Shock And Sirs

Shock and Systemic Inflammatory Response Syndrome

By: Bryan Mae H. Degorio, RN

Shock - is a life threatening condition with a variety of underlying causes. - Characterized by inadequate tissue perfusion that ,if untreated , results in cell death. - Systematic blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cellular functions.

- Blalock in 1934, categorized shock etiology or causes: a. Hematogenic b. Neurogenic c. Vasogenic d. Cardiogenic

- 3 Major Factors that Regulate the Circulatory Mechanism: a. Preload b. Ventricular contraction c. Afterload

into 4

-types: 1. Hypovolemic Shock 2. Cardiogenic Shock 3. Circulatory Shock (Distributive Shock) > Septic Shock > Neurogenic Shock > Anaphylactic Shock *Obstructive Shock -Vascular Responses 1. Central Regulatory Mechanisms 2. Local Regulatory Mechanisms

-Blood Pressure Regulation BP= CO x TPR CO= SV x HR >Maintained by: a. nervous system b. endocrine system c. chemicals >Maintain tissue/organ perfusion: a. MAP= systolic BP + 2 (diastolic BP) 3 *should exceed 70-80 mmHg -Stages of Shock 1. Compensatory Stage >BP is maintained within normal limits due to the effect of normally functioning regulatory mechanisms

>s/sx: - cold clammy skin - oliguria - hypoactive bowel sounds can be

assessed.

>medical management:

a. identify the cause of shock b. correction of shock c. support of the regulatory mechanisms >nursing management: a. monitoring tissue perfusion *LOC *urine output *V/S *skin values

*laboratory

b. reducing anxiety c. promoting safety 2. Progressive Stage -exhaustion of the compensatory mechanisms - In this stage, the mechanisms that regulate blood pressure can no longer compensate and the mean arterial pressure falls.

-assessment and dxtic findings: a. respiratory effects hypoxemia and hypercarbia intense inflammatory response decreased surfactant production acute respiratory distress syndrome (acute lung injury, shock lung, non pulmonary edema)

cardiogenic

b. cardiovascular effects dysrhythmias myocardial infarction cardiac depression c. neurologic effects decreased cerebral perfusion *mental status change *behavioral change *pupillary dilation d. renal effects MAP<80mmHg acute renal failure

e. hepatic effects decreased blood flow less ability to perform hepatic functions

f. gastrointestinal effects decreased blood flow *PUD *bloody diarrhea *sepsis

g. hematologic DIC shock

-medical management: a. depends on the type of shock b. depends on the decompensation of the organ systems

Management Common To All Types Of Shock a. optimize intravascular volume b. supporting the pumping action of the heart c. improving the competence of the vascular system

Nursing Management: a. preventing complications b. promoting rest and comfort c. supporting family members

3. Irreversible Stage -severe organ damage -can no longer respond to treatment -survival is less likely -medical management: a. same with the progressive stage b. the use of life supporting drugs like epinephrine and investigational medications.

-nursing management: a. same with progressive shock b. moral support to the family c. ethical issues (living will)

Clinical Findings in the Stages of Shock Finding

Compensatory

Progressive

Irreversible

BP

normal

Systolic <80 -90mmHg

Mechanical or pharma support

HR

>100bpm

>150bpm

erratic, asystole

Respiration >20 breaths/ min Rapid, shallow Intubation crackles Skin

cold, clammy

Mottled, petechiae

Jaundice

Urine Output decreased

0.5ml/kg/hr

anuria, needs dialysis

Mentation

Lethargy

Coma

confusion

Finding

Compensatory

A/B Balance Resp Alkalosis

Progressive Met Acidosis

Irreversible Profound Acidosis

General Management for Shock • fluid replacement to restore intravascular volume • vasoactive medications to restore vasomotor tone and improve cardiac function • nutritional support to address the metabolic requirements that are dramatically increased in shock

A.

Fluid Replacement: - Is administered in all types of shocks. The type of fluids administered and the speed of delivery vary, but fluids are given to improve cardiac and tissue oxygenation. - may include CRYSTALLOIDS (electrolyte solutions that move freely between intravascular and interstitial space), COLLOIDS (largemolecule intravenous solutions) or blood components.

COMLICATIONS OF FLUID ADMINISTRATION

- The most common and serious side effect of fluid replacement are cardiovascular overload and pulmonary edema. B. VASOACTIVE MEDICATION THERAPY - Administered in all forms of shocks to improve the patients hemodynamic stability when fluid therapy alone cannot maintain adequate MAP.

-Vasoactive medications are selected for their action on receptors of the sympathetic nervous system. - when vasoactive medications are administered, vital sign must be monitored frequently(at least every 15min until stable or more often if indicated)

C. NUTRITIONAL SUPPORT -Nutritional

support is an important aspect of care for the patient with shocks. -Increased metabolic rates during shock increase energy requirements. The patients in shocks requires more than 3000 calories daily. - The release of catecholamines early in the shocks continuum causes glycogen stores to the depleted in about 8 to 10 hours.

TYPES OF SCHOCK

HYPOVOLEMIC SHOCK -most common type of shock -characterized by decreased intravascular volume of 15-25% -predisposing factors: External: Fluid Losses Internal: Fluid Shifts a. trauma a. hemorrhage b. surgery b. burns c. vomiting c. ascites d. diarrhea d. peritonitis e. diuresis e. dehydration f. diabetes insipidus

Manifestations: 1. Decreased Level of Consciousness 2. Tachycardia (pulse: weak and thready) 3. Decreased B/P 4. Decreased Cardiac Output (CO= SV x HR) 5. Decreased Urinary Output 6. Cool, Clammy Skin

PATHOPHYSIOLOGY DECREASED IN BLOOD VOLUME

DECREASE IN VENOUS RETURN

DECREASE IN STROKE VOLUME

DECREASED IN CARDIAC OUTPUT

DECREASE IN TISSUE PERFURION

-medical management: >goals: a. restore intravascular volume b. redistribute fluid volume c. correct the underlying cause *pharmacologic therapy desmopressin anti-emetic insulin anti-diarrhea -nursing management: a. administer O2 as ordered b. administering blood and fluids safely c. assess type client hydration status

d. monitor hemoglobin and hematocrit level e. Monitor the circulatory status (HR, arterial pressure, peripheral perfusion, and UO.) f. Monitor Vs and for hypotension g. Monitor I and O, urine output, and insert FBC as ordered h. Monitor LOC e. Administer small doses of narcotic analgesic as ordered f. Antibiotic for severely injured g. Pressure on site- severe trauma

CARDIOGENIC SHOCK -failure of the heart to pump blood adequately to the circulation causing reduction in CO -due to cardiac failure -either coronary and non coronary Coronary Factors Non Coronary Factors a. myocardial a. cardiomyopathies infarction b. valvular damage c. cardiac tamponade d. dysrhythmias -signs and symptoms: a. anginal pain b. hemodynamic instability c. dysrhythmias

Decreased cardiac contractility

Decreased stroke volume and Cardiac output Ineffective ventricular emptying

Pulmonary congestion Decreased systemic tissue perfusion Pathophysiology

Decreased coronary artery perfusion

-medical management: a. correction of underlying cause b. initiation of first line treatment *supplemental oxygen *vasoactive medications *controlling chest pain *controlling HR *selected fluid support *mechanical cardiac support

c. pharmacologic therapy *dobutamine *nitroglycerine *dopamine *vasoactive meds *anti-arrhythmic meds d. fluid therapy -nursing management: a. administer IV morphine sulfate b. administer O2 c. Prepare client for mechanical ventilation d. administer diuretics and nitrates while constantly monitoring the BP

e. Administer vasopressin, and postive inotropic f. Prepare the client for the insertion of intraaortic balloon pump. g. Prepare for emergency reperfusion such as transluminal coronary angioplasty h. Monitor blood gas i. UO monitor

CIRCULATORY SHOCK - is also called distributive shock - occurs when the blood is abnormally distributed in the vasculature Pathophysiology:

vasodilation

maldistribution of blood volume

decreased venous return

decreased stroke volume

decreased cardiac output

decreased tissue perfusion

Types of Circulatory shock: Septic shock  Anaphylactic shock  Neurogenic shock 

Risk Factors for Circulatory Shock Septic shock

Anaphylactic shock

Neurogenic shock

Imunnosuppresion Extreme ages (<1 and >65) Malnourishment Chronic illness Invasive procedure

Penicillin sensitivity Transfusion Bee sting allergy Latex sensitivity

Spinal cord injury Spinal anesthesia Depressant action Glucose deficiency

A.

Septic Shock - circulatory collapse due to infection - due to invasive infection such as viruses, parasites and bacteria - Gram (-) bacteria is the most common cause - genito-urinary system- the most common source of causative organism usually after instrumentation in the tract

- caused by the released of bacteria toxin that directly act on the on the blood vessel causing vasodilation and pooling of blood , resulting mostly from gram negative septicemia - the goal of treatment is controlling the cause of sepsis

Manifestations:

a. The HYPERDYNAMIC PHASE

High cardiac output with systemic vasodilatation.  The BP remains within normal limits.  Tachycardia  Hyperthermic and febrile with warm, flushed skin and bounding pulses b. The HYPODYNAMIC or irreversible phase 

LOW cardiac output with VASOCONSTRICTION  The blood pressure drops, the skin is cool and pale, with temperature below normal.  Heart rate and respiratory rate remain RAPID!  The patient no longer produces urine. 

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MEDICAL MANAGEMENT: • Current treatment involves identifying and eliminating the cause of infection. • Fluid replacement must be instituted to correct Hypovolemia • Intravenous antibiotics are prescribed based on culture and sensitivity.

Nursing management: a.Control of infection b.Administer IV antibiotics c. Administer O2, IV, vasoactive durgs d.Monitor for CVP or pulmonary wedge pressure

e. Obtain specimen for C and S f. Assess hydration and electrolyte imbalance B. Anaphylactic Shock - circulatory collapse due to massive vasodilation from an allergic reaction - massive vasodilation resulting from serious dramatic allergic reaction causing release of histamine and related substances for damaged cell

- can be due to venom, medication, and dyes use in radiologic study 

MEDICAL MANAGEMENT:  Treatment of anaphylactic shock requires removing the causative antigen, administering medications that restore vascular tone, and providing emergency support of basic life functions.  EPINEPHRINE is the drug of choice given to reverse the vasodilatation

• Nursing management:

a. Establish a patent airway b. Prepare for the administration of epinephrene, benadyril, corticosteroid c. administer o2 and IV fluids d. administer vasoactive drugs

C. Neurogenic Shock -occurs due to the loss of sympathetic tone - an interference in the balance of the vasoregulation influences vessels resulting in massive vasodilation and pooling of blood - Aka- Primary shock - vasodilation of both arterioles and venules increases the reservoir capacity thereby decreasing the venous return

Manifestations: a. The patient who suffers from neurogenic shock may have warm, dry skin and BRADYCARDIA!, poiklothermic temp.

Management: - This involves restoring sympathetic tone, either through the stabilization of a spinal cord injury or in anesthesia, proper positioning.

-nursing management: a. elevate the head of the bed 30 degrees ( in spinal/epidural anesthesia) b. immobilize the patient (in spinal cord injury) c. elastic compression stockings d. feet elevation e. heparin/low molecular weight heparin f. pneumatic compression of the legs g. passive ROM

Systemic Inflammatory Response Syndrome

SIRS - clinical response to a nonspecific insult of either infectious or noninfectious origin. - is nonspecific and can be caused by ischemia, inflammation, trauma, infection, or a combination of several insults. SEPSIS - is the systemic response to infection and is defined as the presence of SIRS in addition to a documented or presumed infection

Epidemiology:  500,000 – 750,000 cases annually in the United States and rising  Most common cause of death in non-coronary ICU and two-thirds of cases occur in hospitalized patients  Increasing incidence of severe sepsis is attributable to the aging population with chronic diseases  Widespread use of antimicrobial agents, indwelling catheters, mechanical devices and ventilators  increase incidence ·30% mortality when shock is present · Severe sepsis $22K/pt, $16 billion/year

Criteria for Diagnosing: 

Systemic Inflammatory Response System(SIRS) o Widespread inflammatory response o Two or more of the following  Temp > 38°C or ˂ 36°C  Heart Rate > 90 bpm  Tachypnea (RR > 20) or hyperventilation (PaCoz ˂ 32 mmHg)  WBC > 12,000 cells/mm3, < 4000 cells/mm3 or presence of >10% immature neutrophils



Sepsis -SIRS + definitive source of infection



Severe Sepsis -Sepsis + organ dysfunction, hypoperfusion, or hypotension -Hypoperfusion and perfusion abnormalities may include but not limited to lactic acidosis, oliguria or an acute mental state.

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Septic Shock - Sepsis + hypotension despite fluids -Perfusion abnormalities a. Lactic acidosis b. Oliguria c. Acute AMS Multiple Organ System Failure -Abnormal function of two or more organs such that homeostasis cannot be achieved without intervention

Pathophysiology: Local Injury (trauma, infection, ischemia) Bacteria enters the damage tissue Release of bacterial toxin Toxin enters the blood and is circulated in the body

Release of systemic chemical mediators: a. Bradykinin b. Histamine c. interleukin-1 d. TNF e. complement

Damage the endothelial cells

Massive vasodilation

Multiple organ damage

Pathophysiology of SIRS 

The antigen-antibody reaction stimulates multiple interacting systems such as: • Complement Cascade • Cytokine cascades • Arachidonic Acid Metabolites • Cell Mediated Immunity • Humoral Immune Mechanisms • Clotting Cascade

Cytokines 

 

Are Intercellular signaling proteins or messengers More than 30 recognized Act through binding to specific receptors on the target cells triggering other cascades or its own cascade

Pathophysiology of SIRS

Pathophysiology of SIRS

TNF-α 





The earliest and most potent mediator in SIRS It activates neutrophils, causing the production of Interleukin-1(IL-1), Interleukin-6 (INL-6), and Interleukin -8 (INL-8). It stimulates platelet activating factors and prostaglandin, and promotes leukocyte or vessel cell wall adhesion.

Pathophysiology of SIRS

IL-1 



 



Pathophysiology of SIRS

During an inflammatory response, it facilitates the movement of WBCs toward the injury, ischemia, or infected area It stimulates the release of arachidonic acid from phospholipids in the plasma membranes, leading to fever, hypotension, and decrease systemic vascular resistance. IL-1 also leads to muscle protein breakdown IL-1 works with other cellular immunity components to produce IL-2, which decreases blood pressure, systemic vascular resistance, and left ventricular ejection fraction. IL-2 may also increase left ventricular end diastolic volume, cardiac output, and heart rate

Pathophysiology of SIRS

IL-6 





Is a key messenger that can either trigger the rest of the cascade or its arrest Stimulates the release of acute phase reactors Its serum levels are consistent with the gravity of the immune reaction

Nitric Oxide 



Nitric oxide is synthesised by inducible nitric oxide synthase (iNOS) in the vascular endothelium and smooth muscle in response to pro-inflammatory cytokines NO is the vasoactive mediator responsible for the fall in systemic vascular resistance underlying the hypotension in the late stages of SIRS and septic shock

Pathophysiology of SIRS

Arachidonic Acid Cascade 

Thromboxane A2 • Is a potent vasoconstrictor and platelet aggregator • Leads to tissue ischemia from hypoperfusion.



Leukotrienes leads to • ↑Capillary endothelial permeability • Bronchoconstriction • Activation of neutrophils

Pathophysiology of SIRS

The Complement Cascade 

Controls the inflammatory process • Chemotaxis • Opsonization • Promotion of phagocytosis

Pathophysiology of SIRS

Clotting Cascade 

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

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Fibrin is formed due to the injury of the vascular endothelium Chemical mediators stimulate the release of Hageman Factor and Thromboplastin These form clots at the site of the injury, attempting to stabilize the site Fibrinolysis is activated by the coagulation cascade, leading to mediator induced (DIC).

Pathophysiology of SIRS

Bradykinin 



The activation of the Hageman Factor stimulates the release of bradykinin Bradykinin creates vasodilatation and capillary leakage, therefore volume depletion.

Pathophysiology of SIRS

Myocardial Depressant Factor





Myocardial depressant factor is a serum protein released by the hypoperfused and ischemic cells of the pancreas It decreases the velocity of contractions of myocardial cells, leading to decreased right and left ventricular ejection fractions

Pathophysiology of SIRS

Beta Endorphins 



Beta endorphins are released, by the pituitary and hypothalamus, in response to hypoperfusion They cause peripheral vasodilatation, and decrease cardiac contractility

Pathophysiology of SIRS

Stages of SIRS 

4 stages according to the gravity of the situation

Pathophysiology of SIRS

SIRS 1 

Release of proinflammatory mediators • These mediators create a web of reactions designed to limit new damage and ameliorate whatever damage has already occurred

Stages

Pathophysiology of SIRS

SIRS 2 

Stages

Pro-inflammatory and antiinflammatory mediators appear in the systemic circulation • Pro-inflammatory mediators recruit neutrophils, lymphocytes, platelets, and coagulation factors

Pathophysiology of SIRS

SIRS 3 

Stages

Massive Systemic Inflammation • Progressive endothelial dysfunction occurs increasing microvascular permeability • Vessels lose tone and profound vasodilatation occurs resulting in severe shock

Pathophysiology of SIRS

SIRS 4 

Stages

Most patients do not make it this far --but if they do-• A compensatory anti-inflammatory response occurs trying to suppress inflammation

Clinical Picture 

The typical 2 or more of: • • • •

Temp. >38°C or <36°C HR >90 bpm RR > 20 cpm or PaCO2 < 4.3 kPa WBCs   



>12 x 109/lit < 4 x 109/lit > 10% immature forms

Symptoms & Signs of each organ sequels

Clinical Picture

Organ Manifestations 

Cardiovascular • Skin warm and flushed • Widened pulse pressure • Cardiac output is ⇑ but SVR is ⇓ • Eventually C.O. declines exacerbating hypoperfusion

Clinical Picture

Organ Manifestations 

Pulmonary • Hypoxemia may be masked by hyperventilation • Respiratory alkalosis • Pulmonary edema • Respiratory failure • Bronchoconstriction • ARDS

Clinical Picture

Organ Manifestations 

CNS • Altered mental status • Confusion • Irritability • Agitation • Disorientation • Lethargy • Seizures • Coma



Renal • Oliguria: < 500 ml/day • Metabolic Acidosis

Clinical Picture

Organ Manifestations 

GIT • • •

Impaired motility ⇑ SGPT & SGOT Hyperbilirubinemi a • Hepatic necrosis • Hypoprothrombin emia • Hypoglycemia

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Blood • • • •

⇑ or ⇓ WBCs ⇑ PT and PTT ⇑ or ⇓ Platelets Anemia

Investigations   

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Cytokines assay (IL-6, IL-8 & TNF) Blood Culture Burn eschar biopsy with culture & sensitivity Serum Procalcitonin • The only lab test that differentiates SIRS (0.5 -2 ng/dl) from  Sepsis (>2 & <10 ng/dl) from  MOD (>10 and often >100ng/dl) 

Treatment = Elimination of triggering factor (LPC & LPS)  LPS • Antibiotics according to C&S • Gut decontamination 

LPC through Prompt early surgical eschar excision  Chemical elimination eg. Cerium Nitrate 

Treatment   

Supportive Medical Surgical

Treatment

Supportive Therapy    

Volume replacement +ve inotropes & vasopressors Ventilation (Pressure support or PEEP) Nutritional Support • • • •

Iso-Osmotic Feedings TPN PPN Immune Modulatory Foods such as Arginine, Glutamine & fish oils

Treatment

Medical 

Potent anti-oxidants • • •



Methylene Blue given IV Acetyl Cysteine Vitamin C

Immune Modulators • • •

Ibuprofen (proved of limited value) Centoxin: an Ab to endotoxins NOSI (nitric oxide synthetase inhibtor) very much accepted • IL-6 blockers Experimental

Surgical Excision 

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

Best option = Early excision + coverage Best performed within the 1st 72 hours and after resuscitation Is the only way to break the circle

Surgical Excision 

⇓⇓ incidence of burn wound colonization

Barret et al, 2003

Prognosis 



Death in 60% of cases of late stages & shock in patients with no previous history of medical conditions Death rate is higher if MOD develops & is dependant on no. of organs affected •3 •4 •5

organs organs organs

85% 95% 99%

Thank You