CH 14 Overview of Shock and Sepsis

Sepsis/Septic Shock Bundle of Care *Antibiotics*

‒ Administered within 1 hour upon arrival ‒ Cultures should be done before antibiotics are administered Antibiotics - Evidence suggests that prompt identification and treatment of the offending microorganism with antibiotics can decrease mortality in sepsis. It is recommended that antibiotics be administered within 1 hour of arrival at the hospital. Cultures should be done before antibiotics are administered to ensure appropriate antibiotic coverage.

Cardiogenic Shock Risk Factors

‒ End stage heart failure ‒ Cardiomyopathy ‒ Hypertension ‒ Diabetes ‒ Multi-vessel disease ‒ Acute vascular disease

Sepsis/Septic Shock Bundle of Care *Blood work*

‒ Serum lactate ‒ Blood cultures ‒ CBC ‒ Coagulation studies ‒ Liver function tests ‒ ABG Obtaining a serum lactate and two sets of blood cultures should be done immediately. Other recommended laboratory work includes: a complete blood count with differential, coagulation studies, chemistries, liver function tests, and arterial blood gasses, as well as the culturing of any other potential sources of infection.

Hypovolemic Shock Laboratory tests

• *ABG's* Initial ABGs may reflect a respiratory alkalosis due to tachypnea. Later stages of shock reveal a metabolic acidosis due to anaerobic metabolism. • *Venous oxygen saturation* • *Hemoglobin and hematocrit* Hemoglobin and hematocrit values may be decreased if the cause of hypovolemic shock is bleeding. • *Metabolic profile* Renal failure and liver failure, as evidenced by increased BUN and creatinine levels and liver function test results, may become evident as a result of decreased organ perfusion. • *Lactate* Increased lactate level and negative base deficit are evidence of poor perfusion at the cellular level. Decreasing lactate level is an endpoint demonstrating adequate resuscitation.

Sepsis/Septic Shock Complications

• *DIC* It occurs because of enhanced coagulation that results from the release of procoagulant factors as part of the inflammatory response associated with sepsis • *MODS* Another complication that occurs as a result of the excessive inflammation associated with severe injury or sepsis.

Cardiogenic Shock Laboratory tests

• ABG's • Venous oxygen saturation • Metabolic profile • Lactate

Anaphylaxis Clinical Manifestations

• SOB • Tachypnea • Wheezing • Stridor • Cyanosis • Confusion • Urticaria • Hypotension • Cool, pale, clammy skin • Weak pulses • Edema

Hypovolemic Shock Assessment and Analysis

• Varies depending upon stage of shock • Progressive: ‒Hypotension ‒Tachycardia ‒Weak pulses ‒Tachypnea The clinical manifestations of hypovolemic shock are related to the decrease in cardiac output and impaired blood flow to all vital organs. The manifestations vary depending on the stage of shock. Without adequate treatment, the results are hypotension; tachycardia with weak pulses; tachypnea; cold, cyanotic, and mottled skin; decreased or absent urine output; severely decreased level of consciousness; and severely decreased or absent bowel sounds. Continuing decompensation results in multiple organ system failures, as evidenced by increased renal studies such as blood urea nitrogen (BUN) and creatinine and increased liver function tests. The refractory stage is evidenced by coma, severe hypotension, bradycardia, and acute respiratory failure due to profound cellular hypoxia. Hemodynamic parameters also vary according to the stage of shock. If a PA catheter is in place, decreased cardiac output will be noted beginning in the initial stage of shock. The compensatory stage is notable for an increase in systemic vascular resistance due to the sympathetic nervous system response. Central venous pressure and PAOP are decreased. Although initial compensation maintains a normal blood pressure, hypotension eventually results.

Neurogenic Shock Clinical Manifestations

• Warm, dry skin • Flushed appearance • Decreased cardiac output • Decreased systemic vascular resistance

Stages of Shock - Compensatory

Neural compensation Endocrine compensation Chemical compensation

Sepsis/Septic Shock Clinical Manifestations

*Early stage* ‒Tachycardia ‒Bounding pulses ‒Fever *Late stage* ‒Cool, pale skin ‒Weak, thready pulses ‒Tachycardia ‒Hypotension The clinical manifestations of septic shock reflect the poor vascular tone and vasodilation that result in increased vascular capacity and blood pooling in the venous system. There is adequate blood volume, but a state of relative hypovolemia exists because of decreased venous return to the right heart. Septic shock is typically divided into early and late stages. Early stages of septic shock, sometimes termed hyperdynamic or warm sepsis, reflect the initial inflammatory response. The patient is tachycardic, with bounding pulses and warm, flushed skin, and is febrile. Blood pressure may be normal as a result of initial compensatory responses. Initial signs of decreased organ perfusion may be present, such as confusion and decreased urine output. Hemodynamic parameters indicate increased cardiac output that occurs as long as there is adequate fluid resuscitation. Filling pressures, CVP, and PAOP remain low. Systemic vascular resistance is low because of profound systemic vasodilation. Venous oxygen levels are temporarily increased due to the increase in cardiac output.

Sepsis/Septic Shock Assessment and analysis

• Early signs • Late signs • Complications ‒Enhanced coagulation ‒Necrotic extremities ‒Excessive bleeding Unlike other forms of shock, the early clinical manifestations of septic shock are related to the initial increase in cardiac output that occurs due to the tachycardia and decreased SVR associated with sepsis. The patient presents as warm and flushed, with bounding pulses. Later manifestations reflect the prolonged poor tissue perfusion. Hypotension, tachycardia, and tachypnea are present. Systemically, the patient has a decreased level of consciousness and weak pulses, with cold, cyanotic, and mottled skin. Urine output and bowel sounds are decreased or absent. Without successful intervention, the clinical manifestations of enhanced coagulation, such as necrotic tissue in the extremities, begin to appear. In later stages, excessive bleeding from any puncture wounds, IV sites, or wounds begins.

Obstructive Shock Risk Factors

• Extracardiac disorders that impair ventricular filling • *Acute pulmonary embolism* • Impaired cardiac emptying • *Cardiac tamponade* • *Tension pneumothorax*

Anaphylaxis Pathophysiology

• Hypersensitivity reaction • Histamine release • Widespread venous dilation • Increased capillary permeability • Smooth muscle contraction

Gastrointestinal Assessment in Shock

• Hypoactive bowel sounds • Nausea • Vomiting The GI system indicates poor perfusion through sluggish, hypoactive bowel sounds that reflect a slowing of intestinal activity. Nausea and vomiting may also be present. The GI system is particularly vulnerable to poor perfusion and ischemia. Cell damage in the GI tract allows translocation of intestinal bacteria to the systemic circulation, increasing the risk of sepsis. Some have suggested that hypoperfusion in the GI system may initiate a systemic inflammatory response, which, if not resolved, may be the precursor to multiple organ dysfunction syndrome (MODS).

Sepsis/Septic Shock Actions

• Meticulous hand washing, aseptic technique • Oxygenation • Prepare for intubation • Lactate level • Blood cultures • Administer antibiotics • Fluid replacement • Vasoactive support • Mouth care

Renal Assessment in Shock

• Oliguria, then anuria • Increased creatinine The renal system provides a clear indication of poor perfusion if urine output decreases. Oliguria is a common finding in early shock because of decreased perfusion of the renal tubules, which stimulates the initiation of the renin- angiotensin-aldosterone system. If unresolved, later stages of shock will present with anuria, increased creatinine level, and other signs of acute renal failure.

Hypovolemic Shock Medical Management

• Optimize oxygenation • Fluid resuscitation • Identify and treat underlying cause: ‒Fluid ‒Blood products Resuscitation priorities in hypovolemic shock include maximizing oxygenation, initiating fluid resuscitation, and identifying and treating the underlying cause. Maximizing oxygenation is essential in the treatment of the patient in shock. Assessing and stabilizing the patient's airway is the immediate first priority. Identifying and controlling further loss of blood or fluid is an obvious priority in this patient. If bleeding or fluid loss is not immediately apparent, diagnostic studies may be necessary to determine the cause of shock.

Stages of Shock - Refractory

• Prolonged inadequate blood supply to cells • Cell death Multisystem organ failure: • Coma • Severe hypotension • Ischemic and necrotic cold extremities • Renal failure • Hepatic failure The refractory stage is marked by prolonged inadequate blood supply to the cells, resulting in cell death and multisystem organ failure. There is a loss of aerobic metabolism, and only extremely inefficient anaerobic metabolism is available. *Shock is irreversible at this stage.*

Changes in CNS perfusion may be the initial indication of inadequate DO2 to the tissues

• Restlessness • Confusion • Irritability • Lethargy • Coma

Neurogenic Shock Medical Management

• Treat cause • Fluid resuscitation • Vasoactive medications • Atropine • Transcutaneous or transvenous pacing • Ventilatory support The treatment focus is on providing cardiovascular support while attempting to resolve the primary cause of shock. Cardiovascular support is done through cautious fluid resuscitation and the use of vasoactive IV medications such as dopamine, epinephrine, norepinephrine, or phenylephrine. If necessary, bradycardia is treated with atropine. Repeated episodes of bradycardia may require transcutaneous or transvenous pacing. Ventilatory support through intubation and mechanical ventilation may be required.

Obstructive Shock Medical Management

• Treat cause • Supplemental oxygen • Vasoactive infusion As with other forms of shock, providing oxygen through a 100% nonrebreather mask is a minimal first step to stabilize oxygenation. Intubation and mechanical ventilation are frequently necessary to support ventilation and maximize oxygenation. Improving or enhancing oxygenation may help decrease myocardial workload, increase myocardial oxygen supply, and help preserve myocardial tissue. Vasoactive drugs may be utilized to help maintain blood pressure in the short term, but early definitive treatment of the cause of obstructive shock is necessary for survival.

Obstructive Shock Pathophysiology

Mechanical barrier to ventricular filling or emptying ‒ Decreased cardiac output ‒ Impaired tissue perfusion Obstructive shock is caused by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload) causing decreased cardiac output. As in cardiogenic shock, symptoms are independent of fluid volume status. The mechanical obstruction to the pumping action of the heart results in decreased cardiac output and poor perfusion at the tissue level. The specific pathophysiology varies depending on the cause of shock. For instance, a PE, typically the result of the mobilization of clot material to the lungs from a deep vein thrombosis (DVT), may result in obstructive shock. This results in extreme increases in right heart afterload due to an obstruction of blood flow into the lungs because of a clot or embolus in the PA. Alveoli are ventilated but not perfused, producing an extreme ventilation-perfusion mismatch. Obstructive shock caused by cardiac tamponade is the result of excessive pressure on the heart muscle that occurs as fluid fills the pericardial sac. This may be the result of trauma to the cardiac muscle that results in bleeding and blood in the pericardial sac or a large, uncontrolled pericardial effusion. As the fluid accumulates around the heart, less blood enters the ventricles with each successive diastole, impairing ventricular filling.

Neurogenic Shock Epidemiology

Neurogenic shock is caused by disruption of the sympathetic nervous system, typically as a result of spinal cord injury, regional spinal anesthesia, or an injury to the brain. The incidence of neurogenic shock is approximately 20% in patients with a cervical spinal cord injury. It is very uncommon in patients with lower spinal cord injuries.

Sepsis/Septic Shock Medical management

Prevention ‒ Hand washing ‒ Aseptic technique for procedures Aggressive mouth care, including brushing the teeth with chlorhexidine products, in ventilated patients may help prevent ventilator-associated pneumonia.

Compensatory Stage: Chemical compensation

Produced through the reaction of chemoreceptors in the aorta and carotid arteries that are stimulated by low oxygen levels. Low oxygen levels occur as a result of decreased blood flow through the alveoli. Tachypnea, or hyperventilation, occurs in an effort to increase circulating oxygen levels. The respiratory alkalosis that results causes a constriction of the carotid arteries.

Hypovolemic Shock

Results when there is a rapid fluid loss resulting in inadequate circulating volume. Most commonly, hypovolemic shock is secondary to blood loss from trauma or severe GI bleed

Distributive Shock is defined as:

The result of disease states such as sepsis, anaphylaxis, or neurogenic shock that cause poor vascular tone and vasodilation, resulting in increased vascular capacity and venous pooling

Overview of Shock

The tissues of the body require a continuous supply of oxygen in order to maintain cellular functioning. Shock is a *life-threatening syndrome* that occurs when the *circulatory system is unable to supply adequate amounts of oxygen to the tissues to meet basic metabolic requirements*. This creates a state of tissue hypoxia, which is an imbalance of cellular oxygen supply and demand. Without immediate treatment to reverse this imbalance, organ system failure and death may result. Important concepts to understand when evaluating shock include cardiac output, oxygen delivery, oxygen consumption, and oxygen debt.

Classifications of Shock

Hypovolemic Cardiogenic Distributive Obstructive

Sepsis/Septic Shock Bundle of Care *Hour 1*

‒ Activities that need to be completed within 1 hour after identifying sepsis ‒ Treatment may not be completed in 1 hour ‒ Treatment should begin immediately

Respiratory Assessment in Shock

• *Tachypnea* Early stages of shock are characterized by increased respirations done in an effort to increase oxygenation and decrease carbon dioxide (CO2) levels due to the metabolic acidosis • *ABG's* • *Pulse oximetry*

Sepsis/Septic Shock Laboratory tests

• ABGs • Venous oxygen saturation • Metabolic profile • Lactate • Clotting studies

Hypovolemic Shock Clinical Manifestations

• Restlessness or confusion • Decreased urine output • Pale, cool, clammy skin • Weak pulses • Delayed capillary refill • Hyperventilation -> respiratory alkalosis • Hypoactive bowel sounds • Hyperglycemia

Neurogenic Shock Pathophysiology

• Sympathetic nervous system disruption ‒ Decreased vascular tone ‒ Increased peripheral vascular volume ‒ Decreased venous return ‒ Decreased cardiac output > relative hypovolemia ‒ Unopposed parasympathetic activity > profound bradycardia ‒ Systemic hypoperfusion

Neurogenic Shock Actions

• *Administer IV fluids as ordered* Cautious fluid resuscitation is provided to increase vascular volume to match the increase in the size of the vascular space due to the massive dilation. • *Administer IV medications as ordered* Vasoactive drips: Administration of vasoactive drips aids in increasing vasomotor tone and systemic vascular resistance. Atropine: Atropine is used for the treatment of bradycardia to block the action of the vagus nerve in the parasympathetic nervous system, increasing the HR. • *Prepare for pacing* Pacing may be necessary to treat recurrent episodes of bradycardia. • *Raise head of bed slowly* Because of loss of systemic vasomotor tone, patients in neurogenic shock are particularly vulnerable to orthostatic hypotension. • *Apply venous thromboembolism prophylaxis* Patients in neurogenic shock are at high risk for venous thromboembolism, particularly in cases where the etiology of neurogenic shock is spinal cord injury.

Cardiovascular Assessment in Shock

• *Hypotension* In shock, blood pressure decreases because of inadequate venous return to the heart, vasodilation, or decreased contractility of the heart muscle. It is important to remember that a return to the baseline blood pressure level does not mean the resolution of the problem, but prolonged hypotension does indicate the continued presence of shock • *Narrow pulse pressure* Results from compensatory vasoconstriction causing an increase in diastolic pressure with only a slight increase in systolic pressure • *Tachycardia, then bradycardia* Tachycardia is a typical finding due to stimulation of the sympathetic nervous system as a way to increase cardiac output. If shock is not resolved but is allowed to progress to later stages, the HR may slow • *Skin color* • *Peripheral pulses* • *Capillary refill* Because of shunting of the blood to vital organs, the skin and periphery become cool, pale, mottled, or cyanotic, with thready pulses and sluggish capillary refill.

Distributive Shock

• *Neurogenic shock* • *Anaphylaxis* Distributive shock is the result of disease states that cause poor vascular tone and vasodilation, resulting in increased vascular capacity and venous pooling. Even though blood volume is adequate, a state of relative hypovolemia exists because of decreased venous return to the right heart. Sepsis is the most common cause of widespread vasodilation and distributive shock. Anaphylaxis, another cause of distributive shock, is caused by the release of histamine, which results in vasodilation, decreased venous return, and hypotension. The least common form of distributive shock is neurogenic shock, which is due to a loss of vasomotor tone. There is a loss of stimulation from the sympathetic nervous system, resulting in the vessel walls relaxing and dilating. Venous return is decreased, and the patient is hypotensive, with a decreased cardiac output. Neurogenic shock can be caused by an injury to the brain, general or spinal anesthesia, or spinal cord injury.

Sepsis/Septic Shock Assessments

• *Neurological status* Decreased level of consciousness occurs a result of decreased cardiac output. • *Vital signs* Hypotension is present because of vasodilation, producing relative hypovolemia and decreased venous return. Tachycardia will be present as one of the compensatory mechanisms. Initially, the patient will be febrile as an adaptive response. In later stages, the patient will be hypothermic, potentially signaling the body's inability to continue the adaptive response. • *Hemodynamic readings* Initially, cardiac output is increased; however, as sepsis progresses, cardiac output decreases as a result of continued decreases in filling pressures, such as right atrial and pulmonary artery occlusion pressures. Initially, systemic vascular resistance is decreased as a result of widespread vasodilation. Later, it may increase due to compensation and vasopressor therapy. • *Urine output* Decreased urine output occurs as a result of decreased cardiac output. • *Skin color and temperature* Initially, the patient's skin is flushed and warm because of increased cardiac output. Later, the skin becomes cold and clammy, signaling the progression of shock. Tissue necrosis in the extremities may indicate the enhanced coagulation of DIC. • *Bleeding* Excessive bleeding from wounds and puncture sites may be present because of consumption of clotting factors in DIC.

Cardiogenic shock is defined as:

A state of hypoperfusion at the tissue level resulting from severe impairment of ventricular contraction in the presence of adequate vascular volume. As a result of damaged myocardium, there is a marked reduction in contractility, which reduces the ejection fraction (the percentage of blood ejected from the ventricle with each contraction) and cardiac output. The result is increased left and right ventricular filling pressures but decreased cardiac output.

Sepsis/Septic Shock Corticosteroid Therapy

Adrenal insufficiency is sometimes a feature of sepsis, but the use of steroids in treatment is not routinely recommended. Studies have been inconclusive as to the benefits of low-dose steroids in septic shock. They have not been shown to decrease mortality in sepsis. The Surviving Sepsis guidelines recommend low-dose steroids only if the patient has not been responsive to fluid and vasopressor therapy.

Compensatory Stage: Endocrine compensation

After a drop in blood pressure, the kidneys respond by releasing the enzyme renin. Renin reacts with angiotensinogen to create angiotensin I. Angiotensin I is then converted in the lungs to angiotensin II via angiotensin-converting enzyme. Angiotensin II is a potent vasoconstrictor that increases blood pressure. Angiotensin II also acts on the adrenals to release aldosterone. The release of aldosterone promotes sodium and water reabsorption in the kidneys, which increases the circulating fluid volume. This is called the renin-angiotensin-aldosterone system (RAAS). Aldosterone release is also stimulated by the release of adrenocorticotropic hormone in response to low blood pressure from the anterior pituitary, which then stimulates the adrenal cortex to release aldosterone. Also in an effort to increase the circulating volume, antidiuretic hormone is released by the posterior pituitary in response to decreased blood volume. It acts on the kidney to conserve water.

Anaphylaxis Medical Management

• *Removal of trigger* If the trigger is the administration of antibiotics or blood, the infusion should be stopped immediately. If the trigger is a bee sting, the stinger should be removed. • *IM epinephrine* The immediate first treatment priority. Intramuscular is the preferred route of administration because it provides a consistent, rapid rise in therapeutic concentration and lowers the risk of cardiovascular complications that can be seen with IV administration. • *Maintain patent airway* The second priority is assessing the airway, maximizing oxygenation through the initiation of oxygen via a 100% nonrebreather, and preparing for intubation if the airway is compromised. • *Circulatory support* Circulatory support via administration of IV fluid is essential. Other medications utilized to treat anaphylaxis include antihistamines, corticosteroids, and inhaled bronchodilators.

Hypovolemic Shock Pathophysiology

• Acute loss of volume ‒Blood or fluid • Decreased venous return • Decreased stroke volume and cardiac output • Decreased tissue perfusion The initial response is the stimulation of the sympathetic nervous system, which increases the HR in an attempt to increase cardiac output. The sympathetic nervous system also stimulates the release of epinephrine and norepinephrine from the adrenal medulla, improving contractility and inducing systemic vasoconstriction. Blood pressure and cardiac output are increased. Blood flow is redirected from nonessential organs to vital organs such as the heart and brain.

Cardiogenic Shock Clinical Manifestations

• Chest pain • Diaphoresis • Nausea and vomiting • Decreased cardiac output ‒Hypotension, decreased LOC, decreased urine output, weak pulses, cool skin, hypoactive bowel sounds • Metabolic acidosis

Neurogenic Shock Assessment and Analysis

• Decreased cardiac output • Bradycardia The clinical manifestations of neurogenic shock are slightly different from the manifestations of other forms of shock. Similar to other forms of distributive shock, the patient has decreased cardiac output as a result of decreased vascular tone and reduced venous return; however, because of the disruption in the sympathetic nervous system, the patient may be bradycardic rather than tachycardic. The patient may appear pink and flushed as a result of vascular vasodilation.

Obstructive Shock Clinical Manifestations

• Decreased level of consciousness • Decreased urine output • Poor pulses • Pale, cool skin • Decreased bowel sounds • Chest pain • Nausea and vomiting • SOB Hemodynamic parameters obtained through a PA catheter indicate variable CVP and PAOP depending on the problem, impaired filling or impaired emptying. Systemic vascular resistance is high, and cardiac output is very low. Venous oxygen saturation is decreased.

Sepsis/Septic Shock Pathophysiology

• Deregulated host response to infection • Excessive release of proinflammatory cytokines ‒Vasodilation ‒Decreased vasomotor tone ‒Increased capillary permeability Sepsis is defined as life-threatening organ dysfunction caused by a deregulated host response to infection. Septic shock occurs when circulatory and metabolic abnormalities are profound, greatly increasing mortality. The invasion of a pathogen initiates a series of complex responses by the host's immune system. The initial, immediate response is the activation of the innate immune response. Sepsis occurs when the inflammatory response is no longer localized. The response becomes amplified and uncontrolled. The excessive release of proinflammatory cytokines results in damage to the endothelial cells lining the blood vessels, producing vasodilation, decreased vasomotor tone, and increased capillary permeability.

Cardiogenic Shock Medical Management

• ECG, cardiac enzymes, chest Xray • Airway/oxygenation • Emergency revascularization, mechanical circulatory support • Vasopressors, inotropes

Obstructive Shock

Caused by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload), causing decreased cardiac output. Examples of disorders resulting in impaired filling include cardiac tamponade and tension pneumothorax.

Hypovolemic Shock Epidemiology

Causes *Acute blood loss* - Trauma, GI bleed *Rapid fluid loss* - Vomiting, diarrhea, burns Hypovolemic shock is defined as inadequate intravascular volume producing decreased cardiac output that results when there is a severe loss of blood or fluids due to acute injury or illness. An acute bleed may be the result of penetrating or blunt trauma or massive GI bleeding. Rapid fluid loss may be due to severe vomiting and diarrhea, excessive urination, or loss of fluids due to burns. The most common cause of hypovolemia is blood loss. Incidence or prevalence data are unavailable because the data are reported for the causative mechanism rather than for the resultant hypovolemic shock.

Compensatory Stage: Neural compensation

Characterized by the detection of hypotension by baroreceptors in the carotid sinus and aortic arch that results in the stimulation of the sympathetic nervous system and the release of the catecholamines epinephrine and norepinephrine from the adrenal medulla. Heart rate and contractility increase, improving cardiac output. Also in response to this catecholamine release, systemic vasoconstriction occurs, resulting in increased blood pressure and redistribution of blood flow from nonessential organ systems, such as the kidneys, GI tract, and skin, to vital organs, such as the heart and brain.

Stages of Shock - Progressive

Failure of compensatory mechanisms Extensive shunting of blood to vital organs • Profound hypoperfusion • Worsening metabolic acidosis • Respiratory acidosis Marked by the failure of compensatory mechanisms to maintain adequate blood pressure and circulating fluid volumes. There is *extensive shunting of blood to vital organs, which results in decreased blood flow to the periphery*. Without effective treatment, profound hypoperfusion occurs, resulting in worsening metabolic acidosis, electrolyte imbalances due to the failure of the sodium-potassium pump, and respiratory acidosis.

Sepsis/Septic Shock Bundle of Care *Fluid resuscitation & Vasopressors*

Fluid resuscitation is essential to restore hemodynamic stability, maximize DO2, and begin repaying oxygen debt. A crystalloid solution such as normal saline or lactated Ringer's is commonly used to improve and maintain filling pressures. Evidence suggests that aggressive resuscitation in early sepsis has been shown to decrease mortality. Fluid resuscitation should be tapered as the patient demonstrates improvement. If fluid resuscitation is not successful at restoring blood pressure during or after administration, initiation of vasopressors to maintain a mean arterial pressure greater than 65 mm Hg may become necessary. The Surviving Sepsis campaign suggests the use of norepinephrine as the first-line vasopressor.

Sepsis/Septic Shock Ongoing Monitoring

Frequent assessment of vital signs, peripheral perfusion, mental status, cultures, and laboratory analyses, including white blood cell count and differential and lactate, are essential. Hemodynamic parameters such as CVP or PAOP and SvO2 or ScvO2 help monitor responsiveness to therapy, but the use of a PA catheter, and thus PAOP and SvO2, is not recommended because the PA catheter has not been shown to have an improved impact on outcomes. Instead, monitoring of responsiveness to therapy can be done through evaluation of CVP and ScvO2 in combination with dynamic measures such as monitoring cardiac output through echocardiology after a passive leg raise (PLR) maneuver. An increase in cardiac output demonstrates a good response to fluid resuscitation.

Cardiogenic Shock

Inadequate pumping of the heart muscle, most typically the result of a heart attack