Responses to Alterations/Problems

and its Pathophysiologic Basis –

Multisystem Problems
Erickson R. Bernardo, MAN, RN
NCM 118
A. Shock
• An acute, widespread process of impaired tissue perfusion → cellular,
metabolic, and hemodynamic alterations.
• Ineffective tissue perfusion:
• imbalance in cellular oxygen supply and cellular oxygen demand
• occur for a variety of reasons → cellular dysfunction → death
Shock Syndrome
• A complex pathophysiologic process → multi-organ dysfunction
syndrome (MODS) and death.
• All types of shock: ineffective tissue perfusion and acute circulatory
failure.
• Shock syndrome:
• pathway involving a variety of pathologic processes
• categorized in four stages: initial, compensatory, progressive, and
refractory.
• progression varies: patient’s prior condition, duration of initiating
event, response to therapy, and correction of the underlying cause
Shock
• Hypovolemic shock: loss of circulating or intravascular volume.
• Cardiogenic shock: impaired ability of the heart to pump.
• Distributive shock: maldistribution of circulating blood volume;
further classified as septic, anaphylactic, or neurogenic.
• Septic shock: host’s dysregulated response to microorganisms entering the
body.
• Anaphylactic shock: severe antibody antigen reaction.
• Neurogenic shock: loss of sympathetic tone
• Obstructive shock: anatomical obstruction of the great vessels of the
heart
Consequences of Shock
• Cardiovascular • Renal
• Ventricular failure • Acute kidney injury
• Microvascular thrombosis • Hematologic
• Neurologic • Disseminated intravascular
• Sympathetic nervous system coagulation
dysfunction • Gastrointestinal
• Cardiac and respiratory depression • Gastrointestinal tract failure
• Thermoregulatory failure • Liver failure
• Coma • Pancreatic failure
• Pulmonary
• Acute lung failure
• Acute respiratory distress syndrome
Assessment and Diagnosis
• Shock state:
• MAP < 60 mm Hg
• with evidence of global tissue hypoperfusion
• Hypotension: may occur late in the process or may normalize even
when tissue perfusion is still inadequate.
• Clinical manifestations: vary – underlying cause of shock, the stage of
the shock, and the patient’s response to shock
• Compensatory mechanisms: produce normal hemodynamic values
even when tissue perfusion is compromised
Medical Management
• Major focus: improvement and preservation of tissue perfusion.
• Adequate tissue perfusion: depends on adequate supply of oxygen
transported to the tissues and the cell’s ability to use it.
• Oxygen transport: influenced by pulmonary gas exchange, CO, and
hemoglobin level.
• Oxygen use: influenced by the internal metabolic environment and
mitochondrial function.
• Management of a patient in shock focuses on supporting oxygen
delivery.
Medical Management
• Adequate pulmonary gas exchange is critical to oxygen transport.
• Establishing and maintaining an adequate airway
• Improving ventilation and oxygenation
• Administration of supplemental oxygen and mechanical ventilatory
support.
• Adequate CO and hemoglobin level are crucial to oxygen transport.
• CO: heart rate, preload, afterload, and contractility.
• Various fluids and medications are used to manipulate these
parameters.
• Fluids: crystalloids and colloids.
• Medications: vasoconstrictors, vasodilators, positive inotropes, and
anti-dysrhythmics.
Medical Management
• Fluid administration: indicated for decreased preload related to
intravascular volume depletion; can be accomplished by use of a
crystalloid or colloid solution, or both.
• Crystalloids: balanced electrolyte solutions that may be hypotonic,
isotonic, or hypertonic; normal saline and lactated Ringer solution.
• Colloids: protein-containing or starch-containing solutions; blood and
blood components, such as albumin, and pharmaceutical plasma
expanders, such as dextran and mannitol.
Medical Management
• Blood: considered to augment oxygen transport if the patient’s
hemoglobin level is critically low
• Stored red blood cells (RBCs): does not substantially increase oxygen
consumption; has been associated with immunosuppression, infection,
impairment of microcirculatory flow, increased pulmonary vascular
resistance, coagulopathy, and increased mortality.
• Transfusion-related acute lung injury (TRALI): from immune and
nonimmune neutrophil activation; leading cause of transfusion-related
death; may occur with transfusion of any plasma-containing blood or
blood product.
Medical Management
• Vasoconstrictor agents: used to increase
afterload by increasing the systemic
vascular resistance (SVR) and improving
the patient’s blood pressure level.
• Vasodilator agents: used to decrease
preload or afterload, or both, by
decreasing venous return and SVR.
• Positive inotropic agents: used to
increase contractility.
• Antidysrhythmic agents: used to
influence heart rate.
Medical Management
• Sodium bicarbonate:
• Not recommended in the treatment of shock-related lactic acidosis.
• No overall benefit has been found
• Significant risks: shifting of the oxyhemoglobin dissociation curve to the
left, rebound increase in lactic acid production, development of
hyperosmolar state, fluid overload resulting from excessive sodium, and
rapid cellular electrolyte shifts.
Medical Management
• Enteral nutrition support therapy should be started within 24 to 48
hours.
• Type of nutrition supplementation: varies according to the cause of
shock; should be tailored to the individual patient’s needs, as indicated
by the underlying condition, laboratory data, and treatment.
• Parenteral nutrition: when enteral feeding is contraindicated; a delay of
7 days is recommended for better outcomes.
• Glucose control to a target level of 140 to 180 mg/dL is
recommended for all critically ill patients.
• Benefits: lower incidences of infection, renal failure, sepsis, and death
Nursing Management
• The patient care management for the patient in shock is a complex
and challenging responsibility.
• Requires an in-depth understanding of the pathophysiology of the
disease and the anticipated effects of each intervention, as well as a
solid understanding of the nursing process.
• The psychosocial needs of the patient and family dealing with shock
are extremely important.
• Based on situational, familial, and patient-centered variables.
Nursing Management
• Nursing interventions:
• providing information on patient status,
• explaining procedures and routines,
• supporting the family,
• encouraging the expression of feelings,
• facilitating problem solving and shared decision making,
• individualizing visitation schedules,
• involving the family in the patient’s care, and
• establishing contacts with necessary resources.
1. Hypovolemic Shock
• Occurs from inadequate fluid volume in the intravascular space.
• The lack of adequate circulating volume leads to decreased tissue
perfusion and initiation of the general shock response.
• Hypovolemic shock is the most commonly occurring form of shock.
Hypovolemic Shock
• Can result from absolute or relative hypovolemia.
• Absolute hypovolemia: occurs when there is a loss of fluid from the
intravascular space
• Relative hypovolemia: occurs when vasodilation produces an increase
in vascular capacitance relative to circulating volume.
Etiologic Factors in Hypovolemic Shock
• Absolute Factors • Relative Factors
• Loss of whole blood • Vasodilation
• Trauma or surgery • Sepsis
• Gastrointestinal bleeding • Anaphylaxis
• Loss of plasma • Loss of sympathetic stimulation
• Thermal injuries • Increased capillary membrane
• Large lesions permeability
• Loss of other body fluids • Sepsis
• Severe vomiting or diarrhea • Anaphylaxis
• Massive diuresis • Thermal injuries
• Loss of intravascular integrity • Decreased colloidal osmotic
• Ruptured spleen pressure
• Long bone or pelvic fractures • Severe sodium depletion
• Hemorrhagic pancreatitis • Hypopituitarism
• Hemothorax or hemoperitoneum • Cirrhosis
• Arterial dissection or rupture • Intestinal obstruction
Assessment and Diagnosis
• Clinical manifestations: depend on the severity of fluid loss and the
patient’s ability to compensate for it.
• Simpler approach: mild, moderate, or severe
• Class I, or mild shock: fluid volume loss up to 15% to 20% or an actual
volume loss up to approximately 750 mL.
• Compensatory mechanisms maintain CO; patient appears free of
symptoms other than possibly slight anxiety; as volume loss worsens,
patient may develop cool extremities and increased capillary refill time
in response to peripheral vasoconstriction.
Assessment and Diagnosis
• Class II and class III hypovolemia is consistent with moderate shock.
• Class II: fluid volume loss of approximately 15% to 30% or an actual
volume loss of 750 to 1500 mL
• Class III: fluid volume loss of 30% to 40% or an actual volume loss of
1500 to 2000 mL.
• May produce progressive stage of shock as compensatory mechanisms
become overwhelmed and ineffective tissue perfusion develops; BP
decreases but often after tissue hypoperfusion is already significant.
• Class IV, or severe shock: usually refractory in nature; fluid volume
loss of greater than 40% or an actual volume loss of greater than
2000 mL
Medical Management
• Major goals: to correct the cause of the hypovolemia, restore tissue
perfusion, and prevent complications.
• identifying and stopping the source of fluid loss,
• administering fluid to replace circulating volume, and
• administering vasopressor therapy to maintain tissue perfusion until
volume is restored.
• Fluid administration: use of a crystalloid solution, a colloid solution,
blood products, or a combination of fluids
• Depends on the type of fluid lost, the degree of hypovolemia, the
severity of hypoperfusion, and the cause of hypovolemia.
Nursing Management
• Prevention of hypovolemic shock is one of the primary
responsibilities of the nurse in the critical care unit.
• Preventive measures: identification of patients at risk and frequent
assessment of the patient’s fluid balance.
• Accurate I/O monitoring and daily weights
• Early identification and treatment → decreased mortality.
Nursing Management
• The patient care management plan for a patient in hypovolemic
shock may include numerous patient problems, depending on the
progression of the process.
• Requires continuous evaluation of intravascular volume, tissue
perfusion, and response to therapy.
• Nursing interventions:
• minimizing fluid loss,
• administering volume replacement and vasopressor agents (if needed),
• assessing response to therapy,
• providing comfort and emotional support, and
• preventing and maintaining surveillance for complications.
Nursing Management
• Measures to minimize fluid loss
• limiting blood sampling,
• observing lines for accidental disconnection, and
• applying direct pressure to bleeding sites
• Measures to facilitate the administration of volume replacement
• insertion of large-bore peripheral intravenous catheters, and
• rapid administration of prescribed fluids
2. Cardiogenic Shock
• Result of failure of the heart to effectively pump blood forward; can
occur with dysfunction of the right or the left ventricle, or both.
• The lack of adequate pumping function leads to decreased tissue
perfusion and circulatory failure.
• It occurs in approximately 5% to 8% of the patients with an ST
segment myocardial infarction (MI), and it is the leading cause of
death of patients hospitalized with MI.
Etiologic Factors in Cardiogenic Shock
• Muscular
• Ischemic injury
• Acute myocardial infarction
• Cardiopulmonary arrest
• Acute decompensated heart failure
• Cardiomyopathy
• Acute myocarditis
• Myocardial contusion
• Prolonged cardiopulmonary bypass
• Septic shock
• Hemorrhagic shock
• Medications (beta-adrenergic blockers,
calcium channel antagonists, cytotoxic
agents)
• Mechanical
• Valvular dysfunction
• Papillary muscle dysfunction or rupture
• Septal wall rupture
• Free wall rupture
• Ventricular aneurysm
• Obstructive hypertrophic cardiomyopathy
• Intracardiac tumor
• Pulmonary embolus
• Atrial thrombus
• Cardiac tamponade
• Massive pulmonary embolus
• Constrictive pericarditis
• Rhythmic
• Bradydysrhythmias
• Tachydysrhythmias
Assessment and Diagnosis
• Various clinical manifestations: depending on etiologic factors, the
patient’s underlying medical status, and the severity of the shock
state.
• Although some clinical manifestations are caused by failure of the
heart as a pump, many are related to the overall shock response.
Clinical Manifestations of Cardiogenic Shock
• Systolic blood pressure <90 mm Hg
• Acute drop in blood pressure >30
mm Hg
• Heart rate >100 beats/min
• Weak, thready pulse
• Diminished heart sounds
• Change in sensorium
• Cool, pale, moist skin
• Urine output <30 mL/h
• Chest pain
• Dysrhythmias
• Tachypnea
• Crackles
• Decreased cardiac output
• Cardiac index <2.2 L/min/m2
• Increased pulmonary artery
occlusion pressure
• Increased right atrial pressure
• Variable systemic vascular resistance
Medical Management
• Treatment of a patient in cardiogenic shock requires an aggressive
approach.
• Major goals: to treat the underlying cause, enhance the effectiveness
of the pump, and improve tissue perfusion; identifying and treating
the etiologic factors of heart failure and administering pharmacologic
agents or using mechanical devices to enhance CO.
Medical Management
• Inotropic agents: used to increase contractility and maintain
adequate blood pressure and tissue perfusion
• Dobutamine: inotrope of choice.
• Vasopressor: preferably norepinephrine, necessary to maintain BP
when hypotension is severe.
• ↑ myocardial oxygen demand, lowest possible doses should be used.
Medical Management
• Diuretics: used for preload reduction.
• Vasodilating agents: used for preload and afterload reduction only in
specific situations in conjunction with an inotrope or when the
patient is no longer in shock.
• Antidysrhythmic agents: used to suppress or control dysrhythmias
that can affect CO.
• Intubation and mechanical ventilation: usually necessary to support
oxygenation.
Nursing Management
• Prevention of cardiogenic shock is one of the primary
responsibilities of the nurse in the critical care unit.
• identification of patients at risk,
• facilitation of early reperfusion therapy for acute MI, and
• frequent assessment and management of the patient’s
cardiopulmonary status.
Nursing Management
• Nursing interventions:
• limiting myocardial oxygen demand,
• enhancing myocardial oxygen supply,
• maintaining adequate tissue perfusion,
• providing comfort and emotional support, and
• preventing and maintaining surveillance for complications.
Nursing Management
• Measures to limit myocardial
oxygen demand
• administering analgesics,
sedatives, and agents to control
afterload and dysrhythmias;
• positioning the patient for
comfort;
• limiting activities;
• providing a calm and quiet
environment and offering
support to reduce anxiety; and
• teaching the patient about the
condition.
• Measures to enhance
myocardial oxygen supply
• administering supplemental
oxygen,
• monitoring the patient’s
respiratory status,
• administering prescribed
medications, and
• managing device therapy.
Nursing Management
• Effective nursing management of cardiogenic shock requires precise
monitoring and management of heart rate, preload, afterload, and
contractility.
• accurate measurement of hemodynamic variables
• controlled administration of fluids and inotropic and vasoactive agents
• close assessment and management of respiratory function
• dysrhythmias are common and require immediate recognition and
treatment
Nursing Management
• Patients who require mechanical device therapy need to be
observed frequently for complications.
• infection,
• bleeding,
• thrombocytopenia,
• hemolysis,
• embolus,
• stroke,
• device malfunction,
• circulatory compromise of a cannulated extremity, and
• sepsis.
3. Anaphylactic Shock
• A type of distributive shock; result of an immediate hypersensitivity
reaction.
• A life-threatening event that requires prompt intervention.
• The severe and systemic response leads to decreased tissue perfusion
and initiation of the general shock response.
Anaphylactic Shock
• Anaphylaxis
• a systemic reaction caused by an immunologic antibody antigen
response or nonimmunologic activation of mast cells and basophils.
• Triggers
• introduced by injection or ingestion or through the skin or respiratory
tract → reaction.
• foods, food additives, diagnostic agents, biologic agents, environmental
agents, medications, and venoms.
• can be physical factors and idiopathic.
• latex can be an extremely problematic antigen.
Etiologic Factors in Anaphylactic Shock
• Common Foods and Food • Diagnostic Agents
Additives • Radiocontrast media
• Eggs and milk • Dehydrocholic acid (Decholin)
• Fish and shellfish • Iopanoic acid (Telepaque)
• Nuts and seeds • Biologic Agents
• Legumes and cereals • Blood and blood components
• Soy • Insulin and other hormones
• Wheat • Gammaglobulin
• Strawberries • Seminal fluid
• Avocados • Vaccines and antitoxins
• Food coloring
• Preservatives
Etiologic Factors in Anaphylactic Shock
• Environmental Agents • Venoms
• Pollens, molds, and spores • Bees, hornets, yellow jackets, and
• Sunlight wasps
• Cold or heat • Snakes, jellyfish
• Animal dander • Deer flies
• Latex • Fire ants
Etiologic Factors in Anaphylactic Shock
• Medications
• Antibiotics • Neuromuscular blocking agents
• Aspirin • Barbiturates
• Nonsteroidal anti-inflammatory • Nonbarbiturate hypnotics
drugs • Protamine
• Opioids • Infliximab (Remicade)
• Dextran • Ethanol
• Vitamins
• Muscle relaxants
Anaphylactic Shock
• Immunologic anaphylactic reactions: either IgE-mediated or non IgE-
mediated responses.
• IgE: an antibody that is formed as part of the immune response.
• The first time an antigen enters the body, an antibody IgE, specific for
the antigen, is formed.
• The antigen-specific IgE antibody is then stored by attachment to mast
cells and basophils.
• This initial contact with the antigen is known as a primary immune
response.
Anaphylactic Shock
• The next time the antigen enters the body, the preformed IgE
antibody reacts with it, and a secondary immune response occurs.
• This reaction triggers the release of biochemical mediators from the
mast cells and basophils and initiates the cascade of events that
precipitates anaphylactic shock.
• Some immunologic anaphylactic reactions are non IgE-mediated.
• These can be IgG mediated, occur as a result of direct activation of the
mast cells, or be mediated by activation of the complement system.
Assessment and Diagnosis
• Anaphylactic shock: severe systemic reaction that can affect multiple
organ systems.
• Various clinical manifestations occur in a patient in anaphylactic shock,
depending on the extent of multisystem involvement.
• The symptoms usually start to appear within minutes of exposure to the
antigen, but they may not occur for hours.
• Symptoms may also reappear after a 1- to 72- hour window of
resolution in what is termed a biphasic reaction.
• These late-phase reactions may be similar to the initial anaphylactic
response, milder, or more severe.
• In protracted anaphylaxis, symptoms may last 32 hours.
Clinical Manifestations of Anaphylactic Shock
Medical Management
• Treatment of anaphylactic shock requires an immediate and direct
approach to prevent death.
• Goals of therapy: remove the offending antigen, reverse the effects
of the biochemical mediators, and promote adequate tissue
perfusion.
• When the hypersensitivity reaction occurs as a result of
administration of medications, dye, blood, or blood products, the
infusion should be immediately discontinued.
• It is often impossible to remove the antigen because it is unknown or
has already entered the patient’s system.
Medical Management
• Reversal of the effects of the biochemical mediators involves the
preservation and support of the patient’s airway, ventilation, and
circulation.
• oxygen therapy,
• intubation,
• mechanical ventilation, and
• administration of medications and fluids.
Medical Management
• Epinephrine
• first-line treatment of choice for anaphylaxis
• promotes bronchodilation, vasoconstriction, and increased myocardial
contractility and inhibits further release of biochemical mediators.
• mild cases:
• 0.2 to 0.5 mg (0.3 to 0.5 mL) of a 1:1000 dilution IM into the anterolateral thigh
• repeated every 5 to 15 minutes until anaphylaxis is resolved.
• SC injection is no longer recommended.
• anaphylactic shock with hypotension:
• IV dose is 0.05 to 0.1 mg (1 mL) of a 1:10,000 dilution administered over 5 minutes.
• If hypotension persists, a continuous infusion of epinephrine is recommended,
administered at 1 to 4 mcg/min with titration up to 10 mcg/min as needed.
Medical Management
• Patients receiving beta-blockers may have a limited response to
epinephrine.
• IV glucagon: 20- to 30-mcg/kg bolus over 5 minutes followed by
continuous infusion at 5 to 15 mcg/min is recommended to treat
bronchospasm and hypotension in these patients.
• Rapid volume replacement with crystalloid or colloid solutions is also
used for patients with hypotension.
• Administration of up to 1 L in 5 to 10 minutes is suggested if needed to
restore perfusion.
• Vasopressors may be necessary to reverse the vasodilation and increase
blood pressure.
Medical Management
• Several medications are used as second-line or third-line adjunctive
therapy but are not to be used as substitutes for epinephrine.
• Inhaled beta-adrenergic agents are used to treat bronchospasm unresponsive
to epinephrine.
• Diphenhydramine (Benadryl), 1 to 2 mg/kg (25 to 50 mg) given by a slow
intravenous push, is used to block histamine response.
• Ranitidine or cimetidine given in conjunction with diphenhydramine has
been found helpful to control cutaneous reactions.
• Corticosteroids are not effective in the immediate treatment of acute
anaphylaxis but may be given with the goal of preventing a prolonged or
delayed reaction.
Nursing Management
• Prevention of anaphylactic shock is one of the primary
responsibilities of the nurse in the critical care unit.
• Preventive measures: identification of patients at risk and cautious
assessment of the patient’s response to the administration of medications,
blood, and blood products.
• A complete and accurate history of the patient’s allergies is an essential
component of preventive nursing care.
• In addition to a list of the allergies, a detailed description of the type of
response for each allergy should be obtained.
Nursing Management
• Nursing interventions:
• administering epinephrine,
• facilitating ventilation,
• administering volume replacement,
• providing comfort and emotional support,
• maintaining surveillance for recurrent reactions, and
• preventing and maintaining surveillance for complications.
Nursing Management
• Measures to facilitate
ventilation:
• positioning the patient to assist
with breathing, and
• instructing the patient to
breathe slowly and deeply.
• Airway protection through
prompt administration of
prescribed medications is
essential.
• Measures to facilitate the
administration of volume
replacement:
• inserting large-bore peripheral
intravenous catheters and
rapidly administering
prescribed fluids.
• Measures to promote comfort:
• administering medications to
relieve itching, and
• applying warm soaks to skin.
Nursing Management
• Observing the patient for clinical manifestations of a delayed or
recurrent reaction is critical.
• Patient education about how to avoid the precipitating allergen is
essential for preventing future episodes of anaphylaxis.
• Education about how to recognize and respond to a future episode
including self-administration of epinephrine is essential to prevent a
future life-threatening event.
4. Neurogenic Shock
• Another type of distributive shock, is the result of the loss or
suppression of sympathetic tone.
• The lack of sympathetic tone leads to decreased tissue perfusion and
initiation of the general shock response.
• Most uncommon form of shock.
Neurogenic Shock
• Can be caused by anything that disrupts the SNS.
• occur as the result of interrupted impulse transmission or blockage of
sympathetic outflow from the vasomotor center in the brain.
• most common cause: spinal cord injury (SCI).
• Neurogenic shock may mistakenly be referred to as spinal shock.
• The latter condition refers to loss of neurologic activity below the level
of SCI, but it does not necessarily involve ineffective tissue perfusion.
Assessment and Diagnosis
• A patient in neurogenic shock characteristically presents with
hypotension, bradycardia, and warm, dry skin.
• The decreased blood pressure results from massive peripheral
vasodilation.
• The decreased heart rate is caused by inhibition of the baroreceptor
response and unopposed parasympathetic control of the heart.
• Hypothermia develops from uncontrolled peripheral heat loss.
• The warm, dry skin occurs as a consequence of pooling of blood in the
extremities and loss of vasomotor control in surface vessels of the skin
that control heat loss.
Medical Management
• Treatment of neurogenic shock requires a careful approach.
• Goals of therapy:
• treat or remove the cause,
• prevent cardiovascular instability, and
• promote optimal tissue perfusion.
• Cardiovascular instability can result from hypovolemia, bradycardia,
and hypothermia.
• Specific treatments are aimed at preventing or correcting these problems as
they occur.
Medical Management
• Hypovolemia is treated with careful fluid resuscitation.
• The minimal amount of fluid is administered to ensure adequate tissue
perfusion.
• Volume replacement is initiated for systolic blood pressure less than 90 mm
Hg or evidence of inadequate tissue perfusion.
• The patient is carefully observed for evidence of fluid overload.
Medical Management
• Vasopressors: used as necessary to maintain BP and organ perfusion.
• Bradycardia: rarely requires specific treatment, but atropine,
intravenous infusion of a beta-adrenergic agent, or electrical pacing
can be used when necessary.
• Hypothermia: treated with warming measures and environmental
temperature regulation.
Nursing Management
• Prevention of neurogenic shock is one of the primary
responsibilities of the nurse in the critical care unit.
• identification of patients at risk
• constant assessment of the neurologic status.
• Vigilant immobilization of SCIs and slight elevation of the head of the
patient’s bed after spinal anesthesia are essential components of
preventive nursing care.
• Early identification allows for early treatment and decreased
mortality.
Nursing Management
• Nursing interventions:
• treating hypovolemia and maintaining tissue perfusion,
• maintaining normothermia,
• monitoring for and treating dysrhythmias,
• providing comfort and emotional support, and
• preventing and maintaining surveillance for complications.
Nursing Management
• Venous pooling in the lower extremities promotes the formation of
deep vein thrombosis (DVT), which can result in a pulmonary
embolism.
• All patients at risk for DVT should be started on prophylaxis therapy.
• monitoring of passive range-of-motion exercises,
• application of sequential pneumatic stockings, and
• administration of prescribed anticoagulation therapy.
5. Sepsis and Septic Shock
• Sepsis: a life-threatening clinical syndrome caused by an infection and
dysregulated physiologic systemic response.
• The host response results in perfusion abnormalities with organ
dysfunction (sepsis) and eventually circulatory, cellular, and metabolic
abnormalities (septic shock).
• Septic shock differs from sepsis in that the complications are more
severe, and the risk of patient mortality is greater.
• Primary mechanisms: maldistribution of blood flow to the
tissues, hypovolemia, and myocardial dysfunction.
Sepsis and Septic Shock
• Sepsis: caused by a wide variety of
microorganisms, including gram-
negative and gram-positive
aerobes, anaerobes, fungi, and
viruses.
• Common sources of infection:
respiratory, GU, and GI systems;
the skin; and the soft tissues.
• Sepsis and septic shock are
associated with a wide variety of
intrinsic and extrinsic precipitating
factors.
Sepsis and Septic Shock
• All factors interfere directly or indirectly with the body’s anatomic and
physiologic defense mechanisms.
• Several of the intrinsic factors are not modifiable or are very difficult to
control.
• Several of the extrinsic factors may be required for diagnosis and
management.
• Therefore all critically ill patients are at risk for septic shock.
Assessment and Diagnosis
• Effective treatment of sepsis and septic shock depends on timely
recognition.
• Sepsis-3 advocates the use of the Sequential (Sepsis-related) Organ
Failure Assessment (SOFA) score to facilitate early identification of
patients.
• The SOFA score is a mortality prediction tool that is based on the
degree of dysfunction of six different organ systems (respiratory,
cardiovascular, hepatic, coagulation, renal, and neurologic).
• The score is calculated on admission and every 24 hours until discharge.
Assessment and Diagnosis
• The two most common organs to demonstrate dysfunction in sepsis
are the cardiovascular system and the lungs.
• Cardiovascular dysfunction: persistent hypotension requiring
vasopressor therapy despite adequate volume resuscitation
• Pulmonary dysfunction: PaO2/fraction of inspired oxygen (FIO2) ratio
of less than 300, indicating ARDS.
• Signs indicating septic shock are hypotension despite adequate fluid
resuscitation and the presence of perfusion abnormalities such as
lactic acidosis, oliguria, or acute change in mentation.
Assessment and Diagnosis
• A patient in sepsis or septic
shock may present with a variety
of clinical manifestations that
may change dynamically as the
condition progresses.
Medical Management
• Treatment of a patient in sepsis
or septic shock requires a
multifaceted approach.
• The goals of treatment:
• control the infection,
• reverse the pathophysiologic
responses, and
• promote metabolic support.
• Approach:
• identifying and treating the
infection,
• supporting the cardiovascular
system and enhancing tissue
perfusion,
• limiting the systemic
inflammatory response,
• restoring metabolic balance,
and
• initiating nutrition therapy.
Medical Management
• Guidelines for the management of
sepsis and septic shock have been
developed and updated under the
auspices of the Surviving Sepsis
Campaign (SSC), an international
effort of more than 11
organizations to improve patient
outcomes.
• Early recognition and treatment of
sepsis and septic shock is critical
for optimal patient outcomes.
• The Hour-1 Bundle lists
interventions that should be
implemented within the first hour
after recognition.
Medical Management
• Immediate resuscitation
• crystalloids
• Intubation and mechanical
ventilatory support
• Antibiotic therapy
• IV insulin
• < 180 mg/dL
• Platelets and RBC transfusions
• < 10,000/mm3, Hgb < 7 g/dL.
• Nutrition therapy
• enteral
Nursing Management
• Patient care management of the patient with sepsis focuses on
infection prevention and transmission, early recognition and
treatment, and supportive nursing care.
• Prevention of sepsis and septic shock is one of the primary
responsibilities of the nurse in the critical care unit.
• identification of patients at risk and
• reduction of their risk factors, including exposure to invading microorganisms
• handwashing, aseptic technique, and an understanding of evidence-based
practice to reduce nosocomial infection
• Early identification allows for early treatment and decreases
mortality.
Nursing Management
• Nursing interventions:
• early identification of sepsis syndrome;
• administering prescribed fluids, medications, and nutrition;
• providing comfort and emotional support; and
• preventing and maintaining surveillance for complications
B. Systematic Inflammatory Responses
Syndrome (SIRS)
• An exaggerated defense response of the body to a noxious stressor
(infection, trauma, surgery, acute inflammation, ischemia or
reperfusion, or malignancy, to name a few) to localize and then
eliminate the endogenous or exogenous source of the insult.
• It involves the release of acute-phase reactants, which are direct
mediators of widespread autonomic, endocrine, hematological, and
immunological alteration in the subject.
• Even though the purpose is defensive, the dysregulated cytokine
storm can cause a massive inflammatory cascade leading to reversible
or irreversible end-organ dysfunction and even death.
Systematic Inflammatory Responses Syndrome
(SIRS)
• SIRS with a suspected source of infection is termed sepsis.
• Sepsis with one or more end-organ failures is called severe sepsis,
and hemodynamic instability despite intravascular volume repletion is
called septic shock.
• Together they represent a physiologic continuum with progressively
worsening balance between pro and anti-inflammatory responses of
the body.
Systematic Inflammatory Responses Syndrome
(SIRS)
• Objectively, SIRS is defined by the satisfaction of any two of
the criteria below:
• Body temp: > 38° or < 36° Celsius
• HR: > 90 bpm
• RR: > 20 bpm
• Leukocyte count: > 12000 or < 4000 /ml
Systematic Inflammatory Responses Syndrome
(SIRS)
• Almost all septic patients have SIRS, but not all SIRS
patients are septic.
• Subgroups of hospitalized patients, particularly at extremes of age,
who do not meet the criteria for SIRS on presentation but progress
to severe infection and multiple organ dysfunction and death.
• Establishing laboratory indices to identify such subgroups of
patients and the clinical criteria that we currently rely upon has
been gaining prominence over recent years.
Systematic Inflammatory Responses Syndrome
(SIRS)
• Sequential Organ Failure Assessment
• Q SOFA
• SBP: < 100 mm Hg
• Highest RR: > 21 cpm
• Lowest GCS: < 15
Assessment and Diagnosis
• A thorough history of location, character, radiation, and exacerbating
– relieving factors of pain, duration, and time correlation of symptom
are important.
• The etiology and primary source are not as obvious.
• History should focus on any alteration from usual activities, including
new medications, food intake, exposure, travel, or recreational agents
of abuse.
Assessment and Diagnosis
• Identification of specific risk factors: preexisting
immunosuppression, diabetes mellitus, solid tumors and leukemia,
dysproteinemias, cirrhosis of the liver, and extremes of age.
• A complete physical examination is not only helpful in localizing the
source but also to assess the true extent of involvement and
complications related to end-organ involvement; helps in guiding the
appropriate investigations and imaging studies.
Assessment and Diagnosis
• The definition of systemic inflammatory response syndrome has its
basis in vital signs other than evaluating leukocyte count.
• However, vital signs can be falsely altered by the stress of arrival to a
healthcare facility in extremes of age or by concomitant use of
medications (beta-blockers, calcium channel blockers).
• Periodic evaluation of vital signs and evidence of persistent instability
becomes important to establish the diagnosis.
Management
• Ensuring hemodynamic stability is of utmost importance.
• initial administration of isotonic crystalloids at a rate of 30 ml/kg bolus
• measurement of pulse pressure variability or stroke volume variability with
passive leg raising
• for a patient on mechanical ventilator support, pulse pressure variability,
stroke volume variability, or IVC diameter variability with respiration is an
option.
• Vasopressors and inotropes
• Primary source control:
• surgical intervention – incision and drainage of wound infection, tube
drainage of a contained abscess and collection, or more exploratory surgery.
Management
• Broad-spectrum antibiotics should still be guided by:
• Suspicion of community vs. hospital-acquired infection
• Prior microbiology patterns in the individual
• Antibiogram for the facility
• Antiviral therapy: respiratory exacerbation and systemic
inflammatory response syndrome in the influenza season.
• Neutropenic patients and those on total parenteral nutrition with
central venous access may need empiric antifungals if they continue
to show SIRS response after empiric antibiotics.
C. Multiple Organ Dysfunction Syndrome
• Results from progressive physiologic failure of two or more separate
organ systems in an acutely ill patient such that homeostasis cannot be
maintained without intervention.
• Major cause of death in patients in critical care units
• linked to the number of organ systems involved.
• dysfunction or failure of two or more organ systems is associated with an
estimated mortality rate of 54%, which increases to 100% when five organ
systems fail.
• Survivors
• may develop generalized polyneuropathy and a chronic form of pulmonary
disease from ARDS, complicating recovery.
• often require prolonged, expensive rehabilitation
Multiple Organ Dysfunction Syndrome
• Trauma patients are particularly
vulnerable to developing MODS,
because they often experience
ischemia-reperfusion events
resulting from hemorrhage,
blunt trauma, or SNS-induced
vasoconstriction.
• Patients 65 years old or older
are at increased risk because of
their decreased organ reserve
and comorbidities.
• Other high-risk patients:
• patients who have experienced
infection,
• a shock episode,
• various ischemia reperfusion
events,
• acute pancreatitis,
• sepsis,
• burns,
• aspiration,
• multiple blood transfusions, or
• surgical complications.
Multiple Organ Dysfunction Syndrome
• Organ dysfunction may be the
direct consequence of an initial
insult (primary MODS) or can
manifest latently and involve
organs not directly affected in
the initial insult (secondary
MODS).
• Patients can experience both
primary and secondary MODS.
Multiple Organ Dysfunction Syndrome
• Primary MODS: results from a
well-defined insult in which organ
dysfunction occurs early and is
directly attributed to the insult
itself.
• Direct insults initially cause
localized inflammatory responses.
• Primary MODS accounts for only a
small percentage of MODS cases.
• The inflammatory response in
primary MODS has a less apparent
presentation and may resolve
without long-term implications.
• Examples of primary MODS:
• immediate consequences of
posttraumatic pulmonary
failure,
• thermal injuries,
• AKI, or
• invasive infections.
• Primary MODS may “prime”
physiologic systems for a more
sustained exaggerated
inflammatory response that
leads to secondary MODS.
Multiple Organ Dysfunction Syndrome
• Secondary MODS: a consequence of widespread sustained systemic
inflammation that results in dysfunction of organs not involved in the initial
insult.
• Secondary MODS develops latently after an initial insult.
• The early impairment of organs normally involved in immunoregulatory
function, such as the liver and the GI tract, intensifies the host response to
the insult.
• The initial insult may prime the inflammatory system in such a way that
even a mild second insult (hit) may perpetuate a sustained
hyperinflammatory response.
• This “two-hit hypothesis” has been increasingly recognized as an
important contributor to morbidity and mortality in patients with
secondary MODS.
Assessment and Diagnosis
• Secondary MODS: a systemic disease with organ-specific
manifestations.
• Organ dysfunction:
• organ host defense function,
• response time to the injury,
• metabolic requirements,
• organ vasculature response to vasoactive medications,
• organ sensitivity to damage, and
• physiologic reserve.
A. Gastrointestinal Dysfunction
• The GI tract plays an important role in MODS.
• GI organs normally have immunoregulatory functions, and the GI
tract contains approximately 70% to 80% of the immunologic tissue of
the entire body.
• A normally functioning GI tract prevents bacteria from entering the
systemic circulation.
• Normal gut flora and gut environment are altered in patients with
severe inflammation.
• Healthy probiotics are decreased in an inflammatory state, and
pathogenic organisms proliferate.
A. Gastrointestinal Dysfunction
• With microcirculatory failure to the GI tract, the gut’s barrier function
may be lost, which leads to bacterial translocation, sustained
inflammation, endogenous endotoxemia, and MODS.
• Hypoperfusion and shock-like states damage the normal GI mucosa
barrier by decreasing mesenteric blood flow, leading to
hypoperfusion of the villi, mucosal edema, ischemic necrosis,
sloughing of the mucosa, and malabsorption.
B. Hepatobiliary Dysfunction
• The liver plays a vital role in host homeostasis related to the acute
inflammatory response.
• The liver responds to sustained inflammation by selectively altering
carbohydrate, fat, and protein metabolism.
• Consequently, hepatic dysfunction threatens the patient’s survival.
• The liver normally controls the inflammatory response by several
mechanisms.
B. Hepatobiliary Dysfunction
• Kupffer cells, which are hepatic macrophages, detoxify substances
that may normally induce systemic inflammation and vasoactive
substances that cause hemodynamic instability.
• Failure to detoxify gram-negative bacteria causes endotoxemia,
perpetuates inflammation, and may lead to MODS.
• The liver also produces proteins and antiproteases to control the
inflammatory response; however, hepatic dysfunction limits this
response.
C. Pulmonary Dysfunction
• The lungs are common and early target organs for mediator-induced
injury and are usually the first organs affected.
• ARDS is the pulmonary manifestation of MODS.
• Patients who develop MODS usually have pulmonary symptoms;
however, not all patients with ARDS develop secondary MODS.
• Patients with ARDS who develop sepsis concurrently with acute lung
failure are at the greatest risk for MODS.
D. Kidney Dysfunction
• AKI is a common manifestation of MODS.
• The kidney is highly vulnerable to hypoperfusion and reperfusion
injury.
• Consequently, kidney ischemia-reperfusion injury may be a major
cause of kidney dysfunction in MODS.
• A patient with AKI may demonstrate oliguria or anuria resulting from
decreased renal perfusion and relative hypovolemia.
• Early oliguria is likely caused by decreases in renal perfusion related
to shock-like states; late oliguria is typically a sign of evolving kidney
injury and ischemia.
E. Cardiovascular and Hematologic System
Dysfunction
• Initial cardiovascular response in sepsis:
• myocardial depression;
• decreased RAP and SVR;
• and increased venous capacitance, CO, and heart rate.
• Despite an increased CO, myocardial depression occurs and is
accompanied by decreased SVR, increased heart rate, and ventricular
dilation.
• These compensatory mechanisms help maintain CO during the early
phase of sepsis.
• An inability to increase CO in response to a low SVR may indicate
myocardial failure or inadequate fluid resuscitation, and it is
associated with increased mortality.
Medical Management
• A patient with MODS requires multidisciplinary collaboration in
clinical management.
• Focus:
• fluid resuscitation and hemodynamic support,
• prevention and treatment of infection,
• maintenance of tissue oxygenation,
• nutrition and metabolic support,
• comfort and emotional support, and
• preservation of individual organs.
Identification and Treatment of Infection
• Identification and treatment of the underlying source of
inflammation or infection are important ways to reduce mortality.
• Medical and surgical intervention to remove sources of infection or
contamination may limit the inflammatory response and improve
chances of recovery.
• Surgical procedures such as early fracture stabilization, removal of
infected organs or tissue, and burn excision are helpful.
• Appropriate antibiotics are needed if the cause cannot be removed by
surgical debridement or incision and draining.
Maintenance of Tissue Oxygenation
• Normally under steady-state conditions, oxygen consumption (VO2)
is relatively constant and independent of oxygen delivery (DO2)
unless delivery becomes severely impaired.
• The relationship is called supply-independent oxygen consumption.
• Consequently, a percentage of oxygen is not used (physiologic reserve).
• Patients with MODS often develop supply-dependent oxygen
consumption, in which VO2 becomes dependent on DO2, rather than
demand, at a normal or high DO2.
• When VO2 does not equal demand, a tissue oxygen debt develops,
subjecting organs to failure.
Nutrition and Metabolic Support
• Hypermetabolism in MODS results in profound weight loss, cachexia,
and loss of organ function.
• Goal: preservation of organ structure and function.
• Although nutrition support may not definitely alter the course of
organ dysfunction, it prevents generalized nutrition deficiencies and
preserves gut integrity.
• Enteral nutrition may exert a physiologic effect that downregulates
the systemic immune response and reduces oxidative stress.
Nutrition and Metabolic Support
• The enteral route is preferable to parenteral support.
• Enteral feedings are given distal to the pylorus to reduce the risk of
pulmonary aspiration.
• Enteral feedings may limit bacterial translocation.
• In addition to early nutrition support, the pharmacologic properties
of enteral feeding formulas may limit inflammation for selected
critical care populations.
Nursing Management
• Preventive measures include a multitude of assessment strategies to
detect early organ manifestations of this syndrome.
• Patients who continue to experience sites of inflammation, septic
foci, and inadequate tissue perfusion may be at higher risk.
• Handwashing, aseptic technique, and an understanding of how
microorganisms can invade the body are essential components of
preventive nursing care.
Nursing Management
• Nursing interventions:
• preventing development of infection,
• facilitating oxygen delivery and limiting tissue oxygen demand,
• facilitating nutrition support,
• providing comfort and emotional support, and
• preventing and maintaining surveillance for complications.
Nursing Management
• Measures to limit tissue oxygen • Measures to enhance tissue
consumption oxygen supply
• administering analgesics and • administering supplemental
sedatives, oxygen,
• positioning the patient for • monitoring the patient’s
comfort, respiratory status, and
• limiting activities, • administering prescribed fluids
• offering support to reduce and medications.
anxiety,
• providing a calm and quiet
environment, and
• educating the patient and
family about the condition.