling, decreased cap refill platelets under 100,000, serum creatinine increase over 0.5mg/dL, ileus (no bowel sounds), bilirubin above 4mg/dL, INR above 1.5 or PTT over 60, PF under 300, urine output under 0.5mL/kg/hr for 2 hrs with fluid resuscitation

vasopressin drug alert

give with norepi, infuse low dose using IV pump (0.03 units/min), no titration, use cautiously with CAD

neurogenic shock

hemodynamic consequence of sci at or above t5, spinal anesthesia, vasomotor center depression- severe pain, drugs, hypoglycemia, injury

Risk factor for heparin induced thrombocytopenia:

heparin therapy for deep vein thrombosis- receiving heparin therapy for longer than 1 week

Med for DIC:

heparin- decrease formation of microclots which deplete clotting factors

dextran 40

hyperosmotic glucose polymer. Limited with side effects (dilute clotting factors, platelet adhesion) increases bleeding risk, monitor for allergic rxn and AKI, has max volume recommendation

albumin 5-25%

increase plasma colloid osmotic pressure, rapid volume expansion, all types except cardiogenic/neurogenic use 5% in hypovolemic 25% with fluid/sodium restriction. monitor for circulatory overload. Mild side effects-chills, fever, urticaria. More expensive than crystalloids

angiotension II

increases BP, MAP, SVR, use for septic/distributive. Give central. Monitor for thromboembolic events. VTE prophylaxis is used

dobutamine

increases myocardial contractility, CO, SV, CVP, decreases ventricular filling pressure, SVR, PAWP used in cardiogenic shock with severe systolic dysfunction. used in septic shock to increase O2 delivery and raise SvO2 to 70+% if Hgb over 7 or HCt over 30. Give central (infiltration leads to tissue sloughing), don't give witih bicarb, monitor HR, BP (hypotension may worsen, give a pressor). Stop infusion with a tachydysrhythmia

septic shock causes

infection- uti, invasive procedures, pneumonia, peritonitis, indwelling lines and catheters at risk patients- older adults, patients with chronic disease (diabetes, ckd, hf), immunosuppressant therapy, malnourished, debilitated

A patient has a spinal cord injury at T4. Vital signs include falling blood pressure with bradycardia. The nurse recognizes that the patient is experiencing

neurogenic shock from massive vasodilation

Small vessel clotting with a client who has ITP

notify provider and report cyanotic nail beds (microvascular clotting, report immediately to avoid ischemic loss of fingers/toes)

hypovolemic shock

occurs from inadequate fluid volume in the intravascular space to support adequate perfusion. The volume loss may be either an absolute or a relative volume loss. Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. In relative hypovolemia, fluid volume moves out of the vascular space into the extravascular space (e.g., intracavitary space). We call this type of fluid shift third spacing. One example of relative volume loss is fluid leaking from the vascular space to the interstitial space from increased capillary permeability, as seen in burns. -Whether the loss of intravascular volume is absolute or relative, the physiologic consequences are similar. The reduced intravascular volume results in a decreased venous return to the heart, decreased preload, decreased SV, and decreased CO. A cascade of events results in decreased tissue perfusion and impaired cellular metabolism, the hallmarks of shock. -The patient's response to acute volume loss depends on several factors, including extent of injury, age, and general state of health. The clinical presentation of hypovolemic shock is consistent. An overall assessment of physiologic reserves may indicate the patient's ability to compensate. A patient may compensate for a loss of up to 15% of the total blood volume (around 750 mL). Further loss of volume (15% to 30%) results in a sympathetic nervous system (SNS)-mediated response. This response results in an increase in heart rate, CO, and respiratory rate and depth. The decreased circulating blood volume causes decreases in SV, central venous pressure (CVP), and PAWP. -The patient may appear anxious. Urine output begins to decrease. If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is generally reversible. If volume loss is greater than 30%, compensatory mechanisms may fail and immediate replacement with blood products should be started. Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with loss of more than 40% of the total blood volume. Common laboratory studies and assessments that are done include serial measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood gasses, mixed central venous O2 saturation (SvO2), and hourly urine outputs

compensatory stage manifestations of shock

oriented, restless, apprehensive, confused, change in LOC, release of epi/noepi (vasoconstriction), increased HR, contractility, MVO2, coronary artery dilation, narrow pulse pressure, decrease BP, pale and cool or warm and flushed, normal or abnormal temp, decreased blood supply, decreased gi motility, hypoactive bowel sounds, increased risk for paralytic ileus, decreased blood to lungs, tachypnea, increased minute ventilation and ventilation perfusion mismatch and physiologic dead space

obstructive shock causes

physical obstruction impeding the filling or outflow of blood resulting in reduced CO- cardiac tamponade, tension pneumothorax, superior vena cava syndrome, abdominal compartment syndrome, pulmonary embolism

Lab values with DIC that indicate clotting factors are depleted:

platelets 100,000 (decreased, clotting times increase raising risk for fatal hemorrhage), fibrinogen levels 120 mg/dL (decreased), increased FDP (D-Dimer)

dopamine

positive inotropic effects: increased myocardial contractility, automaticity, AV conduction, HR, CO, BP, MAP, MVO2, progressive vasoconstriction at high dose cardiogenic shock central line (infiltration leads to tissue sloughing), don't give with bicarb, monitor for peripheral vasoconstriction (paresthesias, cold extremities) at mod to high dose

Hypovolemic shock treatment

provide extra O2, monitor ScvO2/SvO2, rapid fluid replacement using 2 large bore 14-16 gauge peripheral or IO or central cath, resotre fluid volume (blood/blood product, crystalloid), end resuscitation when CVP 15mmHg, PAWP 10-12 mmHg correct cause (stop bleeding, GI loss), use warm IV fluids (blood)

septic shock treatment

provide extra O2, monitor ScvO2/SvO2, intubation/mech vent aggressive fluid resuscitation (30mL/kg crystalloids repeated if no hemodynamic improvement), end resuscitation with vitals/cardiopulmonary assesement, cap refill, peripheral pulses, skin on physical exam, or 2 of ScvO2 over 70 or SvO2 over 65, CVP 8-12 mmHg, cardiovascular ultrasound, responsiveness to fluid with passive leg raise or fluid challenge obtain cultures (blood/wound before abx), monitor temp, control bg, stress ulcer prevent anticoagulants (LMWH), inotrope (dobutamine), pressor (norepi), abx

cardiogenic shock treatment

provide supplemental O2 (nasal cannula, nonrebreather, intubate, mech vent), monitor ScvO2/SvO2. Restore blood flow with angioplasty with stenting (emergent coronary revascularization), reduce workload of heart with CAD, IABP, VAD, treat dysrhythmias, nitrates (nitroglycerin), inotropes (dobutamine), diuretics (furosemide), beta adrenergic blocker (contraindicated with low EF)

pathophys of hypovolemic shock

relative hypovolemia or absolute hypovolemia- decreased circulating volume, venous return, stroke volume, CO, cellular oxygen supply leads to decreased tissue perfusion and impaired cellular metabolism

diagnostic studies shock

respiratory alkalosis (hyperventilation) early, metabolic acidosis (late, lactate accumulation from anaerobic metabolism) -base deficit- more than -6 acid production with hypoxia, growth of organisms in culture, increased BUN- impaired kidney function caused by hypoperfusion from severe vasoconstriction or occurs due to cell catabolism (trauma, infection), increased creatinine kinase (trauma, MI in response to cellular damage and/or hypoxia), creatinine increased, DIC screen- increased PTT, Pt, INR, thrombin time, d-dimer, and fibrin split products, decreased fibrinogen, platelets (acute happens within hours to days of initial assault) -increased glucose early- release of liver glycogen stores in response to sns stimulation and cortisol. Insulin insensitivity develops, decreased depleted glycogen stores with liver dysfunction possible as shock progresses increased sodium early- increased aldosterone, renal retention, decreased later (iatrogenic if hypotonic excess fluid given); potassium increased with dead cell release, aki and acidosis, decreased early with increased aldosterone and renal excretion, increased lactate (impaired o2 at cellular level, byproduct of anaerobic metabolism, liver enzymes (ALT, AST, GGT) increased with liver cell destruction in progressive phase, procalcitonin increased (biomarker with bacterial infections), increased troponin MI, WBC increased or decreased (infection or septic shock); rbc/hct/hgb normal (relative hypovolemia, pump failure and hemorrhagic shock before fluid resuscitation, decreased after fluid resuscitation besides blood in hemorrhagic shock, increased in non hemorrhagic shock caused by actual hypovolemia and hemoconcentration

A 78-yr-old man with a history of diabetes has confusion and temperature of 104°F (40°C). There is a wound on his right heel with purulent drainage. After an infusion of 3 L of normal saline solution, his assessment findings are BP 84/40 mm Hg; heart rate 110; respiratory rate 42 and shallow; CO 8 L/min; and PAWP 4 mm Hg. This patient's symptoms are most likely indicative of

septic shock

cardiogenic shock causes

structural factors (valvular stenosis, regurgitation, ventricular septal rupture, tension pneumothorax), systolic dysfunction: inability of heart to pump blood forward- MI, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, myocardial depression from metabolic problems, dysrhythmias (brady or tachy), diastolic dysfunction: inability of heart to fill (cardiac tamponade, ventricular hypertrophy, cardiomyopathy)

etiology of shock

surgical- aortic dissection, gi bleed, postop bleed, ruptured ectopic pregnancy/ovarian cyst, ruptured organ/vessel, vaginal bleed medical: addisonian crisis, dehydrated, diabetes, diabetes inspidus, MI, PE, sepsis, trauma, fractures, spinal injury multiorgan injury

anaphylactic shock symptoms

tachycardia, Increased co, decreased cvp, Pawp, chest pain, third spacing of fluid, sob, stridor, rhinitis, wheezing, edema of larynx and epiglottis, incontinent, flushed, pruritus, urticaria, angioedema, anxiety, feeling of doom, confusion, metallic taste, decreased LOC, abd pain/cramps, n/v/d, sudden, history of allergies, exposed to contrast media

symptoms for cardiogenic shock

tachycardia, decreased BP, CO, cap refill, SV, increased SVR, PAWP, CVP, increased RR, crackles, cyanosis, increased NA and h20 retention, decreased urine and renal blood flow, pale, cool, clammy, decreased cerebral perfusion, anxiety, confusion, agitation, decreased bowel sounds, n/v, increased cardiac biomarkers (increased bnp), increased glucose and bun, left ventricular dysfunction, pulmonary infiltrates

obstructive shock symptoms

tachycardia, decreased BP, preload, CO, increased SVR/CVP, tachypnea to bradypnea (late), SOB, decreased urine, pale, cool, clammy, decreased cerebral perfusion, anxiety, confused, agitated, decreased/absent bowel sounds,

hypovolemic shock symptoms

tachycardia, decreased preload,, CO, CVP, PAWP, cap refill, increased SVR, bradypnea late/tachypnea early, decreased urine, pale, cool, clammy, decreased cerebral perfusion, anxious, confused, agitated, no bowel sounds, decreased hct/hgb, increased lactate, urine specific gravity, electrolyte changes

compensatory stage

the body activates neural, hormonal, and biochemical compensatory mechanisms to try to overcome the increasing consequences of anaerobic metabolism and maintain homeostasis. The patient's clinical presentation begins to reflect the body's responses to the imbalance in O2 supply and demand. A classic sign of shock is a drop in BP. This occurs because of a decrease in CO and a narrowing of the pulse pressure. The baroreceptors in the carotid and aortic bodies immediately respond by activating the SNS. The SNS stimulates vasoconstriction and the release of the potent vasoconstrictors epinephrine and norepinephrine. Blood flow to the heart and brain is maintained. Blood flow to the nonvital organs, such as kidneys, GI tract, skin, and lungs, is diverted or shunted. -The myocardium responds to the SNS stimulation and the increase in O2 demand by increasing the heart rate and contractility. Increased contractility increases myocardial O2 consumption. The coronary arteries dilate to try to meet the increased O2 demands of the myocardium. Shunting blood away from the lungs has an important clinical effect in the patient in shock. Decreased blood flow to the lungs increases the patient's physiologic dead space. Physiologic dead space is the anatomic dead space (the amount of air that will not reach gas-exchanging units) and any inspired air that cannot take part in gas exchange. The clinical result of an increase in dead space ventilation is a ventilation-perfusion mismatch. Some areas of the lungs that are being ventilated will not be perfused because of the decreased blood flow to the lungs. Arterial O2 levels will decrease, and the patient will have a compensatory increase in the rate and depth of respirations. -The shunting of blood from other organ systems results in clinically important changes. The decrease in blood flow to the GI tract results in impaired motility and a slowing of peristalsis. This increases the risk for a paralytic ileus. -Decreased blood flow to the skin results in the patient feeling cool and clammy. The exception is the patient in early septic shock who may feel warm and flushed because of a hyperdynamic state. Decreased blood flow to the kidneys activates the renin-angiotensin system. Renin stimulates angiotensinogen to make angiotensin I, which is then converted to angiotensin II. Angiotensin II is a potent vasoconstrictor that causes both arterial and venous vasoconstriction. The net result is an increase in venous return to the heart and an increase in BP. Angiotensin II stimulates the adrenal cortex to release aldosterone. This results in sodium and water reabsorption and potassium excretion by the kidneys. The increase in sodium reabsorption raises the serum osmolality and stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH increases water reabsorption by the kidneys, further increasing blood volume. The increase in total circulating volume results in an increase in CO and BP. -A multisystem response to decreasing tissue perfusion starts during the compensatory stage of shock. At this stage, the body can compensate for the changes in tissue perfusion. If the cause of the shock is corrected, the patient will recover with little or no residual effects. If the cause of the shock is not corrected and the body is unable to compensate, the patient enters the progressive stage of shock.

refractory stage of shock

unrepsonsive, areflexia (loss of reflexes), nonreactive pupils, bad hypotension, decreased CO/BP (can't perfuse organs), decreased HR (irregular), severe refractory hypoxemia, resp failure, ischemic gut, anuria, accumulation of waste products (NH3, lactate, CO2), DIC progresses, hypothermia, mottled, cyanotic

nitroglycerin

venous dilation, dilates coronary arteries, decreased preload, MVO2, SVR, BP cardiogenic shock continuously monitor BP, HR since reflex tachy is happening, glass bottle recommended for infusion

complications of fluid resuscitation

warm crystalloid and colloid solutions during massive transfusion to prevent hypothermia, when giving large volumes of packed RBCs remember they don't clot, replace clotting factors based on clinical picture and labs