Begins with severe infection. Can be bacterial, viral or fungal. Infection starts local and gets into blood stream.

Initiates inflammatory defense mechanism

"Problem with the pipes"

Anything that can severely alter blood volume, causing decreased cardiac output.

Ex: vomiting, diarrhea, trauma, surgery, GI bleed, hemorrhage, burns

"Problem with the tank"

hearts inability to pump affectively, could be from heart damage, unable to keep up with the demand of the body, decreased cardiac output

Ex: heart attack, cardiac tamponade, dysthymias

"Problem with the pump"

Hypersensitivity reaction to an allergen or substance. Severe allergic reaction.

Could be from a spinal cord injury, disturbing the CNS response.

"Problem with the pipes"

Wheezing, labored breathing

Dyspnea

Bronchospasm

Flushing

Erythema

Cyanosis

Urticaria (hives)

Pruritis

N/V/D

Chest pain

Feeling of impending doom

Hypotension

Tachycardia

Stridor

Oxygen therapy - mechanical ventilation if necessary

Medications

• Vasopressors (norepinephrine), aspirin, inotropic (dobutamine), antiplatelets (clopidogrel), heparin

IV fluids - NS

Stent placement

Balloon pump

Coronary artery bypass surgery

Ventricular assist devices (VAD)

Heart transplant

First line treatment: Epinephrine

Ensure patent airway

Diphenhydramine

Famotidine

Oxygen

Albuterol

Methylprednisolone

IV Fluids (two large bore IV's)

Possible intubation

Tachypnea

Tachycardia

SOB

Weak pulses

Pale, cool

Diaphoretic

Altered mental status

Decreased urine output

Cyanosis

Abnormal heart rhythm

Antibiotics

Fluids

Corticosteroid

Vasoconstrictor- Norepinephrine

Antipyretics

Oxygen

Blood

Vasopressors- help increase BP and perfusion (MAP > 65 to perfuse vital organs)

Lower head of bed

hypotension

warm pink skin-extremities

hypothermia

restless

lethargy

Decreased LOC

MAP decreases 10 mmHg from normal BP

Circulatory blood volume may decrease (usually by 500 ml)

Oxygenation is adequate

Compensatory mechanisms are affective

Nsg interventions:

Give fluids

Monitor VS

Tachycardia

Vasoconstriction

Tachypnea

Retention of fluid

Decreased urine output

Pale/cool clammy skin

anxiety

Normal to slightly decreased

MAP is decreased by 10-15 mmHg from normal

*Organ perfusion is restored. Organ dysfunction can be reversible if compensatory mechanisms and medical interventions can keep the patient stable. Also, the shock cause is corrected.

Nsg interventions:

IV fluids

Oxygen

I&Os

daily weight

HOB elevated

Correcting cause of shock (antibiotics, blood)

Hypotension

blood volume loss of 30-40%

Cells switch from aerobic to anaerobic metabolism

Metabolic acidosis

Lactic acidosis

endothelial damage- worsen edema

Impending sense of doom

Rapid, weak pulse or bradycardia

Shallow respirations

Cold and clammy skin

O2 sat decreased by 2-20%

Can lead to MODS if not treated

**Medical interventions should be initiated within one hour of onset.

less vital organs become anoxic and more vital become hypoxic

Signs of DIC

Interventions:

Mechanical ventilation (monitor side effect of ventilation) or BIPAP

Vasopressors

IV fluids cautiously, monitoring for fluid overload

Treat DIC

Organ damage

Can lead to death

Medical interventions are not helping

Tissue are anoxic

Wide spread cell death

Cardiac collapse

Severe metabolic acidosis

Petechia -DIC

Interventions:

continue fluid rescitation and vasopressors

Mechanical ventilation with OG tube

Discuss living will or AD and code status

Possible comfort care?

4 - extremely concerned, immediate interventions are needed.

Cancer - leukemia

Damage to organs or tissue

• liver, pancreatitis

Severe tissue injuries - burns

Major surgeries

Complications from pregnancy and delivery

• placental abruption

• hemorrhage

• amniotic fluid entering bloodstream

Severe immune reactions - blood transfusion reactions

In cases of trauma: control bleeding, then give fluids and blood products (FFP, cryoprecipitate, platelets).

Control clotting and thrombosis with anticoagulation therapy but used cautiously due to bleed risk. (Heparin or danaparoid). only tPA in extreme circumstances.

Vasopressors like norepinephrine for hemodynamic support if needed.

Dialysis may be needed in cases of acute kidney injury.

Mechanical ventilation?

Antifibrinolytics- if needed to prevent the breakdown of fibrin clots to control bleeding.

-The first stage of DIC is the body producing mass amounts of clotting factors such as platelets, thrombin, and fibrin into the blood stream to the site of injury (or infection.)

-This causes microthrombi to clot off small vessels within the body, causing impaired perfusion.

-Next, the body senses the clots within the vessels and activates the anticoagulant factors in the body (proteins C and S, Antithrombin 3, etc.)

-The clotting factors are now depleted and the anticoagulation factors are activated, causing the hemorrhage process.

• Continuous O2 sat monitoring

• Fowler or high fowler positioning

• Pain management (analgesics/anti-anxiety)

• Heparin therapy

• Plasma transfusions to replace blood clotting factors

• Treatment of underlying disorder (antibiotics, blood products, etc.)

• IV fluids

• Oxygen therapy

• Closely monitoring vitals

• Monitor I&O

CBC- decreased platelet count is common in DIC due to platelet consumption. Schistocytes (fragmented RBCs) may be noted because of cell trapping and damage within fibrin thrombi

D-dimer elevated in DIC (d-dimer is produced when blood clots and breaks down)

Fibrin degradation products or fibrin split products are increased because of the fibrinolysis that occurs with DIC.

S/S; relate to the decreased perfusion to the body.

Impaired perfusion

• Tachycardia

Shock

• Hypotension

• Circulatory collapse

Impaired clotting, tissue necrosis, and gangrene

• Major vessel thrombosis

Impaired gas exchage

• Tachypnea

Impaired cerebral perfusion

• Progressive reduction in LOC

Impaired renal perfusion

• Oliguria (↓ urine output)

• Anuria

• Renal failure

Urinary tract bleeding

• Hematuria

GI tract bleeding

• Bleeding from mouth or rectum

Integumentary bleeding

• Petechiae

• Purpura

• Ecchymosis

Impaired tissue perfusion

• Pallor/cool extremities

PT- prolonged

aPTT- prolonged

Fibrinogen- decreased

D-Dimer- elevated

TT- prolonged

AT3- decreased

FDP's- elevated

Kidney function - BUN, creatinine

Blood tests - blood cultures, CBC w/diff, CMP

Lactate

Coagulation studies

CRP

Echocardiogram

Pulmonary function tests

ABGs

CT/MRI

Ultrasounds

Renal scan - elastography

Brain scans

Antibiotics for infection

IV fluids

Blood products

Resp may require mech vent

Vasopressors/inotropic meds to increase blood flow and improve tissue perfusion

Renal may require dialysis (to remove waste production from the blood)

Protein rich nutrition

Transplant to replace failing organ

2: Endothelial dysfunction and microcirculatory failure. The widespread inflammation causes activation of endothelial cell activation which leads to vascular permeability resulting in leakage of fluids and proteins into tissues causing edema. This can lead to decrease in tissue perfusion and hypoxia. Then small blood clots form in the capillaries imparing bloodflow further and contribute to ischemia.

3: Tissue hypoxia and cellular injury occur as a result of poor perfusion and oxygen deliver. As the organs experience hypoxia the organs get injured especially the heart, kidneys, liver, and lungs.

4: activation of coagulation and fibrinolysis occurs in response to the inflammatory state of the body which leads to DIC.

5: organ disfunction occurs which includes:

Lungs: alveolar damage, pulmonary edema, and ventilation-perfusion mismatch.

Heart: Decreased cardiac output

Liver: Impaired detoxification, synthesis of proteins and metabolism.

Kidneys: Tubular damage causes AKI.

GI: ischemia leads to gut permeability and bacterial translocation further contributing to systemic inflammation.

Immune dysfunction: immunosuppression follows, leading to susceptibility of secondary infections.

6: Progression and feedback loops- progresses in a cascade-like manner, where one organ failure leads to another. ex renal failure leads to retention of toxic ,metabolites worsening cardiac function and hemodynamic instability that worsens liver and kidney function.

Heart- Heart failure (Hypotension, edema)

Kidneys- Renal failure (Impaired urine output, high creatinine levels)

Liver- Liver failure (Jaundice, Elevated ALT, AST)

Brain- Brain dysfunction- confusion or loss of consciousness

Blood- Internal or external bleeding (problems bleeding or clotting)

S/Sx:

N/V

Fatigue

Fever

Chills

Confusion

Tachypnea

Tachycardia

Dysrhythmias

Abdominal edema

Edema

Jaundice

Impaired perfusion

Blue/gray tint to mucous membranes

• First event is the triggering event

  • Sepsis, major trauma (MVA), or severe heart attack

• Second event occurs within the immune system

  • Causing widespread infection due to a dangerous overreaction

• Third event takes place if an infection develops, or the need for surgery in order to treat the first event causing the initial illness

  
  

hyperinflammation

hypercoagulation

hyperlactemia

acidosis

dysregulated immune response