Shock, Sepsis, and MODS

Shock-Definition

Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
Imbalance between supply of and demand for O2 and nutrients

Shock-Types

Cardiogenic
Hypovolemic: Absolute, relative
Distributive: Neurogenic, anaphylactic, septic
Obstructive

Cardiogenic Shock-Definition

Systolic/diastolic dysfunction: (S) Heart’s inability to pump the blood forward, most common cause is MI
Decreased filling of the heart will result in decreased stroke volume
Low cardiac output (CO) and cardiac index

Cardiogenic Shock-Causes

MI
Cardiomyopathy
Blunt cardiac injury
Severe systemic/pulmonary HTN
Cardiac tamponade
Myocardial depression from metabolic problems

Cardiogenic Shock-Manifestations

Early: Tachycardia, hypotension, narrowed pulse pressure, increased systemic vascular resistance (SVR), increased myocardial O2 consumption
Physical: Tachypnea, pulmonary congestion, pallor and cool, clammy skin, decreased cap refill time, anxiety, confusion, agitation
Increased pulmonary artery wedge pressure (PAWP)
Stroke volume variation (SVV) and pulmonary vascular resistance
Decreased renal perfusion and urinary output

Cardiogenic Shock-Care

Overall goal: Restore blood flow to myocardium by restoring balance between O2 supply and demand

• Angioplasty w/stenting

• Emergency revascularization

• Valve replacement

Hemodynamic monitoring
Circulatory assist devices: Decrease SVR and left ventricular workload, intraaortic balloon pump, VAD
Heart transplant

Cardiogenic Shock-Drug Therapy

Nitrates to dilate coronary arteries
Diuretics to reduce preload
Vasodilator to reduce afterload
B-Adrenergic blockers to reduce HR

Hypovolemic Shock (Distributive Shock)-Types

Absolute hypovolemia: loss of intravascular fluid volume

• Hemorrhage

• GI loss (V/D)

• Fistula drainage

• Diabetes insipidus

• Diuresis

Relative hypovolemia: When fluid volume moves out of vascular space into extravascular space (third spacing)

Hypovolemic Shock-Definition

Response to acute volume loss depends on: Extent of injury, age, and general state of health
Pt may compensate up to 15% loss
Loss of 15-30-5 results in SNS-mediated response

Hypovolemic Shock-Manifestations

Anxiety
Tachypnea
Increase in heart rate, CO, respiratory rate and depth
Decrease in stroke volume, CVP, PAWP, urinary output
If loss is greater than 30%, blood volume is replaced

Hypovolemic Shock-Care

Management focuses on stopping loss of fluid and restoring the circulating volume
Fluid resuscitation is calculated using a 3:1 rule (3mL of isotonic crystalloid for every 1mL of estimated blood loss)

Neurogenic Shock

Hemodynamic phenomenon
Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above
Can last up to 6 weeks
Can occur in response to spinal cord injury or spinal anesthesia
Results in massive vasodilation, leading to pooling of blood in vessels, tissue hypoperfusion, ultimately impaired cellular metabolism

Neurogenic Shock-Manifestations

Hypotension and bradycardia
Inability to regulate body temperature (resulting in heat loss)
Dry skin
Poikilothermia: Taking on temperature of environment

Neurogenic Shock-Care

Spinal stability
Treatment of hypotension and bradycardia w/vasopressors and atropine
Fluids infused cautiously as hypotension generally is not related to fluid loss
Monitor for hypothermia caused by hypothalamic dysfunction

Anaphylactic Shock (Distributive Shock)

Acute, life-threatening hypersensitivity (allergic) reaction
Massive vasodilation
Release of vasoactive mediators
Increase in capillary permeability
Fluid leaks into interstitial space

Anaphylactic Shock-Manifestations

Anxiety
Confusion, dizziness
Sense of impending doom
Chest pain
Incontinence
Swelling of lips and tongue, angioedema
Wheezing, stridor due to laryngeal edema
Flushing, pruritus, urticaria
Respiratory distress and circulatory failure

Anaphylactic Shock-Care

Epinephrine (drug of choice), diphenhydramine, histamine receptor blockers (famotidine)
Maintain a patent airway

• Nebulized bronchodilators

• Aerosolized epinephrine

• Endotracheal intubation or cricothyroidotomy may be necessary

Aggressive fluid resuscitation: Usually crystalloids
IV corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive therapy

Septic Shock (Distributive Shock)-Definition/Degree

Sepsis: systemic inflammatory response to documented or suspected infection
Severe sepsis: sepsis complicated by organ dysfunction
Presence of sepsis with hypotension despite fluid resuscitation
Presence of inadequate tissue perfusion resulting in hypoxia

Septic Shock-Pathophysiologic Effects

Vasodilation
Maldistribution of blood flow
Myocardial dysfunction: Decreased ejection fraction, ventricular dilation

Septic Shock-Manifestations

Increased coagulation and inflammation

Decreased fibrinolysis: Formation of microthrombi, obstruction of microvasculature

Hyperdynamic state: increased CO and decreased SVR
Decreased urine output

Tachypnea/hyperventilation: Results in respiratory alkalosis, respiratory failure develops in 85% of patients

Altered neurologic status
GI dysfunction, GI bleeding, paralytic ileus

Septic Shock-Care

Fluid replacement to restore instavascular volume and organ perfusion

• Initially 30 ml/l isotonic crystalloid solution

• Fluid Resuscitation is to achieve a target CVP of 8-12 mmHG

• Hemodynamic monitoring

Vasopressor drug therapy (epinephrine)
Exogenous vasopressin can replace stores of physiologic vasopressin
IV corticosteroids considered for patients who cannot maintain an adequate BP with vasopressor therapy despite fluid resuscitation
Start antibiotics within first hour
After cultures are obtained (blood, wound exudate, urine, stool, sputum)
Broad-spectrum antibiotics are given first
More specific antibiotics may be ordered once the organism identified
Glucose levels should be maintained below 180 mg/dL
Stress ulcer prophylaxis with proton pump inhibitors (pantoprazole)
VTE prophylaxis (heparin, Lovenox)

Obstructive Shock-Definiton

Develops when physical obstruction to blood flow occurs with decreased CO

Caused by restricted diastolic filling of right ventricle from compression

Abdominal compartment syndrome: Abdominal pressure compresses inferior vena cava

Obstructive Shock-Manifestations

Decreased CO
Increased afterload
Variable left ventricular filling pressure
Rapid assessment and immediate treatment are important

Obstructive Shock-Care

Primary strategy is early recognition and treatment to relieve obstruction
Mechanical decompression
Thrombolytic therapy
Radiation, debulking, or removal of mass
Decompressive laparotomy

Stages of Shock

4 Overlapping Stages

• Initial

• Compensatory

• Progressive

• Refractory

Initial Stage

Usually not clinically apparent
Metabolism changes at cellular level from aerobic to anaerobic
Lactic acid builds up and must be removed by liver
Process requires O2, unavailable due to decreased tissue perfusion

Compensatory Stage

Compensatory mechanisms: Neural, hormonal, biochemical
Attempt to overcome consequences of anaerobic metabolism and maintain homeostasis
Baroreceptors in carotid and aortic bodies activate SNS in response to decreased BP
Vasoconstriction while blood to vital organs maintained: Heart, brain

Progressive Shock

Begins when compensatory mechanisms fail
Patient moved to ICU for advanced monitoring and treatment
Distinguishing features of decreased cellular
perfusion and altered capillary permeability
Leakage of protein into interstitial space
Increase of systemic interstitial edema
Cardiac output begins to decrease, resulting in a decrease in BP

Progressive Shock-Types

Anasarca: diffuse profound edema

• Fluid leakage affects solid organs and peripheral tissues

• Decreases blood flow to pulmonary capillaries

Sustained hypoperfusion

• Weak peripheral pulses

• Ischemia of distal extremities

Progressive Stage-Myocardial Dysfunction

Dysrhythmias
Myocardial ischemia
Possible myocardial infarction
End result: complete deterioration of cardiovascular system

Progressive Stage-Fluid

Movement of fluid from pulmonary vasculature to interstitium

• Pulmonary edema

• Bronchoconstriction

• Decreased functional residual capacity

Fluid moves into alveoli

• Edema

• Decreased surfactant

• Worsening V/Q mismatch

• Tachypnea

• Crackles

• Increased work of breathing

Progressive Stage-GI

Mucosal barrier of GI system becomes ischemic

• Ulcers

• GI bleeding

• Risk of migration of bacteria

• Decreased ability to absorb nutrients

Hypoperfusion leads to renal tubular ischemia

• May result in acute kidney injury

• Worsened by nephrotoxic drugs

• Decreased urine output

• Elevated BUN and serum creatinine

• Metabolic acidosis

Progressive Stage-Liver

Liver fails to metabolize drugs and waste

• Jaundice

• Elevated enzymes

• Loss of immune function

• Risk for DIC and significant bleeding

Refractory Stage

Exacerbation of anaerobic metabolism
Accumulation of lactic acid and waste products
Increased capillary permeability
Profound hypotension and hypoxemia
Tachycardia worsens
Failure of one organ system affects others
Recovery unlikely

Shock-Diagnostics

Thorough history and physical examination
No single study to determine shock
Blood studies
Elevation of lactate
Base deficit
12-lead ECG, continuous ECG monitoring
Chest x-ray
Continuous pulse oximetry
Hemodynamic monitoring

Shock-Care

Identification of patients at risk for developing shock
Integration of patient’s history, physical examination, and clinical findings to establish a diagnosis
Interventions to control or eliminate cause of decreased perfusion
Protection of target and distal organs from dysfunction
Provision of multisystem supportive care
Ensure patent is responsive
Ensure a patent airway
Maximize oxygen delivery

Shock- Oxygen and Ventilation Care

Increase supply

• Optimize CO with fluid replacement or drugs

• Increased hemoglobin by transfusion

• Increased arterial oxygen with supplemental oxygen and mechanical ventilation

Plan care to avoid disrupting O2 supply and demand

Shock-Care (Distributive, septic, hypovolemic, and anaphylactic)

Volume expansion
1 or 2 large-bore IV catheters , intraosseous access device, or central venous catheter
Isotonic crystalloids (NS, LR)
RBCs for volume loss due to bleeding

Shock Care-Fluids

Fluid responsiveness is determined by clinical assessment

• Vital signs

• Cerebral and abdominal perfusion pressures

• Capillary refill

• Neurologic status

• Skin temperature

• Urine output

Other interventions to monitor fluid response include passive leg raise challenge and IVC evaluation

2 major complications of large volumes: Hypothermia and coagulopathy
Persistent hypotension after adequate fluids: Vasopressor may be added

Fluid resuscitation

• Warm crystalloid and colloid solutions

• Replace clotting factors

• Assess for hypocalcemia and DIC

Primary goal is correction of decreased tissue perfusion

Shock Care-Vasopressors

Achieve/maintain MAP greater than 65 mm Hg
Reserved for patients unresponsive to fluid resuscitation
Continuously monitor end-organ perfusion

Shock-Drug Therapy

Vasodilator therapy (nitroglycerin, nitroprusside): Decrease afterload, Achieve/maintain MAP greater than 65 mm Hg
Monitor hemodynamic parameters and assessment

Shock-Nutrition Therapy

Start enteral nutrition (EN) within first 24 hours: Start trophic feeding: slow drip of small amounts of enteral nutrition; Early EN enhances perfusion of GI tract
Parenteral nutrition (PN) used only if enteral nutrition contraindicated
Weigh patient daily and monitor labs

ABCs

Airway
Breathing
Circulation

Shock-Nursing Assessment

Focus on tissue perfusion
VS
Peripheral pulses
LOC
Cap refill
Skin (temp, color, moisture)
Urine output

Shock-Care Goals

Adequate tissue perfusion
Restoration of normal/baseline BP
Recovery of organ function
Avoiding complications from prolonged states of hypoperfusion
Preventing health care-associated complications

Shock-Nursing Implementation

Cardiovascular status: Monitor HR, continuous ECG, BP, CVP, PA pressures, CO, SVR, SVV, dysrhythmias, heart sounds (murmurs, S3, S4)
Give prescribed fluid and drug therapy
Fluid resuscitation is to achieve to target CVP of 8-12mmHg

Respiratory status: Monitor RR, depth, and rhythm, breath sounds, continuous pulse ox, arterial blood gases
Many pts will be intubated and on mechanical ventilation

Renal status: Urine output, serum creatinine

Body temp and skin: Core temp; skin temp, pallor, flushing, cyanosis, diaphoresis, piloerection (goose bumps)

GI status: Auscultate bowel sounds, NG drainage/stools for occult blood

Personal hygiene: Perform bathing, turn Q1-2, passive/active ROM, oral care

Systemic Inflammatory Response Syndrome (SIRS)-Definition

A systemic inflammatory response to a variety of insults
Generalized inflammation in organs remote from the initial insult

SIRS-Triggers

Mechanical tissue trauma: burns, crush injuries, surgery
Abscess formation: intraabdominal, extremities
Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
Microbial invasion: bacteria, viruses, fungi
Endotoxin release: gram-negative and gram-positive bacteria
Global perfusion deficits: postcardiac resuscitation, shock states
Regional perfusion deficits: distal perfusion deficits

Multiple Organ Dysfunction Syndrome (MODS)-Definition

A failure of 2 or more organ systems
Homeostasis cannot be maintained w/o intervention
Results from SIRS

SIRS and MODS-Patho Consequences of inflammatory response

Release of mediators
Direct damage to endothelium
Hypermetabolism
Increase in vascular permeability
Activation of coagulation cascade

SIRS and MODS-Patho Organ and metabolic dysfunction

Hypotension
Decreased perfusion
Formation of microemboli
Redistribution/shunting of blood

SIRS and MODS-Patho Respiratory System

Alveolar edema
Decrease in surfactant
Increase in shunt
V/Q mismatch
End result: ARDS

SIRS and MODS-Patho Cardiovascular System

Myocardial depression and massive vasodilation: Results in decreased SVR and BP
Baroreceptors respond to enhance CO
Albumin and fluid move out of blood vessels
Increased CVP and PAWP

SIRS and MODS-Patho Neurologic System

Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion
Often early sign of MODS
Confusion, agitation, combative, lethargy

SIRS and MODS-Patho Renal System

Acute kidney injury (AKI)
Hypoperfusion
Release of mediators
Activation of renin-angiotensin-aldosterone system
Nephrotoxic drugs, especially antibiotics

SIRS and MODS-Patho GI System

Motility decreased: abdominal distention and paralytic ileus
Decreased perfusion: increased risk for ulceration and GI bleeding
Potential for bacterial translocation

SIRS and MODS-Patho Hypermetabolic State

Hyperglycemia-hypoglycemia
Insulin resistance
Catabolic state
Liver dysfunction
Lactic acidosis

SIRS and MODS-Patho

DIC from dysfunction of coagulation system
Electrolyte imbalances
Metabolic acidosis

SIRS and MODS-Care

Prognosis for MODS is poor
Goal: Prevent the progression of SIRS to MODS
Vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction are critical
Care for patients with MODS focuses on

• Preventing and treating infection

• Maintaining tissue oxygenation

• Nutrition and metabolic support

• Appropriate support of individual failing organs

SIRS and MODS-Care Preventing and Treating Infection

Aggressive infection control strategies to decrease risk for hospital acquired infection
Strict asepsis
Assess need for invasive lines

Once an infection is suspected, begin interventions to control source
Aggressive surgery to remove necrotic tissue
Aggressive pulmonary management
Early mobilization

SIRS and MODS-Care Maintain Tissue Oxygenation

Decrease O2 demand and increased O2 delivery
Sedation
Mechanical ventilation
Analgesia
Rest
Treat fever, chills, and pain

SIRS and MODS-Care Nutrition and Metabolic Needs

Goal of nutrition support: preserve organ function
Total energy expenditure is often increased 1.5 to 2.0 times
Use of EN is preferred to parenteral nutrition
Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis
Provide glycemic control

SIRS and MODS-Care Support Failing Organs

ARDS: aggressive O2 therapy and mechanical ventilation
DIC: appropriate blood products
Renal failure: continuous renal replacement therapy or dialysis
Consider that further interventions may be futile
Communicate with caregiver about realistic goals and outcomes