SHOCK, SIRS & MODS

Shock
Decreased tissue perfusion and impaired cellular metabolism Imbalance between supply and demand of oxygen and nutrients Hypoperfusion: demand for oxygen and nutrients exceeds the supply

Classification
Low Blood Flow: Cardiogenic and Hypovolemic shock Maldistribution of blood flow: Neurogenic, Anaphylactic, and Septic shock

Cardiogenic Shock
Systolic Dysfunction: inability of the heart to pump blood forward (MI, Cardiomyopathy). Primarily affects the left ventricle, because systolic pressure and tension is greater on the left side of the heart. When it affects the right side of the heart, blood flow through the pulmonary circulation is compromised Diastolic Dysfunction: inability of the heart to fill during diastole (pericardial tamponade, Cardiomyopathy). This results in decreased stroke volume. Dysrhythmias: bradydysrhythmias and tachydysrhythmias Structural factors: Valvular abnormalities (stenosis, regurgitation), ventricular septal rupture, tension pneumothorax Despite treatment, the mortality rates for patients with Cardiogenic shock ranges from 50- 80% Patient experiences impaired tissue perfusion and impaired cellular metabolism because of Cardiogenic shock Early clinical presentation is similar to that of acute decompensated HF Tachycardia, hypotension, narrowed pulse pressure. Increase in SVR, increases the workload of the heart, thus increasing the myocardial oxygen consumption The inability of the heart to pump the blood forward will result in a low Cardiac Output (< 4L/min) and cardiac index (<2.1L/min/m2) On examination, the patient may be tachypneic and pulmonary congestion may be evident by the presence of crackles. Rhonchi may also be present Hemodynamic profile will demonstrate an increase in Pulmonary artery wedge Pressure (PAWP), and PVR. Chest pain may or may not be present. Peripheral Hypoperfusion: cyanosis, pallor, cool and clammy skin, decreased capillary refill Decreased Renal blood flow: Sodium and water retention, decreased urinary output Decreased Cerebral perfusion: Anxiety, confusion, agitation

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Gastrointestinal problems: Bowel sounds, N/V Labs and Diagnostic findings: cardiac enzymes ( Cardiac markers), troponin levels, ECG (Dysrhythmias), chest x-ray (pulmonary infiltrates), echocardiogram (left ventricular dysfunction), BUN, Blood Glucose.

Hypovolemic Shock
Occurs when there is a loss of intravascular fluid volume, inadequate to fill the vascular space Absolute hypovolemia: fluid lost through hemorrhage, trauma, GI loss (vomiting, diarrhea), fistula drainage, DI, hyperglycemia, or dieresis Relative hypovolemia: fluid moves out of the vascular space into the extravascular space (interstitial, intacavitary space) from increased capillary permeability, as seen in sepsis-------- THIRD SPACING. Can also occur due to pooling of blood or fluids (bowel obstruction), Fluid shifts (burn injuries, ascites), Internal bleeding (fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis), Massive vasodilation (sepsis) Size of the vascular compartment remains unchanged while the volume of blood and plasma decreases Physiologic Consequences: venous return to the heart, preload, stroke volume, cardiac output and capillary refill time A cascade of events results in decreased tissue perfusion and impaired cellular metabolism, the hallmarks of shock Patient may compensate for a loss of up to 15% of the total blood volume (approximately 750 ml) Further loss (15- 30%) will result in a sympathetic Nervous System- mediated response which causes HR, CO, and respiratory rate and depth (Tavhypnea). in stroke volume and PAWP is due to circulating blood volume Patient may appear anxious, and urine output will begin to decrease If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is generally reversible If the volume loss is more than 30%, compensatory mechanisms may begin to fail to be initiated More than 40% loss of total blood volume, there is loss of autoregulation in the microcirculation and irreversible tissue destruction occurs Peripheral Hypoperfusion: pallor, cool and clammy skin Cerebral Hypoperfusion: anxiety, confusion, agitation GI: Absent Bowel sounds Renal: Urine Output Respiratory: Tachypnea, Bradypnea (late)

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Labs and Diagnostic findings: Serial Hemoglobin and Hematocrit values ( hemoglobin, Hematocrit), urine specific gravity ( urine specific gravity), changes in serum electrolytes, blood gases, and lactic acid

Neurogenic Shock
Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks Massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone Massive vasodilation leads to pooling of blood in the blood vessels, tissue Hypoperfusion, and ultimately impaired cellular metabolism In addition to spinal cord injury, spinal anesthesia can block the transmission of impulses from the SNS Depression of vasomotor center of the medulla from drugs (opioids, benzodiazepines), also result in decreased vasoconstrictor tone of the peripheral blood vessels, resulting in Neurogenic shock The most important clinical manifestations are hypotension (due to massive vasodilation), bradycardia (from unopposed parasympathetic nervous system) Patient in Neurogenic shock may also have an inability to regulate temperature, when combined with massive vasodilation promotes heat loss Initially the skin is warm due to massive dilation without compensation As the heat dissipates, the patient is at risk for hypothermia Later the patients skin may be cool or warm depending on the ambient temperature (poikilothermia- taking on the temperature of the environment) In either case the skin will be dry Respiratory: Dysfunction related to the level of injury Renal: Bladder dysfunction Skin: perfusion, cool, warm or dry Neurologic: Flaccid paralysis below the level of the lesion, loss of reflex activity GI: Bowel dysfunction Spinal Shock: transient condition that is present after an acute spinal cord injury which is characterized by absence of all voluntary and reflex neurologic activity below the level of the injury

Anaphylactic Shock

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Acute and life threatening hypersensitivity (allergic) reaction to a sensitizing substance (drug, chemical, vaccine, food, insect venom). Has a sudden onset of symptoms Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability (fluid leaks from the vascular space into the interstitial space) Cardiovascular: Chest pain, Third spacing of fluid, dizziness Pulmonary: wheezing, stridor, swelling of the lips and tongue, SOB, Edema of the larynx and epiglottis respiratory distress, because of laryngeal edema or severe bronchospasm, and circulatory failure, because of massive vasodilation Skin: Flushing, pruritus, urticaria, and angioedema Neurologic: anxious and confused, feel an impending sense of doom, LOC Renal: Incontinence GI: metallic taste, cramping, abdominal pain, N/V, Diarrhea Parenteral administration of the antigen (allergen) is the route most likely to cause anaphylaxis. However, oral, topical and inhalation routes can also cause anaphylactic reactions Quick and decisive action by the nurse is critical to preventing the progression of an anaphylactic reaction to anaphylactic shock

Septic Shock
Systemic inflammatory response to a documented or suspected infection 10-30% of sepsis, defined as sepsis complicated by organ dysfunction, is diagnosed in more than 750,000 patients per year and has mortality rates as high as 28- 50% Septic shock is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of tissue perfusion abnormalities, making it difficult to manage The primary organisms that cause sepsis are gram-negative and gram-positive bacteria Morbidity and mortality rates from infections with gram-negative organisms are greater than in gram-positive organisms Parasites, fungi, and viruses can also lead to the development of sepsis and septic shock

Pathogenesis
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When an antigen (microorganism) enters the body the normal immune/ inflammatory cascade responses are initiated and work together to destroy the antigen In severe sepsis and septic shock, the initiated body response to an antigen is exaggerated There is increase in inflammation and coagulation, and a decrease in fibrinolysis

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Endotoxins from the microorganism cell wall stimulate the release of cytokines, including TNF, 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 the damage of the endothelium, vasodilation , increased capillary permeability, and neutrophil and platelet aggregation and adhesion to endothelium

Clinical Presentation
No single symptom or group of symptoms is specific to the diagnosis Patients will usually experience an initial hyperdynamic state characterized by CO, SVR Despite this the combination of TNF and IL-1 is thought to have a role in sepsis-induced myocardial dysfunction The ejection fraction is decreased for the first few days after the initial insult, because of which the ventricles will dilate in order to maintain the stroke volume The ejection fraction typically improves and the ventricular dilation resolves over 710 days Persistence of a high CO and a low SVR beyond 24 hours is an ominous finding often associated with an increased development of hypotension and MODS Coronary artery perfusion and myocardial oxygen metabolism are primarily altered in septic shock In addition to the cardiovascular dysfunction that accompanies sepsis, respiratory failure is common. The patient will hyperventilate as a compensatory mechanism, resulting in respiratory alkalosis Once the patient can no longer compensate, respiratory acidosis will develop Respiratory failure will develop in 85% of the patients with sepsis and 40% will develop ARDS Cardiovascular: / temperature, Biventricular dilation, ejection fraction Respiratory: Hyperventilation, Respiratory alkalosis to acidosis, hypoxemia, respiratoty failure, ARDS, Pulmonary HTN, crackles Renal: UOP Skin: warm and flushed to cool and mottled (late) Neurologic: Alteration in mental status (confusion), agitation, coma (late) GI: Bleeding, paralytic ileus Diagnostic Findings: / WBC, platelets, Lactate, Glucose, Urine Specific Gravity, Urine Na+ and positive blood cultures

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Shock Continuum:
Begins with the initial stage of shock that occurs at the cellular level and 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 and must be removed by the liver. However, this process requires oxygen which is unavailable because of the decrease in tissue perfusion

Stages of Shock Compensatory Stage

Body activates neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis As BP falls in response to decreased CO and a narrowing of the pulse pressure in shock, the baroreceptors in the carotid artery and aortic bodies immediately responds by activating the SNS SNS stimulates vasoconstriction and the release of potent vasoconstrictors epinephrine and Norepinephrine Blood flow to the vital organs (heart and brain) is maintained while blood flow to the nonvital organs such as the kidneys, GI tract, skin, and lungs is diverted or shunted Decreased blood flow to the kidneys activates the Renin Angiotensin System. Renin is released and activates angiotensinogen to produce angiotensin I, which is then converted to angiotensin II (potent vasoconstrictor that causes both arterial and venous vasoconstriction) The net result is the increase in venous return to the heart and an increase in BP Angiotensin II also stimulates the adrenal cortex to release aldosterone, which results in sodium and water reabsorption, and potassium excretion by the kidneys This increase in sodium reabsorption raises the serum osmolality and stimulates the release of ADH from the posterior pituitary ADH works by increasing water reabsorption by the kidneys, thus further increasing the blood volume The increase in total circulating volume results in an increase in CO and BP The shunting of blood from other organ systems also results in clinically important changes The decrease in blood flow to the GI results in impaired motility and a slowing of peristalsis, thus increasing the risk for paralytic ileus Decreased blood flow to the skin results in cool, clammy skin. The exception of the patient feeling very warm and flushed in early septic shock due to a hyperdynamic state Shunting of blood away from the lungs increases the patients physiologic dead space (the amount of air that will not reach gas-exchanging units) and any inspired air that cannot participate in gas exchange

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The clinical result of an increase in dead space ventilation is a ventilation-perfusion mismatch There will be areas of the lungs participating in ventilation that would not be perfused because of the decreased blood flow to the lungs Arterial oxygen levels will decrease, and the patient will have a compensatory increase in the rate and depth of respirations The myocardium responds to the SNS stimulation and the increase in oxygen demand by increasing the heart rate and contractility However, increased contractility increases myocardial oxygen consumption (MVO2) The coronary arteries dilate in an attempt to meet the increased oxygen demands of the myocardium A multisystem response to decreasing tissue perfusion is initiated in the compensatory stage of shock At this stage, the body is able to compensate for the changes in tissue perfusion If the perfusion deficit (cause of the shock) is corrected, the patient will recover with little or no residual aftereffects If the perfusion deficit is not corrected and the body is unable to compensate, the patient enters the progressive stage of shock

Compensatory Stage : Clinical Manifestations Summary Neurologic Oriented to person, place, and time Restless, apprehensive, confused Changes in LOC Cardiovascular SNS response Release of epinephrine and Norepinephrine----vasoconstriction MVO2 Contractility HR Coronary artery dilation Narrowed pulse pressure BP adequate to perfuse vital organs like heart and brain Respiratory Blood flow to the lungs Physiologic dead space Ventilation-perfusion mismatch Hyperventilation Minute ventilation (VE) Gastrointestinal
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Blood supply Hypoactive bowel sounds Renal Renal blood flow Renin resulting in the release of angiotensin (vasoconstrictor) Aldosterone resulting in Na+ and water reabsorption Antidiuretic hormone resulting in water reabsorption Temperature Skin Normal or abnormal

Pale and cool Warm and flushed (early onset of septic shock) Key lab findings Blood Glucose pH PaO2 PaCO2

Progressive Stage
Begins as compensatory mechanisms fail Aggressive interventions are needed to prevent the development of MODS Distinguishing features: Continued decreased cellular perfusion and resulting altered capillary permeability Altered capillary permeability allows leakage of fluid and protein out of the vascular space into the surrounding interstitial space In addition to decrease in circulatory volume, there is an increase in systemic interstitial edema The patient may have anasarca or diffuse profound edema Fluid leakage from the vascular space also affects the solid organs (liver, spleen, GI tract and lungs) and peripheral tissues by further decreasing perfusion 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) pressures 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

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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 the fluid moves to the alveoli, with resultant 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 cardiovascular system is profoundly affected in the progressive stage of shock CO begins to fall, with a resultant decrease in BP and coronary artery, cerebral, and peripheral perfusion Changes in the patients mental status are important findings in this stage Capillary permeability continues to increase, enhancing the movement of fluid from the vascular space into the interstitial space 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 potentially MI The end result is a complete deterioration of the cardiovascular system The effects of prolonged hypoperfusion on the kidneys is renal tubular ischemia The resulting acute tubular necrosis (ATN) may lead to the development of acute renal failure, which can be worsened by nephrotoxic drugs, including antibiotics, anesthetics and diuretics Renal function is markedly impaired during the progressive stage of shock The patient will have a decreased UOP and elevated BUN and serum creatinine Metabolic acidosis occurs from an inability to excrete acids and reabsorb bicarbonate The GI system is also affected by prolonged decreased tissue perfusion As the blood supply to the GI tract is decreased, the normally protective mucosal barrier becomes ischemic which predisposes the patient to erosive ulcers and GI bleeding and increases the potential risk of bacterial translocation from the GI tract to the blood The decreased perfusion to the GI tract also leads to a decreased ability to absorb nutrients Other systems are also affected by the sustained hypoperfusion in the progressive stage of shock The loss of functional ability of the liver leads to the failure of liver to metabolize drugs and waste products such as ammonia (NH3) and lactate Jaundice results from accumulation of bilirubin As the liver cells die, enzymes become elevated (ALT, AST, GGT) The liver also loses its ability to function as an immune organ

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Bacteria that may translocate from the GI system are unable to be scavenged by the Kupffer cells. Instead, they are released into the blood stream, thus increasing the possibility of the development of bacteremia Dysfunction of the hematologic system adds to the complexity of the clinical picture The patient is at risk for developing dissemination intravascular coagulation (DIC), in which there is a consumption of platelets and clotting factors with secondary fibrinolysis This results in clinically significant bleeding from many orifices, including, but not limited to GI tract, lungs, and puncture sites Altered lab values in DIC include decreased platelets, prolonged prothrombin time, decreased fibrinogen, elevated D-dimer fragments, and increased fibrin split products

Progressive Stage: Clinical Manifestations Summary Neurologic Cerebral perfusion pressure Cerebral blood flow Listless or agitated Responsiveness to stimuli Cardiovascular Loss of autoregulation in microcirculation Capillary permeability systemic interstitial edema CO BP and HR MAP < 60 mm Hg (or 40 mm Hg drop in BP from baseline) Coronary perfusion o Dysrhythmias o Myocardial ischemia o Myocardial infarction o Myocardial dysfunction impaired CO Peripheral perfusion ischemia of distal extremities, diminished pulses, capillary refill Respiratory ARDS o Capillary permeability o Pulmonary vasoconstriction o Pulmonary interstitial edema o Alveolar edema o Diffuse infiltrates o Respiratory rate o Compliance Moist crackles

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Gastrointestinal Vasoconstriction and perfusion ischemic gut (stomach, small and large intestines, gallbladder, pancreas) o Erosive Ulcers o GI bleeding o Translocation of GI bacteria o Impaired absorption of nutrients

Renal Renal tubules become ischemic Acute Tubular Necrosis UOP BUN/ Creatinine ratio Urine Sodium Urine osmolarity and specific gravity Urine Potassium Metabolic acidosis Hepatic Failure to metabolize drugs and waste products Jaundice (decreased clearance of bilirubin) NH3 and lactate Hematologic DIC o Thrombin clots in microcirculation o Consumption of clots in microcirculation Temperature Skin Hypothermia Sepsis: hypothermia or hyperthermia

Cold and clammy Key Lab findings Liver enzymes: ALT, AST, GGT Bleeding times Thrombocytopenia

Refractory Stage
Final stage of shock Decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism

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The accumulation of Lactic acid contributes to an increased capillary permeability and dilation of the capillaries 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 secondary to the constricted venules and dilated arterioles The loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow which in turn leads to worsening myocardial depression and a further decline in CO Cerebral blood flow cannot be maintained, and cerebral ischemia results The patient in the stage of shock will demonstrate profound hypotension and hypoxemia The failure of the liver, lungs and kidneys will result in an accumulation of waste products, such as lactate, urea, ammonia, and carbon dioxide The failure of one organ system will have an effect on several other organ systems In this final stage, recovery is unlikely The organs are in failure and the bodys compensatory mechanisms are overwhelmed

Refractory Stage: Clinical Manifestations Summary Neurologic Unresponsive Areflexia (loss of reflexes) Pupils unreactive and dilated Cardiovascular Profound hypotension CO Bradycardia, irregular rhythm BP inadequate to perfuse vital organs Respiratory Severe refractory hypoxemia Respiratory failure Gastrointestinal Ischemic gut Renal Anuria Hepatic Metabolic changes from accumulation of waste products (NH3, lactate, CO2) Hematologic DIC Temperature Hypothermia Skin Mottled, cyanotic
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Key Lab findings Blood glucose NH3, lactate, and K+ Metabolic acidosis

Diagnostic Studies
There is no single diagnostic study to determine whether a patient is in shock The process of establishing a diagnosis begins with a thorough history and physical examination History may be obtained from patient , family or friends Obtaining a patients medical and surgical history, and a history of recent events (upper respiratory tract infection, surgery, chest pain, trauma), will provide valuable data Decreased tissue perfusion in shock leads to an elevation of lactate and a base deficit (the amount needed to bring the pH back to normal) These lab changes may reflect an increase in anaerobic metabolism Additional diagnostic studies include a 12-lead ECG, continuous cardiac monitoring, chest x-ray, continuous pulse oximetry, and hemodynamic monitoring (arterial pressure monitoring, central venous or PA pressure monitoring)

Lab Abnormalities in Shock

Blood
RBC, Hemoglobin and Hematocrit Normal: Remains within normal limits in shock because of relative hypovolemia and pump failure and in hemorrhagic shock before fluid resuscitation Decreased: Decreases in hemorrhagic shock after fluid resuscitation when fluids other than blood are used Increased: Increases in nonhemorrhagic shock due to actual hypovolemia because fluid lost does not contain erythrocytes DIC Screen Acute DIC can develop within hours to days after an initial assault on the body FSPs increased Fibrinogen level decreased Platelet count decreased PTT and PT prolonged Thrombin time increased D-dimer increased
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Creatine Kinase Increased: due to trauma, myocardial infarction in response to cellular damage, and/or hypoxia Troponin Increased in myocardial infarction BUN Increased: indicating impaired kidney function due to hypoperfusion as a result of severe vasoconstriction or occurs secondary to catabolism of cells in trauma or infection Creatinine Increased: indicating impaired kidney function due to hypoperfusion as a result of vasoconstriction More serious indicator of kidney function than BUN Glucose Increased: Found in early shock because of release of liver glycogen stores in response to SNS stimulation and cortisol; insulin sensitivity develops Decreased: Occurs because of depleted glycogen stores with hepatocellular dysfunction possible as shock progresses

Serum Electrolytes
Sodium Increased: Found in early shock because of increased secretion of aldosterone, causing renal retention of sodium Decreased: May occur iatrogenically when excess hypotonic fluid is administered after fluid loss Potassium Increased: Results when cellular death liberates intracellular potassium; also occurs in acute renal failure and in the presence of acidosis Decreased: Found in early shock because of increased secretion of aldosterone, causing real excretion of potassium ABGs Respiratory alkalosis: Found in early shock secondary to hyperventilation Metabolic acidosis: occurs later in shock when organic acids, such as lactic acid, accumulate in blood from anaerobic metabolism Base Deficit > -6: Indicates acid production secondary to hypoxia Blood Cultures Growth of organisms in people with septic shock Lactic acid Increased: usually once significant hypoperfusion and impaired oxygen utilization at the cellular level have occurred By product of anaerobic metabolism Liver enzymes (ALT, AST, GGT) Increased: indicate liver cell destruction in progressive stage of shock
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Urine
Specific Gravity Increased: secondary to the action of ADH Fixed at 1.010: occurs in renal failure

Collaborative Care: General Measures

Early recognition and prompt intervention to prevent the decline to progressive or refractory stages General management strategies for a patient with shock begin with ensuring that the patient has a patent airway Next oxygen delivery must be optimized Maintain arterial oxygen saturation of 90% or greater (PaO2> 60mmHg) to avoid hypoxemia either through supplemental oxygen or mechanical ventilation

Oxygen and Ventilation

Delivery is dependent on CO, available hemoglobin, and arterial oxygen saturation (SaO2) Goal is to increase the supply and decrease the demand Supply can be increased by o Optimizing the CO with drug therapy or fluid replacement o Increasing the hemoglobin by the transfusion of blood or packed RBCs o Increasing the arterial oxygen saturation with supplemental oxygen and mechanical ventilation Do not disrupt the balance of oxygen supply and demand Activities that increase oxygen consumption (endotracheal suctioning, position changes ) should be appropriately spaced for oxygen conservation Continuously monitor central venous oxygenation (ScvO2) by a central venous catheter or mixed venous oxygen saturation (SvO2) by a PA catheter. Both reflect the dynamic balance between oxygen supply and demand These values are considered in conjunction with arterial oxygen saturation, CO, hemoglobin, and oxygen consumption to evaluate the patients response to treatments or activities

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Fluid Resuscitation
Except for cardiogenic and neurogenic shock, all other classifications of shock involve decreased circulating blood volume The corner stone of therapy for septic, hemorrhagic and anaphylactic shock is volume expansion with the administration of the appropriate fluid Before beginning fluid resuscitation, two large-bore (14-16 gauge) IV catheters must be inserted preferably into the antecubital veins Both crystalloids (normal saline), and colloids (albumin) have a role in fluid resuscitation Currently, it is generally accepted that isotonic crystalloids are used in the initial resuscitation of shock LR should be used cautiously in all shock situation because the failing liver cannot covert lactate to bicarbonate, thus increasing the serum lactate levels `In some cases hypertonic saline can be used to expand the plasma volume Colloids are effective volume expanders because the size of their molecules keeps them in the vascular space for a longer period of time (costly ad no definitive studies to prove it effectiveness) Choice of fluid for resuscitation must also be based on the type and volume of fluid lost and the patients clinical status If the patient does not respond to 2 to 3L of crystalloids, blood administration and central venous or PA pressure monitoring may be instituted Serial blood pressures with an automatic BP cuff or an intra-arterial catheter can be used to monitor the patients response An indwelling catheter to monitor UOP will also assist in monitoring the patients fluid status When large amounts of fluids are required, the patient must be protected against complications: Hypothermia and Coagulopathy Patient can be protected from hypothermia by warming both crystalloid and colloid solutions used during massive fluid resuscitation If the patient is receiving large volumes of packed RBCs, it is important to remember that they do not contain clotting factors. Therefore clotting factors will need to be replaced based on the clinical situation and blood studies If the patient has persistent hypotension after adequate fluid resuscitation, a vasopressor (dopamine [Inotropin], Norepinephrine [Levophed]) or an inotrope (dobutamine [Dobutrex] may be added The goal of fluid resuscitation remains the restoration of tissue perfusion Although BP helps determine whether the patients CO id adequate, an assessment of end organ perfusion (UOP, neurologic function, peripheral pulses) provides information that is more relevant

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Fluid Therapy in Shock

Fluid Type Crystalloids Isotonic 0.9% Nacl LR Hypertonic 1.8%, 3%, 5% Nacl

Blood/Blood Products Whole blood/ packed RBCs Fresh frozen plasma Colloids Hetastarch

Mechanism of Action Fluid primarily remains in the intravascular space, increasing intravascular volume Fluid remains in the intravascular space, rapid volume expansion Replaces blood loss Increases oxygen carrying capacity Replaces coagulation factors Made from starch and acts as volume expander, is at least as effective as albumin; can exert osmotic effect up to 36hr

Type of Shock Initial volume replacement in most types of shock

Nursing Implications Monitor for circulatory overload LR should not be used in patients with liver failure Monitor for hypernatremia (disorientation, convulsions) Precautions same as any blood administration

May be used for initial volume expansion in hypovolemic shock All types of shock if hemoglobin < 12g/dl or if the patient does not respond to crystalloids All types of shock except cardiogenic and neurogenic

May be 50% less costly than albumin. Use cautiously in patients with HF, Renal failure, or bleeding disorders (due to antiplatelet effect) Monitor for circulatory overload. Mild side effects: chills, fever and urticaria may develop. More expensive than other colloids Increases risk of bleeding. Important to monitor patient for allergic reaction and Acute Renal Failure

Human Serum albumin (5%, 25%), plasma protein fraction (5% albumin in 500 ml NSS)

Can increase plasma colloid osmotic pressure, rapid volume expansion

All types of shock except cardiogenic and neurogenic

Dextran 40 and 70

Hyperosmotic glucose polymer; has similar degrees of volume expansion with dextran 40 and 70; longer duration of action with dextran 70

Limited use because of side effects including reducing platelet adhesion, diluting clotting factors

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Drug Therapy
Primary goal of drug therapy for shock is the correction of decreased tissue perfusion Medications used are administered IV via an infusion pump and often via a central venous line. The key reason being that many of the medications have vasoconstrictor properties and may have deleterious effects if administered peripherally and the drug extravasates

Sympathomimetic Drugs Have effect on, and mimic the action of the SNS Bind to -adrenergic or - adrenergic receptors Many of them cause peripheral vasoconstriction and are referred to as a vasopressor drugs (Epinephrine [Adrenalin], Norepinephrine) These drugs have the potential to cause severe peripheral vasoconstriction and an increase in SVR further jeopardizing tissue perfusion directly or indirectly increased work load of the heart and can be detrimental to a patient in cardiogenic shock by causing further myocardial damage Use of vasopressor drugs is generally reserved for patients who have been unresponsive to other therapies Adequate fluid resuscitation must be achieved before the use of any vasopressor because peripheral vasoconstrictor effects in patients with low blood volume will cause further reduction in tissue perfusion Goals of vasopressor therapy are to achieve and maintain a MAP of 60 to 65 mm Hg Nurse must continuously monitor end organ perfusion (UOP, SvO2, serum lactate levels) to ensure that tissue perfusion is adequate

Vasodilator Drugs In cardiogenic shock there is excessive vasoconstriction and poor tissue perfusion in spite of fluid replacement and normal or even high systemic BP Excessive constriction can reduce tissue blood flow and increase the workload of the heart The rationale behind using vasodilator therapy for a patient in shock is to break the deleterious cycle in which widespread vasoconstriction causes a decrease in CO and BP, resulting in further sympathetic-induced vasoconstriction Goal is to maintain a MAP of 60 to 65 mm Hg or greater It is important to closely monitor PA pressures along with MAP so that fluid administration can be increased or the dose of the vasodilator decreased if a serious fall in CO or BP occurs The vasodilator most often used for patient in cardiogenic shock is nitroglycerin (Tridil) Vasodilation may be enhanced with nitroprusside (Nipride) in noncardiogenic shock.

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Nutritional Therapy
Protein-calorie malnutrition is one of the primary manifestation son hypermetabolism in shock Enteral nutrition should be initiated within the first 24 hours Early Enteral feedings are thought to enhance perfusion of the GI tract and help maintain the integrity of the gut mucosa Parenteral nutrition is used if Enteral feedings are contraindicated or fail to meet at least 80% of the patients caloric requirements The patient is started on continuous drip of very small amounts of Enteral feedings Patient with shock should be weighed on a daily on the same scale at the same time of the day If patient experiences a significant weight loss, dehydration should be ruled out before additional calories are provided Large weight gains are common because of third spacing of fluids Therefore daily weights may function better as an indicator of fluid status than caloric needs and balance Serum protein, nitrogen balance, BUN, serum glucose, and serum electrolytes are all used to assess nutritional status

Collaborative Care: Specific Measures

Cardiogenic Shock
Overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand Definitive measures: Thrombolytic therapy, Angioplasty with stenting, emergency revascularization, and valve replacement Cardiac catheterization should be done as soon as possible after the initial insult. Coronary angioplasty with or without stenting may be performed during the cardiac catheterization Until these interventions can be performed, the heart must be supported to optimize stroke volume and CO in an effort to facilitate optimal perfusion Hemodynamic Management is geared toward reducing the workload of the heart through drug therapy or mechanical interventions Drug selection is based on the clinical goal and a thorough understanding of the pharmacodynamics of each drug Drugs can be used to decrease the workload of the heart by dilating coronary arteries (nitrates), reducing preload (diuretics), reducing afterload (vasodilators), and reducing HR and contractility (- adrenergic blockers)

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The patient may also benefit from a circulatory assist device such as a Intraaortic Balloon pump (IABP), or a ventricular assist device (VAD) IABP: inserted into the femoral artery and placed in the aorta just distal to the aortic arch. Goal is to decrease the SVR and thus left ventricular workload VAD: temporary measure for the patient in cardiogenic shock and/or awaiting cardiac transplantation Cardiac transplantation is an option for a small and select group of patients with cardiogenic shock

Summary of specific strategies for the treatment of cardiogenic Shock

Oxygenation Provide supplemental oxygen (nasal cannula, non-rebreather mask) Intubation/mechanical ventilation if necessary Monitor SvO2/ ScvO2

Circulation Restore blood flow with thrombolytics, angioplasty with stenting, emergent coronary revascularization Reduce workload of the heart with circulatory assist Devices: IABP, VAD

Drug Therapy Nitrates- NTG Inotropes- Dobutamine Diuretics- Furosemide - adrenergic blockers (contraindicated with ejection fraction)

Supportive Therapies Correct dysrhythmias

Hypoveolemic Shock
Goal: to stop the loss of fluid and restoring the circulating volume Fluid resuscitation in hypovolemic shock initially is calculated using a 3: 1 rule (3ml of isotonic crystalloid for every 1 ml of estimated blood loss)

Summary of specific strategies for the treatment of Hypovolemic Shock

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Oxygenation

Provide supplemental oxygen Monitor SvO2 and ScvO2

Circulation

Restore fluid volume (blood/blood products, crystalloids) Rapid fluid replacement using two large-bore (14-16 gauge) peripheral IVs End points of fluid resuscitation: CVP 15 mm Hg, PAWP 10-12 mm Hg
Supportive Therapies

Correct the cause (stoop bleeding, GI losses) Use warmed fluids Septic Shock
Patients require large amounts of fluid replacement, sometimes as much as 6-10 L of isotonic crystalloids and 2-4 L of colloids Hemodynamic monitoring with PA or central venous catheter and arterial pressure monitoring may be necessary Overall goal of fluid resuscitation is to restore perfusion If that cannot be accomplished with IV fluids, vasopressor drug therapy may be added Vasodilation and low CO, or vasodilator alone can cause low BP in spite of adequate volume resuscitation Vasopressin (Pitressin) may be given to patients refractory to vasopressor therapy Exogenous vasopressin is used to replace the stores of physiologic vasopressin that are often depleted in septic shock Vasopressor drugs may increase BP but may also result in a decrease stroke volume An inotropic agent (Dobutamine) is added to offset the decrease in stroke volume In addition, IV corticosteroids are recommended for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP In an attempt to meet the increasing tissue demands coupled with low SVR, the patient is able to achieve and maintain an adequate CO and has unmet tissue oxygen demands, the CO may need to be increased with Inotropes The adequacy of CO can be assessed using SvO2 monitoring Normal SvO2 is 65 to 75% and is a reflection of the balance between oxygen delivery and consumption If the balance is maintained, tissue demands will be met

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SHOCK, SIRS & MODS

Antibiotics are an important and early component of therapy Before beginning definitive treatment for the infection, the cause of the infection must first be identified Cultures (blood, wound exudates, urine, sputum, stool) are obtained before antibiotics are started Broad-Spectrum antibiotics are given initially, followed by antibiotics that are more specific once the organism has been identified Mortality rates for septic shock are very high Drotrecogin alpha (Xigris) o recombinant form of activated protein C, has demonstrated promise in treating patients with severe sepsis o Activated protein C is a naturally occurring substance whose exact mechanism of action is unknown- Thought to produce an anti-inflammatory effect by inhibiting TNF production and limiting inflammation o Activated protein C is found in subnormal levels in patient with sepsis o Drotrecogin interrupts the bodys response to severe sepsis, including bleeding and clotting abnormalities o The use of Drotrecogin has resulted in significant decrease in mortality rate when used for patients with severe sepsis and septic shock o Bleeding is the most serious adverse effect associated with its use Glucose levels should be maintained at less than 150 mg/dl Research has shown improved survival rates when continuous infusions of insulin and glucose were used to keep glucose levels between 80 and 110 mg/dl Therefore, frequent monitoring of glucose levels of all patients in septic shock is necessary Stress ulcer prophylaxis: histamine H2-receptor blockers (famotidine [Pepcid]) Deep vein thrombosis prophylaxis: low-dose unfractionated heparin or low-molecular weight heparin (enoxaparin [Lovenox])

Summary of specific strategies for the treatment of Septic Shock

Oxygenation Provide supplemental oxygen Intubation/ mechanical ventilation, if necessary Monitor SvO2 or ScvO2

Circulation
22

Aggressive fluid resuscitation End points of fluid resuscitation: CVP 15 mm Hg, PAWP 10-12 mm Hg

SHOCK, SIRS & MODS

Drug Therapy Antibiotics are ordered Vasopressors (Dopamine) Inotropes (Dobutamine) Anticoagulation (LMWH)

Supportive Therapies Obtain cultures (blood, wound) before beginning antibiotics Monitor temperature Control blood glucose Stress ulcer /DVT prophylaxis

Neurogenic Shock
Specific treatment is dependent on the cause Spinal cord Injury: general measures to promote spinal stability (Spinal precautions, cervical stabilization with a collar) are initially used. Once the spine is stabilized, definitive treatment for hypotension and bradycardia is essential to prevent further spinal cord damage Hypotension results from loss of sympathetic tone, is associated with peripheral vasodilation and decreased return Treatment: Vasopressors (phenylephrine [Synephrine]) to maintain BP and organ perfusion Atropine (Atropen) to treat bradycardia Fluids are administered cautiously as the cause of hypotension is not related to fluid loss Patient with spinal cord injury needs to be monitored for hypothermia due to hypothalamic dysfunction Although corticosteroids do not have an effect in neurogenic shock, methylprednisolone (Solu-Medrol) is used for patients with a spinal cord injury to prevent secondary spinal cord damage caused by the release of chemical mediators

Summary of specific strategies for the treatment of Neurogenic Shock

Oxygenation
23

Maintain a patent airway Provide supplemental oxygen Intubation/mechanical ventilation, if necessary

SHOCK, SIRS & MODS

Circulation Cautious administration of fluids

Drug Therapy Vasopressors (phenylephrine) for adequate BP and organ perfusion Atropine for Bradycardia Methyl Prednisolone to prevent secondary cord damage by chemical mediators

Supportive Therapy Minimize spinal cord trauma with stabilization Monitor temperature

Anaphylactic Shock
First strategy is managing patients at risk for anaphylactic shock is prevention Thorough history is a key in avoiding risk factors Clinical presentation is dramatic, and immediate intervention is required Epinephrine is the drug of choice to treat anaphylactic shock It causes peripheral vasoconstriction and bronchodilation and opposes the effect of histamine Diphenhydramine (Benadryl) is administered to block the massive 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 also be used to treat laryngeal edema Endotracheal intubation or cricothyroidotomy may be necessary to secure and maintain a patent airway Hypotension results from leakage of fluid leakage of fluid out of the intravascular space into the interstitial space as a result of increased vascular permeability and vasodilation Aggressive fluid resuscitation, predominantly with colloids, is necessary IV corticosteroids may be helpful in anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy

Summary of specific strategies for the treatment of Anaphylactic Shock

Oxygenation
24

Maintain a patent airway

SHOCK, SIRS & MODS

Optimize oxygenation with supplemental oxygen Intubation/mechanical ventilation, if necessary

Circulation Aggressive fluid resuscitation with colloids

Drug Therapy Antihistamines (Benadryl) Epinephrine (SubQ, IV, nebulized) Bronchodilators: nebulized (albuterol) Corticosteroids (if hypotension persists)

Supportive therapy Identify and remove offending cause Prevention via avoidance of unknown allergens Premedication with history of prior sensitivity (contrast media)

Nursing Management of Shock

Overall Goals Assurance of adequate tissue perfusion Restoration of normal or baseline BP Return, recovery of organ function Avoidance of Complications from prolonged states of hypoperfusion

Health Promotion Prevent shock, identify patients at risk Patient who is at risk for decreased oxygen delivery or tissue hypoxia is at risk for the development of shock Rest, analgesics, sedation, and judicious use of paralytic agents (if the patient is intubated) can reduce the myocardial demand for oxygen Carefully question about allergies before administering a new drug (even if the patient has received the same drug in the past), or before undergoing diagnostic procedures, involving the use of contrast media If the patients condition warrants receiving a medication to which he or she is at high risk for an allergic reaction (contrast media), the patient should receive a premedication such as Benadryl or methylprednisolone Careful monitoring of fluid status prevents hypovolemia

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SHOCK, SIRS & MODS

Carefully monitor all patients for infection, especially the ones who are immunocompromised

Acute Interventions Neurologic Status Orientation and LOC, should be assessed every hour or more often Best indicator of cerebral blood flow Be aware of changes in behavior, restlessness, hyperalertness, blurred vision, confusion and paresthesias The astute nurse must also be alert to any subtle changes like mild agitation Orient the patient to time, place, person and events Minimize noise and light levels to control sensory input A day-night cycle of activity and rest should be maintained as much as possible Sensory overload and disruption of the patients diurnal cycle may contribute to delirium

Cardiovascular Status HR, BP, central venous pressure, and PA pressures including continuous cardiac output should be assessed at least every 15 minutes PAWP should be measured every 1-2 hours Patients in shock often have hypotension Avoid Trendelenburg position as it may cause compromised pulmonary function and increased ICP ECG should be ,monitored continuously to detect dysrhythmias Assess heart sounds for presence of S3 or S4 or new murmurs. S3 in adult indicates HF Response to fluid and medications is assessed as often as every 10 to 15 minutes

Respiratory Status
26

Ensure adequate oxygenation, detect complications early, and provide data regarding the patients acid-base status Rate, depth, and rhythm of respirations are initially monitored as frequently as every 15 to 30 minutes Breath sounds should be assessed every 1 to 2 hours for any changes that may indicate fluid overload or accumulation of secretions Continuously monitor oxygen saturation. Pulse oximetry should be attached to nose or forehead in advanced shock because of poor peripheral circulation ABGs: Provide definitive information on ventilation and oxygenation status and acidbase balance

SHOCK, SIRS & MODS

Initial interpretation of ABGs is a nursing responsibility A PaO2 below 60 mm Hg (in the absence of chronic lung disease ) indicates the presence of hypoxemia and the need for the administration of higher oxygen concentrations or for a different mode of oxygen administration Low PaCO2 in the presence of low pH and low bicarbonate level may indicate that the patient is attempting to compensate for a metabolic acidosis Rising PaCO2 in the presence of a persistently low pH and PaO2 may indicate the need for intubation and mechanical ventilation Most patients with shock will be intubated and on mechanical ventilation Maintaining a patent airway and monitoring ventilatory related complications are critical

Renal Status Hourly measurement of UOP are essential in assessment of the adequacy of renal perfusion Indwelling bladder catheter is inserted to facilitate measurements UOP less than 0.5ml/kg/hr may indicate inadequate perfusion of the kidneys BUN and Serum Creatinine values are additional indicators used to assess renal function Serum Creatinine is a better indicator, because BUN values are influenced by catabolic state of the individual

Body Temperature and Skin Changes In the presence of an elevated or subnormal temperature, tympanic or pulmonary arterial pressures should be obtained hourly Normal temperature is monitored every 4 hours Keep patient comfortably warm with the use of light covers and the control of environmental temperature If the patients temperature rises above 101.5F (38.6C) and the patient becomes uncomfortable or experiences cardiovascular compromise, the fever may be managed with NSAIDs (ibuprofen [Motrin]), with acetaminophen (Tylenol), or by removing some of the patients covers Patients skin may be monitored for temperature, pallor, flushing, cyanosis, diaphoresis, and piloerection Capillary refill should also be assessed as an indicator of peripheral perfusion

Gastrointestinal
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Bowel sounds auscultated at least every 4 hours

SHOCK, SIRS & MODS

Assess abdominal distention as well If NG tube is inserted, drainage should be measured and checked for occult blood Stools should also be checked for occult blood

Personal hygiene Important for a patient in shock as impaired tissue perfusion predisposes the patient to skin breakdown and infection Bathing and other nursing measures must be carried judiciously because of problems with oxygen delivery to tissues Use clinical judgment in prioritizing care in order to limit the demands for increased oxygen Oral care for the patient is essential as mucous membranes may become dry and fragile in the volume-depleted patient Intubated patients usually have difficulty swallowing, resulting in pooled secretions in the mouth A water-soluble lubricant applied to the lips prevents drying and cracking Moist swabbing of the tongue and oral mucosa with saline solution or diluted mouthwash is also beneficial. Lemon glycerin swabs should not be used because they can cause further drying of the mucosa Passive ROM should be performed 3-4 times a day to maintain joint mobility Patient should be turned at least 1-2 hours and positioned in good body alignment to help prevent pressure ulcers Use of pressure-relieving mattress or specialty bed may be needed If possible, oxygen consumption (SvO2, ScvO2) should be monitored during all interventions to monitor patients tolerance to activity

Emotional Support and Comfort Assess and monitor for anxiety and pain Medications to decrease anxiety and pain are common modes of therapy Continuous infusions of benzodiazepines (lorazepam [Ativan]), an opioid or anesthetic (morphine, propofol [Diprivan]), and occasionally a neuromuscular blocking agent (cisatracurium [Nimbex]) are extremely helpful in decreasing anxiety, pain and oxygen demand Encourage family to talk to patient even if intubated, comatose or sedated Hearing is the last sense to be diminished If intubated patient can write provide magic slate, pencil, paper. Alphabet boards or signboards with common requests (fan, light, turn) are also useful

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SHOCK, SIRS & MODS

Provide simple explanations of procedures before they are carried out, as well as the current plan of care and rationale Family and significant others have a therapeutic effect on the patient, hence need support and comforting Family and significant others o Link patient to the outside world o Facilitate decision making and advise the patient o Assist with ADLs o Act as liaisons to advise the health care team of the patients wishes for care o Provide safe, caring, familiar relationships for the patient Provide family with simple and honest answers regarding progress and prognosis Support family when making difficult decisions regarding continuation of life support Support family decisions and facilitate realistic expectations and outcomes If desired, the family may be encouraged to perform simple comfort measures If possible the same nurses should continuously care for the patient to decrease anxiety, limit contradictory information and increase trust.

Ambulatory and Home Care Rehabilitation of the patient who has experienced critical illness necessitates correction of the cause and prevention or early treatment of complications Continue to monitor for indications of complications throughout the recovery period Complications include o Decreased ROM o Decreased Physical endurance o Renal failure following ATN o Development of fibrotic lung disease as a result of ARDS Thus patients recovering from shock require diverse services on discharge These can include o Admission to transitional care (for mechanical ventilation weaning) o Rehabilitation centers (inpatient or outpatient) o Home health agencies The nurse should begin to anticipate and facilitate a safe transition from the hospital to home on admission

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SHOCK, SIRS & MODS Systemic Inflammatory Response Syndrome (SIRS)

Etiology and Pathophysiology
Systemic response to variety of insults, including infection (referred to as sepsis), ischemia, infarction, and injury Characterized by generalized inflammation in organs remote from the initial insult Normally the inflammatory process is contained within a confined environment Can be triggered by many mechanisms. Examples include Mechanical tissue trauma: burns, crush injuries, surgical procedures Abscess formation: intraabdominal, extremities Ischemic or necrotic tissue: pancreatitis, vascular disease, myocardial infarction Microbial invasion: bacteria, viruses, fungi, parasites Endotoxin release: gram-negative bacteria Global perfusion deficits: post-cardiac resuscitation, shock states Regional perfusion deficits: distal perfusion deficits

Multiple Organ Dysfunction Syndrome (MODS)

Failure of two or more organ systems in an acutely ill patient such that homeostasis cannot be maintained without intervention Results from SIRS These two syndromes represent the ends of a continuum Transition from SIRS to MODS does not occur in a clear-cut manner

Organ and Metabolic Dysfunction

When the inflammatory response is not controlled, consequences occur These include the activation of inflammatory cells and release of mediators, direct damage to the endothelium, and hypermetabolism Vasodilation becomes excessive and leads to a decreased SVR and hypotension There is an increase in vascular permeability that allows the mediators and protein to leak out of the endothelium and into the interstitial space The white blood cells begin to phagocytize the foreign debris, and the coagulation cascade is activated Organ perfusion may be compromised because of hypotension, decreased perfusion, microemboli, and redistributed or shunted blood flow

Respiratory System

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SHOCK, SIRS & MODS

The respiratory system is often the first system to show signs of dysfunction if SIRS and MODS Inflammatory mediators have a direct effect on the pulmonary vasculature The endothelial damage from the release of inflammatory mediators results in an increase in capillary permeability and facilitates movement of proteinaceous fluid from the pulmonary vasculature into the pulmonary interstitial spaces The fluid then moves to the alveoli, causing alveolar edema Type I pneumocytes (alveolar cells) are destroyed Type II pneumocytes become dysfunctional, and there is a decrease in surfactant production The alveoli collapse, creating an increase in shunt (blood flow to the lungs that does not participate in gas exchange) and a worsening of the ventilation-perfusion mismatch The end result is ARDS Patient with ARDS require aggressive pulmonary management with mechanical ventilation Management Prevention Optimize oxygen delivery /minimize oxygen consumption Mechanical ventilation Positive end-expiratory pressure Lung protective modes (pressure control/inverse ratio ventilation, low tidal volumes) Permissive hypercapnia Positioning (continuous lateral rotation therapy, prone positioning)

Clinical Manifestation of Respiratory Failure Development of ARDS Severe Dyspnea PaO2/FiO2 ratio < 200 Bilateral fluffy infiltrates on chest x-ray PAWP <18 mm Hg Ventilation/Perfusion (V/Q) mismatch Pulmonary hypertension Increased minute ventilation Increased respiratory rate Decreased compliance Refractory hypoxemia Cardiovascular System
31

Include myocardial depression and massive vasodilation in response to increasing tissue demands Vasodilation leads to decrease in SVR and BP The baroreceptor reflex causes release of inotropic (increased force of contraction) and chronotropic (increasing heart rate) factors that enhance CO To compensate hypotension, CO increases by an increase in HR and Stroke Volume Increases in capillary permeability cause a shift of albumin and fluid out of the vascular space, further diminishing venous return and thus preload The patient becomes warm and tachycardic with a high CO and low SVR

SHOCK, SIRS & MODS

Other signs include decreased capillary refill, skin mottling, increased central venous pressure and PAWP, and dysrhythmias SvO2 may be abnormally high because the patient is perfusing areas not consuming much oxygen (skin, nonworking muscle) while other areas may have blood shunted away from them Eventually, either perfusion of vital organs becomes in sufficient or the cells are unable to use oxygen and their function is further compromised Management Volume management PA catheter for hemodynamic monitoring Increased preload via volume replacement Maximize myocardial function Maintain CO Arterial Pressure monitoring Maintain MAP > 60 mm Hg Vasopressors Continuous SvO2 monitoring; balance O2 supply and demand Continuous ECG monitoring Circulatory assist devices IABP VAD

Clinical Manifestation of CV Failure Myocardial depression Biventricular failure Systolic/diastolic dysfunction Increased HR/CO/SVR Decreased stroke volume Decreased MAP Decreased ejection fraction/contractility

Neurologic System Dysfunction commonly manifests as mental status changes with SIRS and MODS Acute alteration in mental status can be a early sign of MODS Patient may become confused and agitated, combative, disoriented, lethargic and comatose These changes may be due to hypoxemia, the direct effect of the inflammatory mediators, or impaired perfusion Management Evaluate for hepatic/metabolic encephalopathy Optimize cerebral blood flow Decreased cerebral oxygen requirements Prevent secondary tissue ischemia Calcium channel blockers 9reduce cerebral vasospasm) Prevents further compromise

Clinical Manifestation of CNS Failure Acute change in neurologic status Fever Hepatic encephalopathy Seizures Confusion/disorientation Failure to wean/ prolonged rehabilitation
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SHOCK, SIRS & MODS

Renal System Acute Renal Failure (ARF) is frequently seen in SIRS and MODS ARF can be caused not only by hypoperfusion but also by the effect of the mediators When there is decreased perfusion to the kidneys, the SNS and the renninangiotensin system are activated The stimulation of RAS results in systemic vasoconstriction and aldosteronemediated sodium and water reabsorption Another risk factor to the development of ARF is the use of nephrotoxic drugs Antibiotics commonly used to treat gram-negative bacteria, such as aminoglycosides, can also be nephrotoxic Careful monitoring of drug levels is essential to avoid nephrotoxic effects Management Diuretics Loop diuretics (furosemide [Lasix]) May need to increase dose due to decreased GFR Dopamine (Inotropin) Enhances renal blood flow Improves renal perfusion Increases urine output (if volume resuscitated) May work synergistically with diuretics Continuous renal replacement therapy (CRRT)

Clinical Manifestation of Renal Failure Prerenal: renal hypoperfusion BUN/Creatinine ratio >20:1 Decreased Urine Na+ <20 mEq/L Increased Urine specific gravity >1.020 Increased Urine osmolality Intrarenal: Acute Tubular Necrosis BUN/Creatinine ratio <10:1- 15:1 Increased Urine Na+ >20 mEq/L Decreased Urine osmolality Urine specific gravity (~ 1.020)

Gastrointestinal System GI tract also plays a key role in the development of MODS GI motility is often decreased in critical illness, causing abdominal distention and paralytic ileus In the early stages of SIRS and MODS, blood is shunted away from the GI mucosa, making it highly vulnerable to ischemic injury Decreased perfusion leads to a breakdown of this normally protective mucosal barrier , thus increasing the risk of ulceration and GI bleeding With the breakdown of the mucosal barrier of the gut, the potential for bacterial translocation from the GI tract into circulation exists

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SHOCK, SIRS & MODS

There is a possibility that insult to the GI system may induce the production of inflammatory mediators, thus contributing to the systemic inflammation leading to MODS Management Stress ulcer prophylaxis Antacids (Maalox) Histamine H2-receptor blockers (famotidine [Pepcid]) Proton Pump Inhibitors (omeprazole [Prilosec]) Sucralfate (Carafate) Dietary consultation Enteral Feedings Stimulate mucosal activity Provide essential nutrients and optimal calories

Clinical Manifestation of GI Failure Mucosal ischemia Decreased intramucosal pH Potential translocation of gut bacteria Hypoperfusion leads to decreased peristalsis, paralytic ileus Mucosal ulceration on endoscopy GI bleeding

Metabolic Changes Pronounced in SIRS and MODS Both syndromes trigger a hypermetabolic response Glycogen stores are rapidly converted to glucose (glycogenolysis) Once glycogen is depleted, amino acids are converted to glucose (gluconeogenesis), reducing protein stores Fatty acids are mobilized for fuel Catecholamines and glucocorticoids are released and result in hyperglycemia and insulin resistance The net result is a catabolic state, and lean body mass (muscle) is lost The hypermetabolism associated with SIRS and MODS can last for several days and results in liver dysfunction Liver dysfunction in MODS may exist long before clinical evidence is present Protein synthesis is impaired Liver is unable to synthesize albumin , one of the key proteins that has an essential role in maintaining plasma oncotic pressure Consequently plasma oncotic pressure is altered and fluid and protein leak from the vascular spaces to the interstitial spaces Administration of albumin does not normalize oncotic pressure in these patients As the hypermetabolism persists, the patient is unable to convert lactate to glucose, and lactate accumulates (Lactic Acidosis)

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SHOCK, SIRS & MODS

Despite increases in glycogenolysis and gluconeogenesis, eventually the liver is unable to maintain a glucose level and the patient becomes hypoglycemic

Clinical Manifestation of Hepatic Failure Bilirubin > 2 mg/dl Elevated liver enzymes (ALT,AST,GGT) Increased serum NH3 Decreased serum albumin, prealbumin, transferin Jaundice Hepatic encephalopathy

Management Maintain adequate tissue perfusion Provide nutritional support (Enteral feedings) Judicious use of hepatically metabolized drugs

Clinical Manifestation of Endocrine Failure Hyperglycemia to hypoglycemia

Management Continuous infusion of insulin and glucose to maintain blood glucose < 150 mg/dl

Hematologic System Failure of coagulation system manifests as DIC DIC results in simultaneous microvascular clotting and bleeding because of the depletion of clotting factors and platelets in addition to excessive fibrinolysis Management Observe for bleeding from obvious and/or occult sites Replace factors being lost (platelets) Minimize traumatic interventions (intramuscular injections, multiple venipunctures)

Clinical Manifestation of GI Failure Increased bleeding times Prolonged PT, PTT Decreased platelet counts (thrombocytopenia) Increased Fibrin Split Products (FSPs) Increased D-dimer test

Electrolyte Imbalances
35

Common and related to hormonal and metabolic changes, and fluid shifts These changes exacerbate mental status changes, neuromuscular dysfunction, and Dysrhythmias The release of ADH and aldosterone results in sodium and water retention Aldosterone increases urinary potassium loss Catecholamines cause potassium to move into the cell, resulting in hypokalemia

SHOCK, SIRS & MODS

Hypokalemia is associated with Dysrhythmias and muscle weakness Metabolic Acidosis results from impaired tissue perfusion, hypoxia, and shift to anaerobic metabolism with a resultant increase in Hydrogen ion production Progressive Renal Dysfunction also contributes to metabolic acidosis Hypocalcemia, hypomagnesemia, and hypophosphatemia are common.

Nursing and Collaborative Management of SIRS and MODS

Prognosis for patient with MODS is poor Mortality rates 90 95% when three or more organ systems fail Most important goal is to prevent the progression of SIRS to MODS A critical component of the nursing role is vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction Collaborative care includes

Prevention and Treatment of Infection Aggressive infection strategies are essential to decrease the risk for nosocomial
infections

Despite aggressive interventions host dysfunction may lead to the development of an

infection

Once an infection is suspected, interventions to control the source must be instituted Appropriate cultures should be sent, and broad-spectrum antibiotic therapy should
be initiated

Early aggressive surgery is recommended to remove necrotic tissue (early

debridement of burn tissue) that may provide a culture medium for microorganisms

Once a specific organism is identified, therapy should be modified if necessary Aggressive pulmonary management, including early ambulation, can reduce the risk
for infection

Strict asepsis can decrease infections related to intraaterial lines, endotracheal tubes,
urinary catheters, IV lines and other invasive devices and procedures

Maintenance of Tissue Oxygenation

Hypoxemia frequently occurs in SIRS and MODS These patients have greater oxygen needs and decreased oxygen supply to the tissues Interventions that decrease oxygen demand and increase oxygen delivery are essential

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SHOCK, SIRS & MODS

Sedation, mechanical ventilation, analgesia, paralysis, and rest may decreased
oxygen demand and should be considered

Oxygen delivery may be optimized by maintaining normal levels of hemoglobin

(transfusion of Packed RBCs) and PaO2 (80 to 100 mm Hg), using individualized tidal volumes with PEEP, increasing preload or myocardial contractility to enhance CO, or reducing afterload to increase CO

Nutritional and Metabolic Needs Hypermetabolism in SIRS or MODS can result in profound weight loss, cachexia, and
further organ failure

Protein-calorie malnutrition is one of the primary manifestations of hypermetabolism

and MODS

Total energy expenditure is often increased 1.5 to 2.0 times the normal metabolic
rate

Because of their relatively short half-life, plasma transferrin and prealbumin levels
are monitored to assess hepatic protein synthesis

The goal of nutritional support is to preserve organ function Providing early and optimal nutrition decreases morbidity and mortality rates in
patients with SIRS and MODS

The use of Enteral route is preferable to parenteral nutrition If Enteral route cannot be used or cannot meet the caloric needs, parenteral nutrition
should be initiated or added

Attention to tight glucose control (blood glucose <150 mg/dl) using insulin infusion is
important in these patients

Support of Failing Organs

Support of any failing organ is primary goal of therapy Patient with ARDS requires aggressive oxygen therapy and mechanical ventilation DIC should be treated appropriately (blood product administration) Renal failure may require dialysis CRRT is better tolerated than hemodialysis, especially in patient with hemodynamic instability

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