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Critical Care Exam 3 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

Chest Tubes - purpose of seal chamber**

A

with chest tube (20ml) water seal is what keep air from going back into the lungs (pleural cavity) – so most important part of chest tube

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2
Q

chest tube and pneumothorax

A
  • if pneumnothorax will see bubbling in the water seal chamber, will also see a little floatation
  • don’t clamp chest tube while pt has pneumothorax
  • if come in and don’t see bubbling then listen to lung sounds and should hear bilateral breath sounds
  • can clamp it if lung is expanded for small amount of time to see how they do but watch carefully
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3
Q

chest tube components:

A
  1. Water seal 2. Drainage 3. Suction
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4
Q

chest tube dressing

A

baseline gauze – foam top

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5
Q

Thoracotomy: *

A

surgical opening into thoracic cavity

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6
Q

Thoracostomy: *

A

incision made into chest wall to provide opening for purpose of drainage in order to put in a chest tube

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7
Q

Laparotomy: *

A

surgical incision into peritoneal cavity

• Exploratory – trauma, bleed, infection

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8
Q

Lacerated:*

A

torn, jagged

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9
Q

Ligated: *

A

to tie off a blood vessel or duct with suture or wire

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10
Q

Peritoneum: *

A

extensive serous membrane that lines abdominal wall of body; coverscontained viscera
• Semipermiable
• GI tract surrounded by blood vessels

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11
Q

Thoracentesis –

A

placing needle into the thoracic cavity

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12
Q

MAST

A

Medical antishock trousers, pressurized, trying to get output back to brain

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13
Q

Pulmonary artery (swan guanz) put in bc

A

it will help to see volume in left end diastolic volume in ventricle
• Filling pressure – care bc that amount of pressure to be ejected when ventricle contracts

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14
Q

when give vasopressor make sure

A

pt has volume first

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15
Q

Oxyhemoglobin shift in sepsis

A

to the right – loose bond

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16
Q

Warm, dry flushed skin in sepsis **

A

early sepsis vasodilation, bacteria in the blood produce toxins that cause vasodilation or lose of tone of vessels

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17
Q

Consider infection if:

A
  • Sputum specimen has 25 or greater WBCs
  • Urinalysis shows greater than 10-15 WBCs = infection
  • Positive wound or line culture
  • Positive blood cultures
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18
Q

Infection vs Bacteremia

A
  • Infection: invasion of body with organisms

* Bacteremia: bacteria in the blood

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19
Q

SIRS

A

body’s response to an insult that results in activation of the immune response
• Systemic inflammatory response syndrome

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20
Q

SIRS as 2 or more: **

A
  • Temp >100.4 or < 96.8 some pts won’t be able to have fever bc so immocompromised
  • HR > 90 beats/min
  • RR > 20 breaths/min
  • PaCO2 < 32 mmHg respiratory alkalosis
  • WBC > 12,000 or 10% bands
  • Hyperglycemia
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21
Q

Causes of SIRS: **

A 
Infection is certainly a trigger
BUT ALSO NON-infection causes:
•	Trauma 
•	Burns 
•	Myocardial infarction 
•	Pancreatitis
•	Note: it is possible for a patient to have SIRS without having sepsis *
22
Q

Sepsis**

A

infection + 2 ≥ SIRS criteria
• Sometimes the source of infection cannot be identified: called “sterile sepsis” – cannot identify pathogen
• Its hard to detect fungal/viral infections

23
Q

Severe Sepsis**

A
  • infection 2 + ≥ SIRS criteria + 1 ≥ organ dysfunction
    • Common organs: kidney or lungs, hepatic dysfunction
    • Mr. S is in septic shock
24
Q

Septic Shock **

A

severe sepsis + hypotension despite IVF and vasopressors; presence of lactic acidosis, oliguria, mental status changes

25
Q

MODS*

A

Multi Organ Dysfunction Syndrome (2 or more failing organs)

26
Q

Septic Shock info

A
  • Global hypotension: peripheral vascular failure/vasodilation, decreased SVR, increased HR (possible high CO, early)
  • Leads to hypoperfusion and low oxygenation of vital organs and tissues; changes in microcirculation: leaky capillary membranes, maldistribution of blood and fluids, cellular dysfunction
  • Blood going to pool in vessels so tissues not getting good O2 and nutrients leads to organ hypoperfusion, so blood sitting in tissue but not being delivered to tissues
  • By the time we see clinical s/s that the patient has severe sepsis, usually several body organs are already affected
27
Q

Intrinsic Factors (who is at risk)*

A

• Age: most vulnerable – elderly, newborns
#1 cause of sepsis in elderly is urosepsis (UTI leads to this)
• Coexisting disease: diabetes, COPD, cancer, HIV, immunocompromised
• Malnutrition

28
Q

Extrensic factors (who is at risk)*

A
  • Invasive devices: central lines, foley catheters, ETT’s
  • Drug therapy
  • Surgical wounds
  • Invasive diagnostic procedures
  • Immunosuppressive Rx
  • Infected “hidden” organs: kidneys, bowel, liver, gallbladder, pancreas
29
Q

Gram-negative bacteria:*

A

Escherichia coli, Klebsiella, Enterobacter, Serratia, Pseudomonas aeruginosa, Bacteriodides, Proteus
• Produce exdotoxins that stimulate production of inflammatory mediators (cytokines) interleukins
• These bacteria are known as pyrogenic because they stimulate fever, inflammatory process

30
Q

Gram-positive bacteria:*

A

staphylococcus aureus, Staphlyococcus epidermidits, Streptococcus pyrogenes, Listeria, pneumococcal pathogens
• See text: p. 991 – (“gm + are responsible for more than ½ of septic cases”)
• Produce exotonxins – more vicious than endotoxins
• Viruses
• Fungus

31
Q

THE BIG THREE PROBLEMS OF SEPSIS:*

A
  1. Exaggerated inflammatory response
  2. Endothelial dysfunction – leaky capillaries
  3. Coagulation dysfunction
32
Q

Bacteria entering body are seen as a foreign substances or

A

ANTIGENS. Body responds by making ANTIBODIES that link with antigen, forming antigen/antibody complex.

33
Q

Bacteria also release Endotoxins, triggering:

A

Leukocyte migration to site of infection
Neutrophils – 1st responders that release oxygen cadicals to destroy the antigen (bacteria)
Monocytes/macrophages-2nd responders that release inflammatory mediators:
• Interleukin – 1 (1L-1), Cytokines
• Tumor necrosis factor (TNF)
• Platelet activating factor (PAF)
• Tissue Necrosis Factor
• Myocardial depressant factor

34
Q

Septic Shock early signs*

A
  • Massive vasodilation
  • ↑ temp
  • ↑ RR
  • respiratory alkalosis
  • normal - ↓ BP (due to >CO and vasodailation)
  • bounding to pull pulses
  • widened pulse pressure
  • ↓ CVP
  • ↓ PAP
  • ↓ PWP
  • ↓ SVR (8)
  • clear or congested lung sound depending on dx
  • ↓ UO
  • warm flushed skin
  • ↓ or ↑ WBC
    • BC
  • ↑ lactate
35
Q

Septic Shock late signs*

A
  • ↑ HR
  • ↑ RR and hypoxemia
  • ↓ BP (MAP) (SBP < 90)
  • ↓ LOC obtunded
  • weak pulses
  • narrow pulse pressure
  • ↑ CVP
  • ↑ PAP
  • ↑ PWP
  • ↑ SVR (<600)
  • ↓ CO/CI
  • clear or congested lung sound depending on dx
  • needs mechanical ventilation
  • ↓ UO
  • cold, mottled skin
  • respiratory alkalosis/ metabolic acidosis
36
Q

The release of these inflammatory mediators contribute to septic shock.

A 
Interleukin (1L-1)
•	Fever
•	Vasodilation 
•	Hypotension
•	Edema
•	> WBC
Tumor necrosis factor (TNF)
Cytokines
37
Q

Result of Mediators of Inflammatory Response

A

• Massive Vasodilation: ↓ SVR, ↓ preload, ↓ afterload
Vessels lose ability to respond to SNS
• Sluggish Blood Flow: increased blood viscosity, microemboli develop
• Leaky capillary membrane: 3rd spacing, edema in lungs (acute lung injury), around heart, in skin
• Myocardial Depression

38
Q

Vascular endothelium regulates:

A
  • Blood vessel tone
  • Vascular permeability
  • Coagulation
  • WBC and platelet activity
  • Phagocytosis of bacteria
39
Q

Tissue Factor

A
  • With vessel damage, Tissue Factor that normally is contained in the vessel is now released
  • Tissue Factor activates abnormal clotting – massive clot production through activation of Hageman Factor (factor XII)
40
Q

clotting overproduction

A
  • Hageman factor stimulates “clotting cascade” resulting in Thrombin formation
  • Thrombin stimulates fribrin production
  • Fibrin: a sticky weblike material that traps platelets, RBC’s WBC’s, forming a Fibrin Clot
  • Clots become trapped in capillaries, blocking oxygen and blood flow leading to death of tissue
  • 1st see petechiae then eventually see loss of digits (black toes)
41
Q

COAGULOPATHY

A
  • Inflammatory mediators also activate the clotting cascade
  • All clotting factors are eventually used up
  • “Micro-clots” dispersed everywhere
  • Leads to ischemic organs/necrosis
  • Increased thrombin production attracts platelets, resulting in thrombocytiopenia
  • Activation of fibrinogen, Fibrin split products to break down clots
  • Inhibition of activated Protein C (a substance that blocks microvascular coagulation)
  • Now see bleeding all over the place
  • Now will see ↑ in D-dimers
42
Q

Signs related to microthrombi

A 
Neuro
•	Stroke
Pulmonary
•	RF
•	PE
Heart
•	MI, angina
•	Dysrhythmias
GI
•	Liver ischemia
•	Bowel infarct
GU
•	Renal failure
43
Q

From clotting to bleeding

A
  • Under normal circumstances, Fibrin Spilt Products are “cleared” by Reticuloenothelial System. In sepsis, the system is overwhelmed
  • Fibrin Split Products remain in circulation
  • Fibrin Split Products have an ANTICOAGULANT effect
  • INCREASED BLEEDING EVERYWHERE
  • DISSEMINATED INTRAVASCULAR COAGULATION (DIC) petechiae
44
Q

Clinical Symptoms related to hemorrhage

A
  • Bleeding from gums, venipunctures, surgical sites
  • Hemoptysis
  • Heamturia
  • Abdominal hemorrhage
  • Subarachoid hemorrhage
45
Q

expected lab results

A
  • ↑ Prothrombin Time
  • ↑ Partial Thromboplastin Time
  • ↑ Fibrin Degradation Products
  • ↑ D-dimers
46
Q

Treatment of DIC**

A

DISSEMINATED INTRAVASCULAR COAGULATION *
need to stop the clotting – having over clotting problems, use heprin
• elimination of underlying pathology
• Restoring hemostasis
• Maintaining organ function
• Heprin
• Replacement therapy (fluids, platelets, FFP)

47
Q

Compensation*
High cardiac output shock
• Early s/s:

A
  • Fever
  • Warm, flushed skin
  • Bounding pulses
  • Widened pulse pressure
  • Tachycardia, tachypnea
  • Altered LOC
48
Q

Decompensation *
Low cardiac output shock
• Late s/s:

A
  • Hypotension
  • Weak pulses
  • < cap refilling
  • skin mottling
  • < UO
  • edema/ + fluid balance
  • > BS (>120mg/dl is DM)
  • Altered LOC
49
Q

Role of nurse

A

key to prevention
• HOB at > 30 degrees elevation
• Oral care
• Aggressive mobility plan
• Early enteral feeding – so gut doesn’t sit and become susceptible to a paralytic illeus
• Reduction on ventilator circuit changes

50
Q

Primary goal

A 
Remove the cause
Maintain tissue/organ perfusion (blood flow)/ cellular oxygenation by: 
•	Optimizing volume status
•	Optimizing BP
•	Optimizing CO
51
Q

Treatment

A
  • IVF, Levophed
  • Blood cultures
  • Sputum culture
  • Intubated, high FIO2
  • CVL and arterial line
52
Q

Xigris: Drotrecogin Alfa (x)

A 
(Activated Protein C)
•	First approved cogin
•	Inhibits coagulation
•	Promotes fibrinolysis
•	Decreases inflammatory response
•	Now off market (2012)
•	Contraind: bleeding
•	Side effect: bleeding 
•	24 mg/kg/hr for 96  hrs
•	effects gone within 2 hrs after D/C 
•	cone bottle lasts about 15 hours
•	costs $12,000/bottle
•	Xigris has anti-coagulant, anti-inflammatory, and fibrinolytic properties
•	It reduces IL-1 and IL-6, TNF, and other proinflammatory cytokines
•	(sepsis depletes levels of protein C)
•	Xigiris inhibits factors Va and Viiia, inhibiting trombotic effect
•	Inhibits TNF production by monocytes, blocking leukocyte adhesion

Critical Care Exam 3 (4 decks)

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