NU 373 - Week 1 - Shock

Anaphylactic shock - primary characteristics

(1) Acute onset of symptoms, (2) Presence of two or more symptoms that include respiratory compromise, reduced BP, GI distress, and skin or mucosal tissue irritation, (3) Cardiovascular compromise from minutes to hours after exposure to the antigen.

Hypovolemia - risk factors

(1) External risk factors: fluid losses, such as trauma, surgery, vomiting, diarrhea, diuresis, diabetes insipidus, etc. (2) Internal risk factors: fluid shifts, such as hemorrhage, burns, ascites, peritonitis, dehydration, necrotizing pancreatitis, etc.

Progressive stage of shock - cardiovascular manifestations

A lack of adequate blood supply leads to dysrhythmias and ischemia. The heart rate is rapid, sometimes exceeding 150 bpm. The patient may complain of chest pain and even suffer a myocardial infarction (MI). Levels of cardiac biomarkers (e.g., cardiac troponin I [cTn-I]) increase. In addition, myocardial depression and ventricular dilation may further impair the heart's ability to pump enough blood to the tissues to meet increasing oxygen requirements.

Abdominal compartment syndrome (ACS)

ACS is a serious complication that may occur when large volumes of fluid are given. It may also occur after trauma, abdominal surgery, pancreatitis, or sepsis. In ACS, fluid leaks into the intra-abdominal cavity, increasing pressure that is displaced onto surrounding vessels and organs. Venous return, preload, and cardiac output are compromised. The pressure also elevates the diaphragm, making it difficult to breathe effectively. The renal and GI systems also begin to show signs of dysfunction (e.g., decreased urine output, absent bowel sounds, intolerance of tube feeding). Abdominal compartment pressure can be measured. Normally, it is 0 to 5 mm Hg, and a pressure of 12 mm Hg is considered to be indicative of IAH. If ACS is present, interventions that usually include surgical decompression are necessary to relieve the pressure.

Multiple organ dysfunction syndrome - clinical manifestations after 7-10 days

After approximately 7 to 10 days, signs of hepatic dysfunction (e.g., elevated bilirubin and liver function tests) and renal dysfunction (e.g., elevated creatinine and anuria) are evident. As the lack of tissue perfusion continues, the hematologic system becomes dysfunctional, with worsening immunocompromise, increasing the risk of bleeding. The cardiovascular system becomes unstable and unresponsive to vasoactive agents, and the patient's neurologic response progresses to a state of unresponsiveness or coma. The goal of all shock states is to reverse the tissue hypoperfusion and hypoxia. If effective tissue perfusion is restored before organs become dysfunctional, the patient's condition stabilizes. Along the septic shock continuum, the onset of organ dysfunction is an ominous prognostic sign; the more organs that fail, the worse the outcome.

Sepsis - nutritional therapy

Aggressive nutritional supplementation within 24-48 hours of ICU admission to address hypermetabolic state. Malnutrition further impairs the ability to fight infection. Enteral feedings preferred, unless perfusion to the GI tract reduces peristalsis and absorption.

Anaphylactic shock

Anaphylactic shock is caused by a severe allergic reaction when patients who have already produced antibodies to a foreign substance (antigen) develop a systemic antigen-antibody reaction; specifically, an immunoglobulin E (IgE)-mediated response. This antigen-antibody reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin, and activates inflammatory cytokines, causing widespread vasodilation and capillary permeability. The most common triggers are foods (especially peanuts), medications, and insects.

Progressive stage of shock - neurologic manifestations

As blood flow to the brain becomes impaired, mental status deteriorates. Changes in mental status occur with decreased cerebral perfusion and hypoxia. Initially, the patient may exhibit subtle changes in behavior, become agitated, confused, or demonstrate signs of delirium. Subsequently, lethargy increases, and the patient begins to lose consciousness.

Clinical manifestations during the later stages of sepsis

As sepsis progresses, tissues become less perfused and acidotic, compensation begins to fail, and the patient begins to show signs of organ dysfunction. The cardiovascular system also begins to fail, the BP does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (e.g., AKI, pulmonary dysfunction, hepatic dysfunction, confusion progressing to nonresponsiveness). As sepsis progresses to septic shock, the BP drops and the skin becomes cool, pale, and mottled. Temperature may be normal or below normal. Heart and respiratory rates remain rapid. Urine production ceases, and multiple organ dysfunction progressing to death occurs.

Cardiogenic shock - treating underlying causes - coronary causes

As with all forms of shock, the underlying cause of cardiogenic shock must be corrected. It is necessary first to treat the oxygenation needs of the heart muscle to ensure its continued ability to pump blood to other organs. In the case of coronary cardiogenic shock (e.g., acute coronary syndromes, acute MI), the patient may require thrombolytics (fibrinolytics) therapy, a percutaneous coronary intervention, coronary artery bypass graft surgery, intra-aortic balloon pump therapy, ventricular assist device, or some combination of these treatments.

Compensatory stage of shock - nursing management

Assess the patient for risk of shock. Recognize subtle clinical changes of this stage before the patient's BP begins to drop. Identify cause of shock, administer IV fluids and oxygen, obtain necessary laboratory tests to rule out and treat metabolic imbalances or infection. Monitor tissue perfusion: Level of consciousness, vital signs, urinary output, skin changes, RR, and lab values; Serum NA and blood glucose will elevate initially as a response to aldosterone and catecholamines; If infection is suspected, blood cultures BEFORE administrating antibiotics. Reduce anxiety. Promote safety: Close monitoring, frequent reorientation, hourly rounding, and implementing interventions to prevent falls (e.g., bed alarms) are essential.

Hypovolemia - IV requirements

At least two large-gauge IV lines are inserted to establish access for fluid administration. If an IV catheter cannot be quickly inserted, an intraosseous catheter may be used for access in the sternum, legs (tibia), or arms (humerus) to facilitate rapid fluid replacement. Multiple IV lines allow simultaneous administration of fluid, medications, and blood component therapy if required. Because the goal of the fluid replacement is to restore intravascular volume, it is necessary to administer fluids that will remain in the intravascular compartment to avoid fluid shifts from the intravascular compartment into the intracellular compartment.

Blood pressure - baroreceptors

BP is regulated by baroreceptors (pressure receptors) located in the carotid sinus and aortic arch. These pressure receptors are responsible for monitoring the circulatory volume and regulating neural and endocrine activities. When BP drops, catecholamines (e.g., epinephrine, norepinephrine) are released from the adrenal medulla. These increase heart rate and cause vasoconstriction, restoring BP. Chemoreceptors, also located in the aortic arch and carotid arteries, regulate BP and respiratory rate using much the same mechanism in response to changes in oxygen and carbon dioxide (CO2) concentrations in the blood. These primary regulatory mechanisms can respond to changes in BP on a moment-to-moment basis.

Interventions to be completed ASAP or within first 6 hours of onset of sepsis symptoms

Begin vasopressor agents if hypotension is not improved (MAP < 65 mm Hg) after initial fluid resuscitation. If hypotension persists after initial fluid administration (MAP <65 mm Hg) or initial lactate was ≥4 mmol/L, reassess intravascular volume status and tissue perfusion using two of the following assessment parameters: Measure CVP (goal 8-12 mm Hg); Measure Scv¯O2 (goal > 70%); Bedside cardiovascular ultrasound; Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge.

Hypovolemia treatment - blood products

Blood products, which are also colloids, may need to be given, particularly if the cause of the hypovolemic shock is hemorrhage. The decision to give blood is based on the patient's lack of response to crystalloid resuscitation, the volume of blood lost, the need for hemoglobin to assist with oxygen transport, and the necessity to correct the patient's coagulopathy. Patients requiring massive transfusion respond better when blood products are given in a 1:1:1: ratio, meaning units of plasma, platelets, and packed red blood cells. Packed red blood cells are given to replenish the patient's oxygen-carrying capacity in conjunction with other fluids that will expand volume. Plasma and platelets are transfused to assist with coagulation and hemostasis. The need for transfusions is based on the patient's oxygenation needs and coagulation status, which are determined by vital signs, blood gas, chemistry, coagulation laboratory values, and clinical appearance.

Cardiogenic shock

Cardiogenic shock occurs when the heart's ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and the tissues. The causes of cardiogenic shock are known as either coronary or noncoronary. Coronary cardiogenic shock is more common than noncoronary cardiogenic shock and is seen most often in patients with acute MI resulting in damage to a significant portion of the left ventricular myocardium. Patients who experience an anterior wall MI are at greatest risk for cardiogenic shock because of the potentially extensive damage to the left ventricle caused by occlusion of the left anterior descending coronary artery. Noncoronary causes of cardiogenic shock are related to conditions that stress the myocardium (e.g., severe hypoxemia, acidosis, hypoglycemia, hypocalcemia, tension pneumothorax) as well as conditions that result in ineffective myocardial function (e.g., cardiomyopathies, valvular damage, cardiac tamponade, dysrhythmias).

Potential complications of fluid resuscitation

Care must be taken when rapidly administering isotonic crystalloids to avoid both underresuscitating and overresuscitating the patient in shock. Insufficient fluid replacement is associated with a higher incidence of morbidity and mortality from lack of tissue perfusion, whereas excessive fluid administration can cause systemic and pulmonary edema that progresses to ALI, intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS), and multiple organ dysfunction syndrome (MODS). The most common and serious side effects of fluid replacement are cardiovascular overload, pulmonary edema, and ACS.

Nursing management during the progressive stage of shock - ICU care

Close hemodynamic monitoring, ECG, arterial blood gases, electrolyte levels, physical/mental status changes. Rapid and frequent administration of medications and fluids. Supportive technologies such as mechanical ventilation, dialysis, and intra-aortic balloon pumps. Collaborative care, thorough and complete documentation.

Shock - compensatory vs progressive vs irreversible stages - heart rate

Compensatory: >100bpm. Progressive: >150bpm. Irreversible: erratic.

Shock - compensatory vs progressive vs irreversible stages - respiratory status

Compensatory: >20 breaths/min. PaCO2 <32 mm Hg. Progressive: Rapid, shallow respirations; crackles. PaO2 <80 mm Hg. PaCO2 >45 mm Hg. Irreversible: Requires intubation and mechanical ventilation and oxygenation.

Shock - compensatory vs progressive vs irreversible stages - skin

Compensatory: cold, clammy. Progressive: mottled, petechiae. Irreversible: Jaundice.

Shock - compensatory vs progressive vs irreversible stages - mentation

Compensatory: confusion and/or agitation. Progressive: lethargy. Irreversible: unconscious.

Shock - compensatory vs progressive vs irreversible stages - urinary output

Compensatory: decreased. Progressive: <0.5 mL/kg/h. Irreversible: anuric; requires dialysis.

Shock - compensatory vs progressive vs irreversible stages - blood pressure

Compensatory: normal. Progressive: Systolic <90 mm Hg; MAP <65 mm Hg. Requires fluids resuscitation to support blood pressure. Irreversible: Requires mechanical or pharmacologic support.

Shock - compensatory vs progressive vs irreversible stages - acid-base balance

Compensatory: respiratory alkalosis. Progressive: metabolic acidosis. Irreversible: profound acidosis.

Irreversible / refractory stage of shock - nursing management

Continue to carry out prescribed treatments, continued monitoring, prevent complications, protect from injury, provide comfort. Offer explanations to the patient (unclear if they will hear or comprehend). Comfort measures (reassuring touches). Care for the family (educate, inform, and allow them to see, touch, and talk to the patient). Advanced directives, end of life decisions. Engage palliative care specialists.

Hypovolemia treatment - crystalloids and colloids

Crystalloid solutions such as lactated Ringer's solution or 0.9% sodium chloride solution are commonly used to treat hypovolemic shock, as large amounts of fluid must be given to restore intravascular volume. If hypovolemia is primarily due to blood loss, the American College of Surgeons recommends administration of 3 mL of crystalloid solution for each milliliter of estimated blood loss. This is referred to as the 3:1 rule. Colloid solutions (e.g., albumin) may also be used. Hetastarch and dextran solutions are not indicated for fluid administration because these agents interfere with platelet aggregation.

Progressive stage of shock - hepatic manifestations

Decreased blood flow to the liver impairs the ability of liver cells to perform metabolic and phagocytic functions. Consequently, the patient is less able to metabolize medications and metabolic waste products, such as ammonia and lactic acid. Metabolic activities of the liver, including gluconeogenesis and glycogenolysis, are impaired. The patient becomes more susceptible to infection as the liver fails to filter bacteria from the blood. Liver enzymes (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase,) and bilirubin levels are elevated, and the patient develops jaundice.

Distributive shock

Distributive shock occurs when intravascular volume pools in peripheral blood vessels. This abnormal displacement of intravascular volume causes a relative hypovolemia because not enough blood returns to the heart, which leads to inadequate tissue perfusion. The ability of the blood vessels to constrict helps return the blood to the heart. The vascular tone is determined both by central regulatory mechanisms, as in BP regulation, and by local regulatory mechanisms, such as tissue demands for oxygen and nutrients. Therefore, distributive shock can be caused by either a loss of sympathetic tone or a release of biochemical mediators from cells that causes vasodilation.

Discontinuing vasoactive medications when treating patients with shock

Dosages of vasoactive medications must be tapered. When vasoactive medications are no longer needed or are necessary to a lesser extent, the infusion should be weaned with frequent monitoring of BP (e.g., every 15 minutes). Stopping abruptly can lead to severe hemodynamic instability and worsening state of shock.

Crystalloids - examples, advantages, disadvantages

Examples: 0.9% Sodium chloride (normal saline solution), Lactated Ringer's. Advantages: Widely available, inexpensive. Lactate ion that helps buffer metabolic acidosis. Disadvantages: Requires large volume of infusion; can cause hypernatremia, pulmonary edema, abdominal compartment syndrome. Requires large volume of infusion; can cause metabolic acidosis, pulmonary edema, abdominal compartment syndrome.

Colloids - examples, advantages, disadvantages

Examples: Albumin (5%, 25%). Advantages: Rapidly expands plasma volume. Disadvantages: Expensive; requires human donors; limited supply; can cause heart failure.

Vasoactive inotropic agents to treat shock - examples, desired action, disadvantages

Examples: Dobutamine (Dobutrex), Dopamine (Intropin), Epinephrine (Adrenalin), Milrinone (Primacor). Desired action in shock: Improves contractility, increase stroke volume, increase cardiac output. Disadvantages: Increases oxygen demand of the heart.

Vasodilators to treat shock - examples, desired action, disadvantages

Examples: Nitroglycerin (Tridil), Nitroprusside (Nipride). Desired action in shock: Reduce preload and afterload, reduce oxygen demand of heart. Disadvantages: Cause hypotension.

Vasopressor agents to treat shock - examples, desired action, disadvantages

Examples: Norepinephrine (Levophed), Dopamine (Intropin), Phenylephrine (Neo-Synephrine), Vasopressin (Pitressin), Epinephrine (Adrenalin). Desired action in shock: Increase blood pressure by vasoconstriction. Disadvantages: Increase afterload, thereby increasing cardiac workload; compromise perfusion to skin, kidneys, lungs, gastrointestinal tract. Note: Use a volumetric IV pump when administering vasopressors and monitor for complications and side effects.

Blood products - examples, advantages, disadvantages

Examples: Plasma, packed red blood cells, and platelets. Advantages: Rapidly replaces volume lost due to hemorrhage. Disadvantages: Cross-match type-specific blood is desired for optimal massive transfusion protocols to reduce transfusion-related complications (e.g., transfusion-related acute lung injury, hemolytic reactions, transfusion-associated circulatory overload).

Types of fluid replacement for patients in shock

Fluid replacement, also referred to as fluid resuscitation, is given in all types of shock. The type of fluids given and the speed of delivery vary; however, fluids are given to improve cardiac and tissue oxygenation, which in part depends on flow. The fluids given may include crystalloids (electrolyte solutions that move freely between intravascular compartment and interstitial spaces), colloids (large-molecule IV solutions), and blood components (packed red blood cells, fresh frozen plasma, and platelets).

Progressive stage of shock - GI manifestations

GI ischemia can cause stress ulcers in the stomach, putting the patient at risk for GI bleeding. In the small intestine, the mucosa can become necrotic and slough off, causing bloody diarrhea. Beyond the local effects of impaired perfusion, GI ischemia leads to bacterial translocation and organ dysfunction, in which bacterial toxins enter the bloodstream through the lymphatic system. In addition to causing infection, bacterial toxins can cause cardiac depression, vasodilation, increased capillary permeability, and an intense inflammatory response with activation of additional biochemical mediators. The net result is interference with healthy cellular functioning and the ability to metabolize nutrients.

What are the five key elements of the central line bundle? (to prevent CLABSI)

Hand hygiene. Maximal sterile barrier precautions during line insertion. Chlorhexidine skin antisepsis. Optimal catheter site selection with avoidance of using the femoral vein for central venous access in adult patients. Daily review of line necessity, with prompt removal of unnecessary lines.

Risk factors for anaphylactic shock

History of medication sensitivity, Transfusion reaction, History of reaction to insect bites/stings, Food allergies, Latex sensitivity

Hypertonic crystalloid solutions to replace fluids in patients with shock

Hypertonic crystalloid solution, often 3% sodium chloride, may be given in patients with shock and traumatic brain injury. These solutions exert a large osmotic force that pulls fluid from the intracellular space to the extracellular space to achieve a fluid balance. This osmotic effect results in fewer fluids being given to restore intravascular volume, which is important in a patient with a head injury and cerebral swelling. Current research suggests that using hypertonic crystalloid solution does not improve patient outcomes and may result in unintended complications. Complications that may be associated with the use of hypertonic solutions include excessive serum osmolality, which can cause rapid fluid shifts, overwhelming the heart and leading to hypernatremia.

Hypovolemic shock - Pathophysiology

Hypovolemic shock can be caused by external fluid losses, as in traumatic blood loss, or by internal fluid shifts, as in severe dehydration, severe edema, or ascites. Intravascular volume can be reduced by both fluid loss and fluid shifting between the intravascular and interstitial compartments. The sequence of events in hypovolemic shock begins with a decrease in the intravascular volume. This results in decreased venous return of blood to the heart and subsequent decreased ventricular filling. Decreased ventricular filling results in decreased stroke volume (amount of blood ejected from the heart) and decreased cardiac output. When cardiac output drops, BP drops and tissues cannot be adequately perfused.

Hypovolemic shock

Hypovolemic shock, the most common type of shock, is characterized by decreased intravascular volume. Body fluid is contained in the intracellular and extracellular compartments. Intracellular fluid accounts for about two-thirds of the total body water. The extracellular body fluid is found in one of two compartments: intravascular (inside blood vessels) or interstitial (surrounding tissues). The volume of interstitial fluid is about three to four times that of intravascular fluid. Hypovolemic shock occurs when there is a reduction in intravascular volume by 15% to 30%, which represents an approximate loss of 750 to 1,500 mL of blood in a 70-kg (154-lb) person.

Colloidal solutions to replace fluids in patients with shock

IV colloidal solutions are similar to plasma proteins, in that they contain molecules that are too large to pass through capillary membranes. Colloids expand intravascular volume by exerting oncotic pressure, thereby pulling fluid into the intravascular space, increasing intravascular volume. In addition, colloids have a longer duration of action than crystalloids, because the molecules remain within the intravascular compartment longer. Typically, if colloids are used to treat tissue hypoperfusion, albumin is the agent prescribed. Albumin is a plasma protein; an albumin solution is prepared from human plasma and is heated during production to reduce its potential to transmit disease. The disadvantage of albumin is its high cost compared to crystalloid solutions. Resuscitation with colloid solutions has not reduced the risk of morbidity or death compared to resuscitation with crystalloid solutions; moreover, colloids can be considerably more expensive than crystalloid solutions.

Cardiogenic shock - nursing management - prevention

Identifying at-risk patients early, promoting adequate oxygenation of the heart muscle, and decreasing cardiac workload can prevent cardiogenic shock. This can be accomplished by conserving the patient's energy, promptly relieving angina, and administering supplemental oxygen. Often, however, cardiogenic shock cannot be prevented. In such instances, nursing management includes working with other members of the health care team to prevent shock from progressing and to restore adequate cardiac function and tissue perfusion.

Cardiogenic shock - pain control

If a patient experiences chest pain, IV morphine is given for pain relief. In addition to relieving pain, morphine dilates the blood vessels. This reduces the workload of the heart by both decreasing the cardiac filling pressure (preload) and reducing the pressure against which the heart muscle has to eject blood (afterload). Morphine may also decrease the patient's anxiety.

Cardiogenic shock - mechanical assistive devices

If cardiac output does not improve despite supplemental oxygen, vasoactive medications, and fluid boluses, mechanical assistive devices are used temporarily to improve the heart's ability to pump. Intra-aortic balloon counterpulsation is one means of providing temporary circulatory assistance. Other means of mechanical assistance include left and right ventricular assist devices and total temporary artificial hearts. Another short-term means of providing cardiac or pulmonary support to the patient in cardiogenic shock is through an extracorporeal device similar to the cardiopulmonary bypass (CPB) system used in open-heart surgery. CPB is used only in emergency situations until definitive treatment, such as heart transplantation, can be initiated.

Hypovolemic shock - pharmacologic therapy

If fluid administration fails to reverse hypovolemic shock, then vasoactive medications that prevent cardiac failure are given. Medications are also given to reverse the cause of the dehydration. For example, insulin is given if dehydration is secondary to hyperglycemia, desmopressin (DDAVP) is given for diabetes insipidus, antidiarrheal agents for diarrhea, and antiemetic medications for vomiting.

Sepsis - pharmacological interventions

If infection unknown, broad-spectrum antibiotic agents, then changed to target specific organism. If fluids unsuccessful, vasopressor agents (norepinephrine and dopamine). MAP >65 mm Hg. Inotropic agents to support the myocardium. RBCs to support oxygen transportation. Neuromuscular blockage agents and sedation to reduce metabolic demands and provide comfort. DVT prophylaxis with low-dose heparin and mechanical prophylaxis. Stress ulcer prophylaxis (h2 blockers, PPIs).

MODS - medical management

If preventive measures fail, treatment measures to reverse MODS are aimed at (1) controlling the initiating event, (2) promoting adequate organ perfusion, (3) providing nutritional support, and (4) maximizing patient comfort.

Multiple organ dysfunction syndrome - initial clinical manifestations

In MODS, the sequence of organ dysfunction varies depending on the patient's primary illness and comorbidities before experiencing shock. For simplicity of presentation, the classic pattern is described. Typically, the lungs are the first organs to show signs of dysfunction. The patient experiences progressive dyspnea and respiratory failure that are manifested as ALI or ARDS, requiring intubation and mechanical ventilation. The patient usually remains hemodynamically stable but may require increasing amounts of IV fluids and vasoactive agents to support BP and cardiac output. Signs of a hypermetabolic state, characterized by hyperglycemia (elevated blood glucose level), hyperlactic acidemia (excess lactic acid in the blood), and increased BUN, are present. The metabolic rate may be 1.5 to 2 times the basal metabolic rate. At this time, there is a severe loss of skeletal muscle mass (autocatabolism) to meet the high energy demands of the body.

Positioning during fluid administration of fluids to treat hypovolemic shock

In addition to administering fluids to restore intravascular volume, positioning the patient properly assists fluid redistribution. A modified Trendelenburg position, also known as passive leg raising, is recommended in hypovolemic shock. Elevation of the legs promotes the return of venous blood and can be used as a dynamic assessment of a patient's fluid responsiveness. The nurse assesses for an improvement in the patients vital signs, specifically a rise in the BP and return of the pulse pressure to normal or near normal. A full Trendelenburg position makes breathing difficult and does not increase BP or cardiac output.

Distributive shock - general pathophysiology

In all types of distributive shock, massive arterial and venous dilation promotes peripheral pooling of blood. Arterial dilation reduces systemic vascular resistance. Initially, cardiac output can be high, both from the reduction in afterload (systemic vascular resistance) and from the heart muscle's increased effort to maintain perfusion despite the incompetent vasculature. Pooling of blood in the periphery results in decreased venous return. Decreased venous return results in decreased stroke volume and decreased cardiac output. Decreased cardiac output, in turn, causes decreased BP and ultimately decreased tissue perfusion.

Cardiogenic shock - pathophysiology

In cardiogenic shock, cardiac output, which is a function of both stroke volume and heart rate, is compromised. When stroke volume and heart rate decrease or become erratic, BP falls and tissue perfusion is reduced. Blood supply for tissues and organs and for the heart muscle itself is inadequate, resulting in impaired tissue perfusion. Because impaired tissue perfusion weakens the heart and impairs its ability to pump, the ventricle does not fully eject its volume of blood during systole. As a result, fluid accumulates in the lungs. This sequence of events can occur rapidly or over a period of days.

Cardiogenic shock - pharmacologic therapy

In coronary cardiogenic shock, the aims of vasoactive medication therapy are improved cardiac contractility, decreased preload and afterload, and stabilized heart rate and rhythm. Because improving contractility and decreasing cardiac workload are opposing pharmacologic actions, two types of medications may be given in combination: inotropic agents and vasodilators. Inotropic medications increase cardiac output by mimicking the action of the sympathetic nervous system, activating myocardial receptors to increase myocardial contractility (inotropic action), or increasing the heart rate (chronotropic action). These agents may also enhance vascular tone, increasing preload. Vasodilators are used primarily to decrease afterload, reducing the workload of the heart and oxygen demand. Vasodilators also decrease preload.

Neurogenic shock - pathophysiology

In neurogenic shock, vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation. Sympathetic stimulation causes vascular smooth muscle to constrict, and parasympathetic stimulation causes vascular smooth muscle to relax or dilate. The patient experiences a predominant parasympathetic stimulation that causes vasodilation lasting for an extended period, leading to a relative hypovolemic state. However, blood volume is adequate, because the vasculature is dilated; the blood volume is displaced, producing a hypotensive (low BP) state. The overriding parasympathetic stimulation that occurs with neurogenic shock causes a drastic decrease in the patient's systemic vascular resistance and bradycardia. Inadequate BP results in the insufficient perfusion of tissues and cells that is common to all shock states.

How do cells generate energy while the body is in shock?

In shock, the cells lack an adequate blood supply and are deprived of oxygen and nutrients; therefore, they must produce energy through anaerobic metabolism. This results in low-energy yields from nutrients and an acidotic intracellular environment. Because of these changes, normal cell function ceases. The cell swells and the cell membrane becomes more permeable, allowing electrolytes and fluids to seep out of and into the cell. The sodium-potassium pump becomes impaired; cell structures, primarily the mitochondria, are damaged, and death of the cell results.

Gluconeogenesis during shock

In stress states, catecholamines, cortisol, glucagons, and inflammatory (i.e., cytokines) are released, causing hyperglycemia and insulin resistance to mobilize glucose for cellular metabolism. Activation of these substances promotes gluconeogenesis, which is the formation of glucose from noncarbohydrate sources such as proteins and fats. Glycogen that has been stored in the liver is converted to glucose through glycogenolysis to meet metabolic needs, increasing the blood glucose concentration (i.e., hyperglycemia). Continued activation of the stress response by shock states causes a depletion of glycogen stores, resulting in increased proteolysis and eventual organ failure. The deficit of nutrients and oxygen for normal cellular metabolism causes a buildup of metabolic end products in the cells and interstitial spaces.

Cardiogenic shock - treating underlying causes - noncoronary causes

In the case of noncoronary cardiogenic shock, interventions focus on correcting the underlying cause, such as replacement of a faulty cardiac valve, correction of a dysrhythmia, correction of acidosis and electrolyte disturbances, or treatment of a tension pneumothorax. If the cause of the cardiogenic shock was related to a cardiac arrest, once the patient is successfully resuscitated, targeted temperature management, also called therapeutic hypothermia, may be initiated to actively lower the body temperature to a targeted core temperature (e.g., 32°C [89.6°F] to 36°C [96.8°F]) to preserve neurologic function.

Compensatory stage of shock

In the compensatory stage of shock, the BP remains within normal limits. Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to maintaining adequate cardiac output. This results from stimulation of the sympathetic nervous system and subsequent release of catecholamines (e.g., epinephrine, norepinephrine). Patients display the often-described "fight-or-flight" response. The body shunts blood from organs such as the skin, kidneys, and gastrointestinal (GI) tract to the brain, heart, and lungs to ensure adequate blood supply to these vital organs. As a result, the skin may be cool and pale, bowel sounds are hypoactive, and urine output decreases in response to the release of aldosterone and ADH. If treatment begins in this stage of shock, the prognosis for the patient is better than in later stages.

Cardiogenic shock - oxygenation

In the early stages of shock, supplemental oxygen is given by nasal cannula at a rate of 2 to 6 L/min to achieve an oxygen saturation exceeding 95%. Monitoring of arterial blood gas values, pulse oximetry values, and ventilatory effort (i.e., work of breathing) helps determine whether the patient requires a more aggressive method of oxygen delivery (including noninvasive and invasive mechanical ventilation).

Progressive stage of shock

In the second stage of shock, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits. Patients are clinically hypotensive; this is defined as a systolic BP of less than 90 mm Hg or a decrease in systolic BP of 40 mm Hg from baseline. The patient shows signs of declining mental status. Overworked heart becomes dysfunctional, inability to meet oxygen demands produces ischemia. Biochemical mediators cause myocardial depression leading to heart failure. Autoregulatory function of the microcirculation fails to respond to increased biochemical mediators released by the cells, resulting in capillary permeability. There is a relaxation of precapillary sphincters which causes fluid to leak out of the capillaries, creating interstitial edema and decreased return to the heart. Inflammatory response to injury is activated, releasing anti-inflammatory mediators, which activate the coagulation system - to reestablish homeostasis. Body mobilizes energy stores and increases O2 consumption to meet increased metabolism needs of underperfused cells. Anaerobic metabolism ensues which will create an increased buildup of lactic acid and disruption of normal cell function.

Nutritional support when treating patients with shock

Increased metabolic rates during shock increase energy requirements and therefore caloric requirements. Patients in shock may require more than 3000 calories daily. The release of catecholamines early in the shock continuum causes rapid depletion of glycogen stores. Nutritional energy requirements are then met by breaking down lean body mass. In this catabolic process, skeletal muscle mass is broken down even when the patient has large stores of fat or adipose tissue. Loss of skeletal muscle greatly prolongs the patient's recovery time. Parenteral or enteral nutritional support should be initiated as soon as possible. Enteral nutrition is preferred, promoting GI function through direct exposure to nutrients and limiting infectious complications associated with parenteral feeding. Implementing early enteral nutrition has been found to promote gut-mediated immunity, reduce metabolic response to stress, and improve overall patient morbidity and mortality.

Compensatory stage of shock - clinical manifestations

Increased respiratory rate, increased HR, cool/clammy skin, decreased urinary output, confusion and/or agitation, metabolic acidosis, respiratory alkalosis. The result of inadequate perfusion is anaerobic metabolism and a buildup of lactic acid, producing metabolic acidosis. The respiratory rate increases in response to the need to increase oxygen to the cells and in compensation for metabolic acidosis. This rapid respiratory rate facilitates removal of excess CO2 but raises the blood pH and often causes a compensatory respiratory alkalosis. The patient may experience a change in affect, feel anxious, or be confused.

Isotonic crystalloid solutions to replace fluids in patients with shock

Isotonic crystalloid solutions are often selected because they contain the same concentration of electrolytes as the extracellular fluid and, therefore, can be given without altering the concentrations of electrolytes in the plasma. IV crystalloids commonly used for resuscitation in hypovolemic shock include 0.9% sodium chloride solution (normal saline) and lactated Ringer's solution. Ringer's lactate is an electrolyte solution containing the lactate ion, which should not be confused with lactic acid. The lactate ion is converted to bicarbonate, which helps buffer the overall acidosis that occurs in shock. A disadvantage of using isotonic crystalloid solutions is that some of the volume given is lost to the interstitial compartment and some remains in the intravascular compartment. This occurs as a consequence of cellular permeability that occurs during shock. Diffusion of crystalloids into the interstitial space means that more fluid may need to be given than the amount lost to support tissue perfusion.

Neurogenic shock - nursing management

It is important to elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when a patient receives spinal or epidural anesthesia. Elevation of the head helps prevent the spread of the anesthetic agent up the spinal cord. In suspected spinal cord injury, neurogenic shock may be prevented by carefully immobilizing the patient to prevent further damage to the spinal cord. Nursing interventions are directed toward supporting cardiovascular and neurologic function until the usually transient episode of neurogenic shock resolves. A patient who has experienced a spinal cord injury may not report pain caused by internal injuries. Therefore, in the immediate postinjury period, the nurse must monitor the patient closely for signs of internal bleeding that could lead to hypovolemic shock.

Nursing management during the progressive stage of shock - supporting family members

Keep comfortable and informed. Encourage rest. Spiritual services.

Cardiogenic shock - laboratory marker monitoring

Laboratory biomarkers for ventricular dysfunction (e.g., B-type natriuretic peptide), cardiac enzyme levels and biomarkers (cTn-I), and serum lactate are measured, a transthoracic echocardiography may be performed at the bedside, and serial 12-lead electrocardiograms are obtained to assess the degree of myocardial damage. Continuous ECG and ST segment monitoring is also done to closely monitor the patient for ischemic changes.

Goals of treatment to address hypovolemia

Major goals in the treatment of hypovolemic shock are to restore intravascular volume to reverse the sequence of events leading to inadequate tissue perfusion, to redistribute fluid volume, and to correct the underlying cause of the fluid loss as quickly as possible. Depending on the severity of shock and the patient's condition, often all three goals are addressed simultaneously.

Mean arterial blood pressure equation

Mean arterial BP = Cardiac output × Peripheral resistance. Three major components of the circulatory system—blood volume, the cardiac pump, and the vasculature—must respond effectively to complex neural, chemical, and hormonal feedback systems to maintain an adequate blood pressure (BP) and perfuse body tissues. BP is regulated through a complex interaction of neural, chemical, and hormonal feedback systems affecting both cardiac output and peripheral resistance.

Irreversible / refractory stage of shock - medical management

Medical management during the irreversible stage of shock is similar to interventions and treatments used in the progressive stage. Although the patient may have progressed to the irreversible stage, the judgment that the shock is irreversible can be made only retrospectively on the basis of the patient's failure to respond to treatment. Strategies that may be experimental (e.g., investigational medications, such as immunomodulation therapy) may be tried to reduce or reverse the severity of shock.

Compensatory stage of shock - medical management

Medical treatment is directed toward identifying the cause of the shock, correcting the underlying disorder so that shock does not progress, and supporting those physiologic processes that thus far have responded successfully to the threat. Because compensation cannot be maintained indefinitely, measures such as fluid replacement and medication therapy must be initiated to maintain an adequate BP and reestablish and maintain adequate tissue perfusion.

Cardiogenic shock - medications used

Medications commonly combined to treat cardiogenic shock include dobutamine, nitroglycerin, and dopamine. Additional vasoactive agents that may be used in managing cardiogenic shock include norepinephrine, epinephrine, milrinone, vasopressin, and phenylephrine. Also antiarrhythmic medications: Multiple factors, such as hypoxemia, electrolyte imbalances, and acid-base imbalances, contribute to serious cardiac dysrhythmias in all patients with shock. In addition, as a compensatory response to decreased cardiac output and BP, the heart rate increases beyond normal limits. This impedes cardiac output further by shortening diastole and thereby decreasing the time for ventricular filling. Consequently, antiarrhythmic medications are required to stabilize the heart rate.

Beta-blockers can mask ...

Medications such as beta-blocking agents (metoprolol [Lopressor]) used to treat hypertension may mask tachycardia, a primary compensatory mechanism to increase cardiac output, during hypovolemic states. Be aware of this particularly when dealing with potential shock in older patients.

Nursing management during the progressive stage of shock - preventing complications

Monitor levels of medication. Monitor invasive vascular lines for infection. Interventions to reduce the risk of VAP (ventilation associated pneumonia). Frequent oral care, aseptic suctioning techniques, elevate HOB to >30 degrees. Daily interruption of sedatives to assess readiness for extubation. Positioning and repositioning for comfort and skin integrity. Monitor for delirium and prevention techniques. Frequent reorientation, assessing and treating pain, promoting sleep, early mobilization activities, limiting sedation.

Multiple organ dysfunction syndrome (MODS)

Multiple organ dysfunction syndrome (MODS) is altered organ function in acutely ill patients that requires medical intervention to support continued organ function. It is another phase in the progression of shock states. MODS may be a complication of any form of shock, but it is most commonly seen in patients with sepsis and is a result of inadequate tissue perfusion. The precise mechanism by which MODS occurs remains unknown. However, MODS frequently occurs toward the end of the continuum of septic shock when tissue perfusion cannot be effectively restored. The clinical presentation of MODS is insidious; tissues become hypoperfused at both a microcellular and macrocellular level, eventually causing organ dysfunction that requires mechanical and pharmacologic intervention to support organ function. Organ failure usually begins in the lungs, and cardiovascular instability, as well as failure of the hepatic, GI, renal, immunologic, and central nervous systems, follows.

Pulse pressure as an indicator of shock

Narrowing or decreased pulse pressure is an earlier indicator of shock than a drop in systolic BP

Neurogenic shock - causes / risk factors

Neurogenic shock can be caused by spinal cord injury, spinal anesthesia, or other nervous system damage. It may also result from the depressant action of medications or from lack of glucose (e.g., insulin reaction).

Neurogenic shock - course, clinical manifestations

Neurogenic shock may have a prolonged course (spinal cord injury) or a short one (syncope or fainting). Normally, during states of stress, the sympathetic stimulation causes the BP and heart rate to increase. In neurogenic shock, the sympathetic system is not able to respond to body stressors. Therefore, the clinical characteristics of neurogenic shock are signs of parasympathetic stimulation. It is characterized by dry, warm skin rather than the cool, moist skin seen in hypovolemic shock. Another characteristic is hypotension with bradycardia, rather than the tachycardia that characterizes other forms of shock.

Interventions to be completed within three hours of patient presentation of sepsis symptoms

Obtain serum lactate level. Obtain blood culture prior to administration of antibiotics. Administer prescribed broad-spectrum antibiotics. Initiate aggressive fluid resuscitation in patients with hypotension or elevated serum lactate (>4 mmol/L): Minimum initial fluid bolus of 30 mL/kg using crystalloid solutions. Monitor for effectiveness: BP, CVP, fluid responsiveness with passive leg raise, urine output, serum lactate.

Multiple organ dysfunction syndrome - risk factors

Older adult patients are at increased risk for MODS because of the lack of physiologic reserve and the natural degenerative process, especially immune compromise. Early detection and documentation of initial signs of infection are essential in managing MODS in older adult patients. Subtle changes in mentation and a gradual rise in temperature are early warning signs. Other patients at greater risk for MODS are those with chronic illness, malnutrition, immunosuppression, or surgical or traumatic wounds. While it is not possible to predict MODS, clinical severity assessment tools may be used to anticipate patient risk of organ dysfunction and mortality. These clinical assessment tools include APACHE (Acute Physiology and Chronic Health Evaluation); SAPS (Simplified Acute Physiology Score); PIRO (Predisposing factors, the Infection, the host Response, and Organ dysfunction); and SOFA score.

What is involved in first-line treatment of cardiogenic shock?

Oxygenation, pain control, hemodynamic monitoring, laboratory marker monitoring, fluid therapy (Incremental IV fluid boluses are cautiously given to determine optimal filling pressures for improving cardiac output), pharmacological therapy, mechanical assistive devices (as necessary).

Neurogenic shock - VTE

Patients with neurogenic shock have a higher risk for venous thromboembolism (VTE) formation because of increased pooling of blood from vascular dilation; this risk is greater in patients with neurogenic shock related to spinal cord injury. The nurse must check the patient daily for any lower extremity pain, redness, tenderness, and warmth. If the patient complains of pain and objective assessment of the calf is suspicious, the patient should be evaluated for DVT. Passive range of motion of the immobile extremities helps promote circulation. Early interventions to prevent VTE include the application of pneumatic compression devices often combined with antithrombotic agents (e.g., low-molecular-weight heparin).

Anaphylactic shock - nursing management - prevention

Prevent and early recognition. Assess patients for allergies or previous reactions and communicate to others. Assess patient and family understanding of allergies and strategies to avoid exposure. Encourage use of ID band with allergy identification. Observe for reactions after giving new medications (antibiotics, beta-blockers, ACE inhibitors, aspirin, NSAIDS). Must have knowledge about s/s of anaphylaxis, must take immediate action, and must be prepared to initiate CPR. Community health and home care nurses who administer medications, including antibiotic agents, in the patient's home or other settings, must be prepared to administer epinephrine intramuscularly in the event of an anaphylactic reaction. Teaching about allergies and medications used at home.

Septic shock - risk factors

Primary risk factors: immunosuppression, extremes of age (<1 yr and >65 yr), malnourishment, chronic illness (e.g., diabetes, hepatitis, CKD, immunosufficiency disorders, etc.), invasive procedures and indwelling medical devices, and emergent and/or multiple surgeries. Hospital-acquired conditions, which may include hospital-associated infections (i.e., infections not present at the time of admission to the health care setting) in critically ill patients that may progress to septic shock most frequently originate in the bloodstream (bacteremia), lungs (pneumonia), and urinary tract (urosepsis). Other infections include intra-abdominal infections and wound infections. Of increasing concern are bacteremias associated with intravascular catheters and indwelling urinary catheters. Additional risk factors are the increased number of antibiotic-resistant microorganisms, and the increasingly older population. Older adult patients are at particular risk for sepsis because of decreased physiologic reserves, an aging immune system, comorbid conditions and often nonspecific presentation of infection.

Pulse pressure

Pulse pressure correlates well with stroke volume. Pulse pressure is calculated by subtracting the diastolic measurement from the systolic measurement; the difference is the pulse pressure. Normally, the pulse pressure is 30 to 40 mm Hg (e.g., 120 mm Hg - 80 mm Hg = 40 mm Hg pulse pressure).

Nursing management during the progressive stage of shock - promoting rest and comfort

Reduce patient physical activity to minimize cardiac workload. Treat pain and anxiety. Cluster care. Protect from temperature extremes.

Physiologic responses common to all forms of shock

Regardless of the initial cause of shock, certain physiologic responses are common to all types of shock. These physiologic responses include hypoperfusion of tissues, hypermetabolism, and activation of the inflammatory response. The body responds to shock states by activating the sympathetic nervous system and mounting a hypermetabolic and inflammatory response. Failure of compensatory mechanisms to effectively restore physiologic balance is the final pathway of all shock states and results in end-organ dysfunction and death.

Interventions to decrease tissue oxygen requirements and increase perfusion

Sedating agents may be given to lower metabolic demands, or the patient's pain may be treated with IV opioid agents to decrease metabolic demands for oxygen. Supplemental oxygen and mechanical ventilation may be required to increase the delivery of oxygen in the blood. Administration of IV fluids and medications supports BP and cardiac output, and the transfusion of packed red blood cells enhances oxygen transport. Monitoring tissue oxygen consumption with Scv−O2 is an invasive measure to more accurately assess tissue oxygenation in the compensatory stage of shock before changes in vital signs detect altered tissue perfusion.

Clinical manifestations during the early stages of sepsis

Sepsis is an evolving process that may result in septic shock and life-threatening organ dysfunction if not recognized and treated early. In the early stage of septic shock, BP may remain within normal limits, or the patient may be hypotensive but responsive to fluids. The heart rate increases, progressing to tachycardia. Hyperthermia and fever, with warm, flushed skin and bounding pulses, are present. The respiratory rate is elevated. Urinary output may remain at normal levels or decrease. GI status may be compromised, as evidenced by nausea, vomiting, diarrhea, or decreased gastric motility. Hepatic dysfunction is evidenced by rising bilirubin levels and worsening coagulopathies (e.g., decreasing platelet counts). Signs of hypermetabolism include increased serum glucose and insulin resistance. Subtle changes in mental status, such as confusion or agitation, may be present. The lactate level is elevated because of the maldistribution of blood. Inflammatory markers such as WBC counts, plasma C-reactive protein (CRP), and procalcitonin levels are also elevated.

Septic shock

Septic shock is the most common type of distributive shock, is caused by widespread infection or sepsis. It is "a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality."

Three types of distributive shock

Septic shock, neurogenic shock, and anaphylactic shock

Shock

Shock can best be defined as a clinical syndrome that results from inadequate tissue perfusion, creating an imbalance between the delivery of oxygen and nutrients needed to support cellular function. Adequate blood flow to the tissues and cells requires an effective cardiac pump, adequate vasculature or circulatory system, and sufficient blood volume. If one of these components is impaired, perfusion to the tissues is threatened or compromised. Without treatment, inadequate blood flow to the cells results in poor delivery of oxygen and nutrients, cellular hypoxia, and cell death that progresses to organ dysfunction and eventually death. Many conditions may cause shock; irrespective of the cause, tissue hypoperfusion prevents adequate oxygen delivery to cells, leading to cell dysfunction and death.

Anaphylactic shock - assessment

Signs and symptoms of anaphylaxis may present within 2 to 30 minutes of exposure to the antigen; however, occasionally some reactions may not develop for several hours. The patient may complain of headache, lightheadedness, nausea, vomiting, acute abdominal pain or discomfort, pruritus, and feeling of impending doom. Assessment may reveal diffuse erythema and generalized flushing, difficulty breathing (laryngeal edema), bronchospasm, cardiac dysrhythmias, and hypotension. Characteristics of severe anaphylaxis usually include rapid onset of hypotension, neurologic compromise, respiratory distress, and cardiac arrest. Anaphylactoid reactions present similarly to anaphylaxis but are not mediated by IgE responses. Anaphylaxis and anaphylactoid reactions are often clinically indistinguishable.

Progressive stage of shock - medical management

Specific medical management in the progressive stage of shock depends on the type of shock, its underlying cause, and the degree of decompensation in the organ systems. Although medical management in the progressive stage differs by type of shock, some medical interventions are common to all types. These include the use of appropriate IV fluids and medications to restore tissue perfusion by the following methods: Supporting the respiratory system; Optimizing intravascular volume; Supporting the pumping action of the heart; Improving the competence of the vascular system. Other aspects of management may include early enteral nutritional support, targeted hyperglycemic control with IV insulin and use of antacids, histamine-2 (H2) blockers, or PPI / antipeptic medications to reduce the risk of GI ulceration and bleeding.

Stress ulcers and shock

Stress ulcers occur frequently in acutely ill patients because of the compromised blood supply to the GI tract. Therefore, antacids, H2 blockers (e.g., famotidine [Pepcid]), and proton pump inhibitors (e.g., lansoprazole [Prevacid], esomeprazole magnesium [Nexium]) are prescribed to prevent ulcer formation by inhibiting gastric acid secretion or increasing gastric pH.

Interventions to address sepsis during early management

Support blood pressure to achieve a urine output >0.5 mL/kg/h. Administer vasopressor agents if fluid resuscitation does not restore an effective BP and cardiac output: • Norepinephrine centrally given is the initial vasopressor of choice; • Epinephrine, phenylephrine, or vasopressin should not be given as the initial vasopressor in septic shock. Support the respiratory system with supplemental oxygen and mechanical ventilation. Transfuse with packed red blood cells when hemoglobin is <7 g/dL to achieve a target hemoglobin of 7-9 g/dL in adults. Provide adequate IV sedation and analgesia; avoid the use of neuromuscular blockade agents when possible. Control serum glucose <180 mg/dL with IV insulin therapy. Implement interventions and medications to prevent deep vein thrombosis and stress ulcer prophylaxis. Discuss advance care planning with patients and families.

General management strategies when supporting patients in shock

Support of respiratory system. Supplemental oxygen and/or mechanical ventilation to optimize oxygenation. Fluid replacement to restore intravascular volume. Vasoactive medications to restore vasomotor tone and improve cardiac function. Nutritional support to meet metabolic demands that typically increase in shock.

Purpose of a central venous pressure (CVP) line in patients receiving IV fluids to address shock

The CVP is used to assess preload in the right side of the heart. The CVP value assists in monitoring the patient's response to fluid replacement, especially when it is used in conjunction with additional assessment parameters (e.g., urine output, heart rate, BP response to fluid challenge). A normal CVP ranges from 4 to 12 mm Hg or cm H2O. Several readings are obtained to determine a range, and fluid replacement is continued to achieve a CVP between 8 and 12 mm Hg.

Older patients with shock - fever

The aging immune system may not mount a truly febrile response (temperature greater than 38.3°C [101°F]); however, a lack of a febrile response (temperature less than 37°C [98.6°F]) or an increasing trend in body temperature should be addressed. The patient may also report increased fatigue and malaise in the absence of a febrile response.

Progressive stage of shock - hematologic manifestations

The combination of hypotension, sluggish blood flow, metabolic acidosis, coagulation system imbalance, and generalized hypoxemia can interfere with normal hemostatic mechanisms. In shock states, the inflammatory cytokines activate the clotting cascade, causing deposition of microthrombi in multiple areas of the body and consumption of clotting factors. The alterations of the hematologic system, including imbalance of the clotting cascade, are linked to the overactivation of the inflammatory response of injury. Disseminated intravascular coagulation (DIC) may occur either as a cause or as a complication of shock. In this condition, widespread clotting and bleeding occur simultaneously. Bruises (ecchymoses) and bleeding (petechiae) may appear in the skin. Coagulation times (e.g., prothrombin time, activated partial thromboplastin time) are prolonged. Clotting factors and platelets are consumed and require replacement therapy to achieve hemostasis.

MODS - nursing management

The general plan of nursing care for patients with MODS is the same as that for patients with shock. Primary nursing interventions are aimed at supporting the patient and monitoring organ perfusion until primary organ insults are halted. Providing information and support to family members is a critical role of the nurse. The health care team must address end-of-life decisions to ensure that supportive therapies are congruent with the patient's wishes. Nurses should encourage frequent and open communication about treatment modalities and options to ensure that the patient's wishes regarding medical management are met. Patients who survive MODS must be informed about the goals of rehabilitation and expectations for progress toward these goals, because massive loss of skeletal muscle mass makes rehabilitation a long, slow process.

Cardiogenic shock - goals of medical management

The goals of medical management in cardiogenic shock are to limit further myocardial damage and preserve the healthy myocardium and to improve cardiac function by increasing cardiac contractility, decreasing ventricular afterload, or both. In general, these goals are achieved by increasing oxygen supply to the heart muscle while reducing oxygen demands.

Older patients - effects of hypoxia/hypoxemia

The heart does not function well in hypoxemic states, and the aging heart may respond to decreased myocardial oxygenation with dysrhythmias that may be misinterpreted as a normal part of the aging process. There is a progressive decline in respiratory muscle strength, maximal ventilation, and response to hypoxia. Older patients have a decreased respiratory reserve and decompensate more quickly. Changes in mentation may be inappropriately misinterpreted as dementia. Older adults with a sudden change in mentation should be aggressively assessed for acute delirium (hypo- and hyperdelirium states) and treated for the presence of infection and organ hypoperfusion.

Prevention of sepsis

The incidence of sepsis can be reduced by using strict infection control practices, beginning with thorough hand hygiene techniques. Other interventions include implementing programs to prevent central line infection; ensuring early removal of invasive devices that are no longer necessary (e.g., indwelling urinary catheters); implementing prevention programs to prevent ventilator associated events and pneumonia; promoting early ambulation; timely debriding of wounds to remove necrotic tissue; carrying out standard precautions and adhering to infection prevention/control practices, including the use of meticulous aseptic technique; and properly cleaning equipment and the patient environment.

Irreversible / refractory stage of shock

The irreversible (or refractory) stage of shock represents the point along the shock continuum at which organ damage is so severe that the patient does not respond to treatment and cannot survive. Despite treatment, BP remains low. Renal and liver dysfunction, compounded by the release of biochemical mediators, creates an acute metabolic acidosis. Anaerobic metabolism contributes to a worsening lactic acidosis. Reserves of ATP are almost totally depleted, and mechanisms for storing new supplies of energy have been destroyed. Respiratory system dysfunction prevents adequate oxygenation and ventilation despite mechanical ventilatory support, and the cardiovascular system is ineffective in maintaining an adequate MAP for tissue perfusion. Multiple organ dysfunction progressing to complete organ failure has occurred, and death is imminent. Multiple organ dysfunction can occur as a progression along the shock continuum or as a syndrome unto itself and is described in more detail later in this chapter.

Blood pressure - influence of kidneys

The kidneys regulate BP by releasing renin, an enzyme needed for the eventual conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This stimulation of the renin-angiotensin mechanism and the resulting vasoconstriction indirectly lead to the release of aldosterone from the adrenal cortex, which promotes the retention of sodium and water (i.e., hypernatremia). Hypernatremia then stimulates the release of antidiuretic hormone (ADH) by the pituitary gland. ADH causes the kidneys to retain water further in an effort to raise blood volume and BP. These secondary regulatory mechanisms may take hours or days to respond to changes in BP.

Progressive stage of shock - respiratory manifestations

The lungs, which become compromised early in shock, are affected at this stage. Subsequent decompensation of the lungs increases the likelihood that mechanical ventilation will be needed. Respirations are rapid and shallow. Crackles are heard over the lung fields. Decreased pulmonary blood flow causes arterial oxygen levels to decrease and CO2 levels to increase. Hypoxemia and biochemical mediators cause an intense inflammatory response and pulmonary vasoconstriction, perpetuating pulmonary capillary hypoperfusion and hypoxemia. The hypoperfused alveoli stop producing surfactant and subsequently collapse. Pulmonary capillaries begin to leak, causing pulmonary edema, diffusion abnormalities (shunting), and additional alveolar collapse. This condition is called acute lung injury (ALI); as ALI continues, interstitial inflammation and fibrosis are common consequences, leading to acute respiratory distress syndrome (ARDS).

Cardiogenic shock - nursing management - enhancing safety and comfort

The nurse must take an active role in safeguarding the patient, enhancing comfort, and reducing anxiety. This includes administering medication to relieve chest pain, preventing infection at the multiple arterial and venous line insertion sites, protecting the skin, and monitoring respiratory and renal function. Proper positioning of the patient promotes effective breathing without decreasing BP and may also increase patient comfort while reducing anxiety. Brief explanations about procedures that are being performed and the use of comforting touch often provide reassurance to the patient and the family. The family is usually anxious and benefits from opportunities to see and talk to the patient. Explanations of treatments and the patient's responses are often comforting to family members.

Cardiogenic shock - nursing management - maintaining intra-aortic balloon counterpulsation

The nurse plays a critical role in caring for the patient receiving intra-aortic balloon counterpulsation. The nurse makes ongoing timing adjustments of the balloon pump to maximize its effectiveness by synchronizing it with the cardiac cycle. The patient is at risk of circulatory compromise to the leg on the side where the catheter for the balloon has been inserted; therefore, the nurse must check the neurovascular status of the lower extremities frequently.

When should the nurse contact the provider about a patient's blood pressure?

The nurse should report a systolic BP lower than 90 mm Hg or a drop in systolic BP of 40 mm Hg from baseline or a MAP less than 65 mm Hg. If the patient is concurrently diagnosed with an infection or if an infection is suspected, the nurse should promptly notify the primary provider if the patient exhibits any two of the three following signs: Respiratory rate ≥22/min; Altered mentation; Systolic BP ≤100 mm Hg.

Use of Sepsis-related Organ Failure Assessment Score in ICU settings - components involved

The parameters that are monitored on the SOFA, which include assessment of respiratory rate, platelets, bilirubin, MAP (and use of any vasopressors), serum creatinine, urine output, and Glasgow Coma Scale (GCS) score, may all be gathered and assessed by the nurse in the ICU setting. A drop of 2 points or more in a patient's SOFA score from baseline is suggestive of organ dysfunction. In a patient with infection, the presence of organ dysfunction suggests the development of sepsis

What should be monitored when a patient is receiving fluid administration to address shock?

The patient receiving fluid replacement must be monitored frequently for adequate urinary output, changes in mental status, skin perfusion, and changes in vital signs. Lung sounds are auscultated frequently to detect signs of fluid accumulation. Adventitious lung sounds, such as crackles, may indicate pulmonary edema and ALI. Often, a central venous pressure (CVP) line is inserted (typically into the subclavian or jugular vein) and is advanced until the tip of the catheter rests near the junction of the SVC and the right atrium.

Quick SOFA (qSOFA) - components (in non-ICU settings)

The qSOFA is an easy measurement tool that nurses may readily use; the presence of any two of the three parameters on this scale suggests the development of sepsis. These parameters include a respiratory rate of 22 breaths per minute or higher, a GCS score of less than 15, and a systolic BP of 100 mm Hg or less. The GCS parameter is considered positive for any score less than 15; therefore, any change in the patient's mentation status is considered positive.

Anaphylactic shock - medical management

Treatment of anaphylactic shock requires removing the causative antigen (e.g., discontinuing an antibiotic agent), administering medications that restore vascular tone, and providing emergency support of basic life functions. Fluid management is critical, as massive fluid shifts can occur within minutes due to increased vascular permeability. Intramuscular epinephrine is given for its vasoconstrictive action. Diphenhydramine (Benadryl) is given intravenously to reverse the effects of histamine, thereby reducing capillary permeability. Nebulized medications, such as albuterol (Proventil), may be given to reverse histamine-induced bronchospasm. If cardiac arrest and respiratory arrest are imminent or have occurred, cardiopulmonary resuscitation (CPR) is performed. Endotracheal intubation may be necessary to establish an airway. IV lines are inserted to provide access for administering fluids and medications.

Neurogenic shock - medical management

Treatment of neurogenic shock involves restoring sympathetic tone, either through the stabilization of a spinal cord injury or, in the instance of spinal anesthesia, by positioning the patient properly. Specific treatment depends on the cause of the shock.

Vasoactive medications to treat patients in shock

Vasoactive medications are given in all forms of shock to improve the patient's hemodynamic stability when fluid therapy alone cannot maintain adequate MAP. Specific medications are selected to correct the particular hemodynamic alteration that is impeding cardiac output. These medications help increase the strength of myocardial contractility, regulate the heart rate, reduce myocardial resistance, and initiate vasoconstriction.

Vasoactive medications to treat patients with shock - alpha vs beta

Vasoactive medications are selected for their action on receptors of the sympathetic nervous system. These receptors are known as alpha-adrenergic and beta-adrenergic receptors. Beta-adrenergic receptors are further classified as beta-1 and beta-2 adrenergic receptors. When alpha-adrenergic receptors are stimulated, blood vessels constrict in the cardiorespiratory and GI systems, skin, and kidneys. When beta-1 adrenergic receptors are stimulated, heart rate and myocardial contraction increase. When beta-2 adrenergic receptors are stimulated, vasodilation occurs in the heart and skeletal muscles, and the bronchioles relax. The medications used in treating shock consist of various combinations of vasoactive medications to maximize tissue perfusion by stimulating or blocking the alpha- and beta-adrenergic receptors.

What should nurses monitor during fluid administration?

Vital signs, blood gases, chemistry, coagulation labs, clinical appearance. Also complications: The nurse monitors the patient closely for cardiovascular overload and signs of difficulty breathing, a condition known as transfusion-associated circulatory overload. Transfusion-related acute lung injury may occur and is characterized by pulmonary edema, hypoxemia, respiratory distress, and pulmonary infiltrates, usually within hours after massive transfusion. The risk of these complications is increased in older adults, in patients with preexisting cardiac disease, and with increasing number of blood products given. ACS is also a possible complication of excessive fluid resuscitation and may initially present with respiratory symptoms (difficulty breathing) and decreased urine output. Hemodynamic pressure, vital signs, arterial blood gases, serum lactate levels, hemoglobin and hematocrit levels, bladder pressure monitoring, and fluid intake and output (I&O) are among the parameters monitored. Temperature should also be monitored closely to ensure that rapid fluid resuscitation does not cause hypothermia. IV fluids may need to be warmed when large volumes are given. Physical assessment focuses on observing the jugular veins for distention and monitoring jugular venous pressure. Jugular venous pressure is low in hypovolemic shock; it increases with effective treatment and is significantly increased with fluid overload and heart failure. The nurse must monitor cardiac and respiratory status closely and report changes in BP, pulse pressure, CVP, heart rate and rhythm, and lung sounds to the primary provider.

Systemic inflammatory response syndrome

When microorganisms invade body tissues, patients exhibit an immune response. This immune response provokes the activation of biochemical cytokines and mediators associated with an inflammatory response and produces a complex cascade of physiologic events that leads to poor tissue perfusion. Increased capillary permeability results in fluid seeping from the capillaries. Capillary instability and vasodilation interrupt the body's ability to provide adequate perfusion, oxygen, and nutrients to the tissues and cells. The widespread inflammatory response that occurs is called the systemic inflammatory response syndrome (SIRS). SIRS results from a clinical insult that initiates an inflammatory response that is systemic, rather than localized to the site of the insult. The insult may be a significant injury (e.g., multitrauma) or an infection (e.g., sepsis). A patient presenting with manifestations of SIRS may be exhibiting a protective inflammatory response to the initiating insult or may be exhibiting a response to infection, which may lead to sepsis.

Progressive stage of shock - renal manifestations

When the MAP falls below 65 mm Hg, the glomerular filtration rate of the kidneys cannot be maintained, and drastic changes in renal function occur. Acute kidney injury (AKI) is characterized by an increase in blood urea nitrogen (BUN) and serum creatinine levels, fluid and electrolyte shifts, acid-base imbalances, and a loss of the renal-hormonal regulation of BP. Urinary output usually decreases to less than 0.5 mL/kg per hour (or less than 30 mL per hour) but may vary depending on the phase of AKI.

Vasoactive medications to treat patients with shock - monitoring and dosage

When vasoactive medications are given, vital signs must be monitored frequently (at least every 15 minutes until stable, or more often if indicated). Monitor urinary output every hour. Vasoactive medications should be given through a central venous line, because infiltration and extravasation of some vasoactive medications can cause tissue necrosis and sloughing. Individual medication dosages are usually titrated by the nurse, who adjusts drip rates on the basis of the prescribed dose and target outcome parameter (e.g., BP, heart rate) and the patient's response. Dosages are changed to maintain the MAP at a physiologic level that ensures adequate tissue perfusion (usually greater than 65 mm Hg). Infuse via controller or pump, and verify the dose with another RN.

Clotting during shock

With significant cell injury or death caused by shock, the clotting cascade is overproductive, resulting in small clots lodging in microcirculation, further hampering cellular perfusion. This upregulation of the clotting cascade further compromises microcirculation of tissues, exacerbating cellular hypoperfusion. Cellular metabolism is impaired, and a self-perpetuating negative situation (i.e., a positive feedback loop) is initiated.