What is the Reversal or state that will give Nurses a basis that a patient is doing ok?

BP- +/- 20 mmHg of pre-shock state

Temp-within normal limits

HR-60-100 BPM

Alert and Oriented-Glasgow to pre-shock

Urine output->30 cc/hr

Hypovolemic Shock-Volume Loss

What are the Hemodynamic parameters?

Transport Shock

Hemodynamic Parameters?

Decreased HCT/Hgb

Cardiogenic Shock

Hemodynamic Parameters?

Hypovolemic Shock-Septic Shock

Hemodynamic Parameters?

1-Inflammation Stimulus

2-Inflammation Mediators

3-Effects on Capillaries

4-Effects on Phagocytes

5-Acute Inflammation

6-Inflammatory Repair

What are the Inflammatory Mediators?

What can Inflammatory Mediators Stimulate?

Cytokines, Tumor Necrosis Factor (TNF), nitric oxide (NO),

and histamines. 

Stimulate nerve endings with stimulation of pain and pressure with increased capillary permeability.

SHOCK

What Does Vasodilation have to do with it?

SHOCK

What does Activation of the Endothelial Cells have to do with it?

SHOCK

What does Increased Vascular Permiability have to do with it?

SHOCK

What does Chemotactic Factors Production have to do with it?

Macrophages

What do they do?

Activated Macrophages produce nitric oxide (NO)

Kill microbes and tumors

Scavenge dead cells and debris during inflammatory repair

Monocytes

What are they and what do they do?

-Immature Macrophages

-Release pro-inflammatory cytokines like TNF-alpha and -Interleukin-6 (IL-6) (fever)

-First line of Defense

-Up regulate Tissue Factor

Platelets

Do what?

What substance in the body is introduced by  bacterial products and proinflammatory cytokines (TNF)?

and

Responsible for cytotoxic effects of macrophages on bacteria protozoa, and tumor cells?

Nitric Oxide

What substance in the body

Reduces internal Ca2+ and dampens

Cardiac contractility?

Nitric Oxide

on

Cardiac Myocytes

What substance in the body decreases intracellular Ca2+ leads to muscle relaxation?

Nitric Oxide

on

Smooth Muscle

What substance in the body

Inhibits platelet aggregation?

Platelets

Nitric Oxide

Nitric Oxide

to

Shock

What is the treatment to nitric oxide

and what does it do?

Methaline Blue

Binds the nitric oxide and inhibits  nitric oxide form causing vasodilation on blood vessels

This turns the patient's urine really dark blue, then green because it cannot be absorbed

What do Prostaglandins and Leukotrienes do

and

what are they?

Produced in response to inflammatory mediators

Acts as inflammatory mediators

Prostoglandins are a large family of compounds-cause pain

Leukotrienes are a complex mixture of molecules

When inflammation is turned on what else turns on with it?

What are the pathways for this answer?

Clotting Cascade

Fast and slow pathway

The extrinsic and intrinsic pathway

What is the extrinsic pathway(fast) activated by?

What is the intrinsic pathway(slow) activated by?

What do both pathways lead to?

extrinsic-tissue factor

intrinsic-a contant process and is part of homeostasis

Both lead to the formation of thrombin which causes fibrin to be sticky and leads to clotting.

What is the normal process of thrombin?

What happens to thrombin is shock or sepsis state?

Normal-Thrombin activates a pathway to turn off whatever cascade is active

Shock or Sepsis state-leads to systemic inflammatory response syndrome and pathway of thrombin becomes less potent than the activation of the clotting cascade

causing Pro-inflammatory state- leads to fibrin which is sticky-formation of clots and DVTS

Sepsis is what?

What does it cause blood pressure to do?

How can this system develop?

Sepsis-some sort of infection that is within the blood

BP-drops low

Developed-either by a result of the body's own defense system or from toxic substances made by the infecting agent (such as bacteria, virus, or fungus).

What happens to the vital signs in Septic Shock?

HR

RR

WBC

Temp

BP

Abnormally high temperature (Fever) or low temperature (hypothermia)

Plus 1 or more of the following:

Rapid HR

Rapid breathing rate

An abnormally high or low number of WBC

How is sepsis diagnosed?

As sepsis worsens what begins?

Diagnosed when BP remains low despite intensive treatment

 Severe organ malfunction

and

blood pressure may decrease

During Sepsis when toxins produced by bacteria cause cells in the body to release substances it triggers what?

What can this trigger cause in the body?

Triggers inflammation (cytokines)

Althoug cytokines are good to fight infection locally, when systemic it can cause harmful effects

-blood vessels widen (dilate), decreasing BP

-Blood clots in tiny blood vesses in organs

After blood vessels widen decreasing BP and blood clots in tiny vessels inside the organs from cytokines

What harmful complications arise to this happening?

-Blood flow decreases to vital organs-(kidneys, heart, and brain)

-The heart attempts to compensate by working harder, increasing HR and amt of blood pumped

-Eventually blood toxins and increased work of pumping weaken the  heart-heart pumps less blood, and vital organs recieve even less blood

 When tissues do not receive enough blood to the body what is the compensatory release?

What happens to the kidneys in septic shock?

The tissues release excess lactic acid (a waste product) into the bloodstream, making the blood more acidic.

Kidneys excrete little or no urine, and metabolic waste products (such as urea nitrogen) accumulate in the blood.

What happens to the walls of blood vessels during septic shock?

What happens to lung function?

Walls of blood vessels may leak, allowing fluid to escape from the bloodstream into tissue and cause swelling

Lung Function worsens because leaking blood vessels in the lungs cause fluid to accumulate, making breathing difficult.

A client who suffers an MI have documented increases in free radicals after supplemental oxygen is given

This often manifests itself as arrhythmias

Anaerobic Metabolism-->Decreased ATP-->Hypoxanthane Production-->Reperfusion, Fluids, Supplemental O2-->Xanthane + O2--> Oxygen Free Radicals-->

Both Damages cell membranes --- and Increased cellular permeability

Damaged cell membranes lead to further anaerobic metabolism with leukocytes clogging microvascular circulation

Organs

Vasodilation with Nitric Oxide that causes:

Organs and Shock

Increased Capillary Permiability:

leaking fluid into tissue causes hypovolemia intravascularly

Interstitial edema can decrease perfusion and cause pain

Sypathetic Nervous System

Prostaglandin-

Cortisol-

Prostaglandin-pain response and activation of the sympathetic nervous system

Cortisol-Increased blood sugar and immune suppression

Manifestation of SIRS include, but are not limited to:

(4)

When any of at least 2 of the following criteria are present

-Body Temp. less than 36 C or greater than 38 C

-HR greater than 90 beats per minute

-Tachypnea (high respiratory rate) with greater than 20 breaths; or arter partial pressure of carbon dioxide less than 4.3 kPa

-WBC count less than 4,000 cells or greater than 12,000 cells; or the presence of greater than 10% immature neutraphils (band forms)

What are some etiologies that can cause SIRS?

(5)

-Infectious process(bacterial, fungal, viral, protozoa infections)

-Massive ischemia or injury

-one or multiple blood transfusions

-Burns

-Cancers

(MODS) Multiple Organ Dysfunction Syndrome

What is Primary MODS and 2ndary MODS?

Primary-Organ failure is related to the intial injury/insult

2ndary-Organ failure is the result of the SIRS response to the inital injury/insult

Occurs latent (7-10 days) after original insult

Occurs in organs distant from the orginal insult

What is the Transition from SIRS to MODS?

(4)

1.  Failure to control the source of infection or inflammation.

2.  Persistent hypoperfusion (prolonged shock state)

3.  Presence of necrotic tissue

4.  Altered (increased) cellular oxygen consumption

What is the MODS system failure order?

(1-7)

1. Pulmonary

2. Cardiovascular

3. Renal

4. Neurologic

5. Hepatic

6. GI

7. Hematologic

During MODS in the Pulmonary system what happens?

Cardivascular System?

Patients will get swelling at the alveolar cappillary membrane and will have difficulty diffusing oxygen.

Symptoms of vasodilation and increased capillary permeability causes maldistribution of blood and a cardiovascular sympathetic response; changes in BP and increases in HR

MODS system to renal failure (3rd in order to fail)?

4th Neurological?

5th Hepatic?

6th GI?

7th Hemotologic?

 3rd-changes in urine output and the kidneys

4th-confusion is a sign that the patients are getting inappropriate oxygen to brain tissue.

5th-changes in liver enzymes

6th-parastalsis and the integrity of the gut wall

7th-coagulopathies

2ndary MODS leads to:

(4)

1. Impaired gut barrier leading to translocation of bacteria

2. Generation and release of inflammatory mediator

3. Reticuloendothelial dysfunction(immune function and distribution of immune cells)

4. Disruption of oxygen supply to the tissues or when tissues have an inability to use oxygen

MODS 2ndary Diseases

Bacterial Translocation?

The normal gut contains enough bacterial and endotoxins to kill the host thousands of times over, we reasoned that even small increases in gut permiability could have profound physiologic consequences-

which leads to leaky gut-barrier failure allows bacteria and toxin products, such as endotoxins escape from gut and enter into systemic circulation-systemic sepsis--> to MODS

Millions of micro thrombi,  Uses all of the body's clotting factors, Hemorrhage everywhere, Increased in Fibrin Split Products as the body is trying to break down all of those clots(Imbalance of clotting and bleeding)

D-Dimer

Explain what is happening to The Neurological System with MODS?

Early Failure-

Late Failure-

Neurologically-Neuroendrocrein exhaustion and ischemia

Early Failure- Confusion, disorientation

Late Failure- Progressive decreased LOC to Irreversible Coma

MODS

What is happening to the Pulmonary System?

Early Failure-

Late Failure-

Pulmonary-Alveolar capillary injury, starts to disrupt surfactant

Early Failure-requires ventilator support for 3-5 days

Late Failure-Progressive ARDS

(PEEP>+10 and FiO2> 50%)

MODS

What happens with the Cardiovascular System?

Early Failure-

Late Failure-

Cardiovascular-Decreased perfusion related to MDF (mycardial depressant factor) production

Early Failure-Ejection fraction, 65%;capillary leak syndrome

Late Failure-Increased inflammatory mediators that depress CO; hypodynamic despite inotropes-refractory to B stimulation

MODS

What happens in the Renal System?

Early Failure-

Late Failure-

Renal-Renal ischemia leads to (ATN) acute tubular necrosis

Early Failure-Oliguria of <480 cc/day; Creatine >2-3; increased urine osmolality

Late Failure-Dialysis dependent(specific slow and more gentle type, pt cannot handle massive fluid shifts

MODS

What happens to the Intestinal System?

Early Failure-

Late Failure-

Intestinal-Bacterial translocation, abdominal hypertension

Early Failure- decreased parastalsis and inability to absorb food-->Ileus(enteral intolerant) for > 5 days; abdominal HTN

Late Failure-Stress ulcer(requiring transfusion);Cholecystitis (without stones);abdominal compartment syndrome

MODS

What happens to the Hepatic System?

Early Failure-

Late Failure-

Hepatic-Reticuloendothelial system (Kupffner cells) failure

Early Failure-Bilirubin>2mg;LFTs 2X normal values;decreased albumin;decreased production of clotting factors, impaired immune cells, failure to be able to metabolize

Late Failure-Jaundice and Biliruben> 8-10 mg;coagulopathy

MODS

What happens to the Hematologic System?

Early Failure-

Late Failure-

Hematologic-Clotting mechanism>fibrinolytic system=progcoagulant state

Early Failure-Pt/Ptt>25%; Platelets <80,000; decreased fibrinogen

Late Failure-Evidence of DIC increased FSP/FDP(fibrin split products) and D-dimer titers

Transport Shock

Is What?

Related to the fact that the

Supply of Hgb that carries O2 to tissues

Is greatly diminished

Resulting in Decreased O2 supply for body.

decreased Hgb volume

Inappropriate hgb binding

What do we do for Transport Shock when there is a Decreased Hgb volume

What are examples of decreased Hgb volume?

Administer (Crystalloid) fluid therapy which causes a thinning of the Hgb in the blood.  Fluid is usu. given and then a blood product to correct this state.

Anemia and Hemmorrhage

What happens with Inappropriate hemoglobin binding?

and with what substance?

can also happen with heavy metal poisoning

The Hgb bus seats are occupied by carbon monoxide, leaving no room for O2.

Carbon monoxide poisoning 200x binding affinity

Oxygen cannot be transported to tissues

false reading on pulse Oximetry

Impaired Oxygenation because of a Mechanical barrier to blood flow

blocks O2 delivery to tissues

It is the inhibition of blood leaving either side of the heart

SV, CO, BP decreases and contractility is impaired

Because the ventricle can't propel all of its contents forward, blood begins to "back up" into the pulmonary system, causing pulmonary congestion.

During an MI (Cardiogenic Shock) what happens if there is a dysfunction of the right ventricle and what happens after?

ejects too little blood so less blood enters the left ventricle

SV,CO,BP decreases

Because the R ventricle cant effectively pump all blood recieved, blood begins to "back up" into the systemic circulation. (look for JVD and edema)

Cardiogenic Shock

Cardiac Dysrhythmias what happens?

Complex neuro-endocrine response

baroreceptors in the aorta and carotid arteries sense decrease in BV and CO

baroreceptor and chemo-receptors--> alert

hypothalamus=releases ACTH=activation of Aldosterone=Na+ and H2O retention--> increase in BV and BP

To increase venouse return Na+ and H2O are retained by?

The rennin-angiotension-aldosterone cycle is activated to increase what? (2)

By aldosterone and ADH

BV and venous return

Blood to Kidneys decrease-->rennin release-->angio I in liver release-->angio I to angio II in lungs =

equals what?

VASOCONTRICTION

1-Initial-cellular anaerobic metabolism

2-Compensatory-SNS stimulated

3-Progressive-failure of compensatory mechanisms

4-Refractory-unresponsive to therapy

Cellular anaerobic metabolism

decreased CO and tissue perfusion are evident

decreased O2 delivery results in anaerobic metabolism and Lactic Acid

BEST STAGE TO CATCH AND TX SHOCK, if O2 delivery is restored recovery is good

Augment CO

Redistribute blood flow-Shunting Occurs

Restore blood volume-ACTIVATION OF SNS

Neuro-endocrine responses to restore CO and O2 delivery

Increased HR 10 bpm may be a subtle indication

BP may drop and then rise to an adequate level

FAILURE OF COMPENSATORY MECHANISMS when body can't restore homeostasis

Progressive shock results in MAJORY DYSFXN OF MANY ORGANS

decrease continued in blood flow, tissue perfusion, O2 delivery, and increase of metabolic wastes= over time lead to MODS

Unresponsive to therapy

so profound shock state, cell destrxn so severe

DEATH IS ENEVITABLE

Profound hypotension despite potent vaso-active drugs

pt remains hypoxic despite O2 therapy

A state of intractable circulatory failure leads to total body failure and DEATH

WHAT ARE THE INITIAL 1ST SIGNS OF SHOCK?

S/S

LOC and mentation changes, decreased UO, there is no SNS STIMULATION

this is the best stage to catch and tx shock and restore delivery of O2

diaphoresis and cool skin, decreased UO, decrease peristalsis,

Increased HR, RR, glycolysis

Increased HR by 10bpm

BP may drop and then rise to an adequate level

3RD STAGE OF SHOCK- PROGRESSIVE S/S?

pts are dependant on interventions provided:

HR erratic, NO UO, pt is confused, low BP as compensatory mechanisms begin to fail

Drug therapy: Ace Inhibitors, +chronotropes

Mechanical ventilation is still an appropriate intervention

What are 4 signs to traditionally assess SHOCK?

why are these signs often underestimated

BP- 90/60 may be norm for one pt and not for another

HR-many factors to tachycardia

MENTATION-may be hard to assess in the presence of head injury, ETOH, drugs, or chronic disease (Alzheimer's)

UO-several factors false sense of security such as hyperglycemia, and DI

What can be used as a indirect measure of impaired O2 and shock?

Normal Levels are?

What can this substance cause?

Serum Lactate Levels

Normal levels are below <2mMol/L

metabolic acidosis

Lactate levels indicate the degree of?

How many hrs does a pt have for an increased survival rate and decreased occurance of organ dysfxn for levels to return to norm?

Hypo-perfusion

24 hrs

Hypovolemic Shock

Clinical Findings S/S are r/t?

SVR

CO

BP

PAP

CVP

PCWP

Related to the degree of volume depletion

SVR-increases

CO, BP, PAP, decreases

CVP,PCWP, decreases

Tachycardia is evident and UO is low

1-What is the TX for Hypovolemic Shock?

2-Caution?

3-For every 1000mL administered only ___ mL will stay in the vascular circulation

4-Vasodilation=?

1-2-3 L crystalloid till blood replacement available

2-Caution is used as too much fluids could lead to transport shock

3-  200mL

4-Vasodilation=interstitial fluid resulting in edema.

Vasodilation-Warm decreased SVR (persistent vasodilation)-below the injury

Produces warm skin d/t venous pooling

Fluid is in dependent areas

Decreased CO, BP-produces deminish venouse return producing lower RAP, PAP, PSWP, and CO

Decreased sympathetic response-decreased HR as a result of parasympathetic innervation

*Hypthermia and absences of sweating below the level of the SCI may be present

Treat bradycardia-Atropine

Fluid resuscitation

Anapylactic Shock

How soon can it develop?

What is the typical pattern?

What happens during upper airway destruction?

It can develop rapidly (5-30 mins) or slowly (6-12 hrs)

Follows a typical pattern of generalized itching, followed by cutaneous flushing, urticaria, a fullness in the throat, anxiety, tightness in the chest, faintness, and loss of consciousness.

Severe upper airway obstruction by edema can lead to asphyxia, whereas lower airway obstruction with wheezing and chest tightness is caused by bronchospasm

Respiratory distress initally-edema in the airway

Vasodilation(warm, decreased SVR)

Decreased output (edema, CO, BP)

HR increases in a normal sympathetic response

What is the Treatment for Anaphylactic Shock?

Airway management-priority intervention

Epinephrine and antihistamines-histamine is the cause

Fluid resuscitation-for BP maintenance to avoid renal failure

Steroids given for capillary seal-leaky membranes

What is Septic Shock?

A multitude of metabolic, hematologic, and hemodynamic abnormalities occur as a systemic response to the invasion of microorganisms in the bloodstream.

Early recognition is crucial

Compensation to vasodilation (bacterial toxins lead to vasodilation problem)

Early (hyperdynamic phase)

Febrile/warm to hot skin-100.3 F

Increased output (HR, BP, CO)

CO- increased 8-14

BP may be normal even if it should be low d/t vasodilation

Increased CO

Decreased SVR

Hypotension

Increased Lactate levels-decreased lactate clearance

SVO2-V/Q mismatching due to pulmonary endothilial damage and microthrombi--increased atelectosis and intrapulmonary shunting

What is a Late-(hypodynamic phase) of Shock?

First dose of Antibiotics given w/in 1 hr of order, or w/in 1-3 hrs of Admission

Fluid resuscitation

Xygris-activated protein C;interferes w/ inflammation and the clotting cascade

Tight blood glucose control 80-150

What are the parameters of Sepsis

and manifested by 2 or more of these S/S?

(4)

1-Temperature greater than 38 C or less than 36 C

2.  HR greater than 90 bpm

3.  RR>20 bpm or PaCO2 greater than 32

4. WBC count>12000 or less than 4000 or greater than 10% immature (bands) form

What is severe Sepsis before Shock?

Sepsis associated with organ dysfunction, hypoperfusion, or hypotension.  Hypoperfusion and perfusion abnormalities may include byt are not limited to lactic acidosis, oliguria, or an acute alteration in mental status

Hallmark:endothelial damage and coagulation dysfunction

Diminished O2 carrying capacity of the blood produces the clinical manifestations

Decreased hct/hgb-(Shock caused by carbon monoxide poisoning)

RAP and PAWP may be normal, depending on volume status

An elevated level of carboxyhemoglobin if poisoned by

What is the Treatment for Transport Shock?

What is the Treatment for Obstructive Shock?

Tamponade

Pulmonary Embolus

Pneumothorax

Blood replacement and hyperbaric therapy

Tamponade-Remove pericardial fluid, pericardocentesis

Pulmonary embolus-thrombolytics;Med management

Pneumothroax-chest tube placement

What are the S/S of

Tamponade?

PE?

Pneumothorax?

Tamponade-Pulsus paradoxus-decrease greater than 10 of systolic BP during inspiration, Beck's triad-elevated RAP, decreased BP, widening pulse

PE-SOB, hypoxia, hypotension, T-wave inversion

Pneumothorax-increased pleural pressure, decreased breath sounds or none, trachial deviation, and bradycardia, decreased CO, poor ventilation, decreases venous return

What are the findings of Cardiogenic Shock regardless if it is on Left or Right Side pump failure?

 What is the Treatment given for?

Vasoconstriction(cool, increased SVR, HR)

Decreased output (CO, BP, PAP)

Increased filling pressures (CVP, PCWP)

Support myocardium (IABP, VAD)

Revascularization-stent placement

What are the clinical manifestations of Cardiogenic Shock on the Left side?

(associated with hypoperfusion and pulmonary congestion)

Dyspnea, bilateral rales (crackles)

Distant heart sounds, and 3rd and 4th heart sounds are usu. present

Elevated PAWP (>15mm Hg)

Low cardiac index (<2.2)

Sustained Systolic hypotension (<90 for greater than 30 minutes)

What are the clinical findings for Cardiogenic Shock for Right Ventricular Failure?

(Associated with systemic venous congestion)

Periperal edema

Lung sounds will be clear unless ther is also left ventricular dyfxn

A split 2nd ehart sound may be heart-means a distended R ventricle

Elevated RAPs in the presences of normal or low PAWP

What's the primary goals of treatment for shock states?

(3)

Identify and treat the underlying cause of shock

Optimize oxygen delivery

Decrease oxygen consumption

Fluids (crystlloid, colloid, or blood) to restor preload and increase the CO component of O2 delivery

Rapid infuser 500 mL/min in septic shock or trauma

Usu. a combo of crystalloids and Colloids

Can also give PRBC and Blood

+ Inotropes-Dopamine(alpha and beta)

Dobutamine (beta 1)

Milirinone-(phosphodiesterase inhibitor)

Vasopressors

epinephrine, norepinephrin, dopamine, and vasopressin

Afterload reduction

Nitroprusside, Nitroglycerine(decreases SVR)

Decrease pain and anxiety

Normal Temperatures to keep metabolic rate down

Minimize activity- this might be considered by giving a sedative like Diprovan(short life)

or

Mechanical Ventilation

Describe what MODS is

Multiple Organ Dysfunction Syndrome?

What are the Mortality rates for: (%)

one organ failure?

2 organs?

3 organs?

MODS is a syndrome characterized by the progressive dysfunction of 2 or more organ systems

Single organ- 30%

Double organ- 60%

Triple(or more) organ-90%

Chronically ill with an acute illness

Major tauma (acute insult to 2 or more ststems)

Immunosuppression and/or infection (sepsis)-vascular and GU

What are the risk factors of getting MODS?

(5)

Diagnosis of sepsis

(persistent infection, or bowel infarction)

# of organs dysfunction

Baseline organ dysfunction/Significant tissue injury from initial insult

Severity of disease on hospital admission

Age >65yrs old

Immunosuppression

What are the severities of disease that can happen before hospital admission that can worsen the chances of

MODS?

Poor/delayed resuscitation

Malnutrition

Coma on admission

>6 units of blood in 12 hours

What do Mediators do? (3 things)

What are they released from?

Mediators stimulate the inflammatory process, recruit WBC, and promote the clotting cascade, and increase capillary permiability

endothelial cells that activate during trauma to blood vessels, transient bacterial, and stress

What Chemical Mediators are involved during Shock:

Catagories and Names

(5)

Vasoconstrictors: Thromboxane, Endothlin, Angiotension II-balance inflammation

Vasodilators: Bradykinin, Complement, Nitric Oxide, Prostaglandins, Leukotrienes, Pro-inflammatory

Stimulate T & B lymphocytes: Interleukins (1-6)-anti-inflammatory

Mediate endotoxins and stimulate leukocytosis: TNF (tumor necrosis factor)

Block virus production and transmission: Interferons

What is the extrinsic system?

What is the intrinsic system?

What do both pathways do?

extrinsic-fast pathway that is activated by tissue factor

intrinsic-slow pathway that is a constant process and part of homeostasis

Both pathways-->formation of thrombin-->fibrin sticking to everthing-->

Tissue injury to both occur

Local-has local inflammation-->increased O2 and glucose to injured tissues-->promotes healing

Systemic-systemic inflammation-->widespread cellular hypoxia and O2 consumption-->reperfusion injury

Major shunting is the key!!!

Seen when an area of tissue suffers and ischemic or hypoxic event and then increased amounts of O2 are delivered by returned blood supply.  This causes free radical formation and can lead to further tissure damage.

Conversion from anaerobic to aerobic metabolism.

Patients becomes more clinically unstable in an organ system when O2 is perfused to an area that has had hypoperfusion

Explain the mechanisms of Reperfusion Injury in order?

(7) steps

Prostaglandin-pain response and activation of the SNS

Cortisol-increased blood sugar and immune suppression

What is SIRS?

What can SIRS be caused by?

exaggerated inflammatory response that becomes systemic and results in the excessive productionof chemical mediators.

May be caused by infection, trauma, major surgery, acute pancreatitis, or burns

Temperature greater than 38 C or less than 36 C

HR>90 bpm

Tachypnea RR >20 breaths/min or PaCO2> 32 mm Hg

WBC count> 12,000 or <4000 or >10% immature (bands) forms

When the cause of SIRS is infection, the process is called____.

When there are excessive pro-inflammatory responses-?

When there is excessive anti-inflammatory responses-?

Sepsis

 SIRS and then Organ dysfunction is likely to occur

 CARS-The patient is at risk for 2ndary or opportunistic infections, which serve as additional insults to trigger the SIRS response

What is the transition from SIRS to MODS?

(4)

*Failure to control the source of infection or inflammation

*Persistent hypoperfusion (prolonged shock state)

*Presence of necrotic tissue

*Altered (increase) cellular oxygen comsumption (hypermetabolism)