Cv System - Sepsis Syndrome And Septic Shock By Jackson

Front 1

What is sepsis?

Back 1

Systemic Inflammatory Response Syndrome (SIRS) due to infection. Mostly it's bacterial, but it can be caused by virus, fungi, parasites, etc.

Front 2

What is sepsis syndrome?

Back 2

sepsis plus evidence of altered organ perfusion with at least one of the following: hypoxemia, elevated lactate, oliguria, altered mentation.

Front 3

What is septic shock?

Back 3

Sepsis with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities: lactic acidosis, oliguria, altered mentation

Front 4

What are some likely settings of the development of sepsis.

Back 4

E.Coli- UTIs
Pseudomonas- burn victims, ICU
Staph aureus- nosocomial, IVs, ICU
Coagulase Neg. Staph- post-surgical, IV
Group B Strep- neonatal

Front 5

What are some signs and symptoms of SIRS?

Back 5

First of all, SIRS is a systemic inflammatory response to a variety of severe clinical insults. It is manifested by 2 or more of the following: changes in temperature, heart rate respiratory rate, or WBC count.

Front 6

Describe pseudomonas aeruginosa.

Back 6

Gram negative bacilli
Ubiquitous; opportunistic pathogen
Oxidase +, non-fermentative.

Virulence Factors:
Slime capsule, toxins, attachment organisms, green pigment

Front 7

Describe Septic Shock caused by pseudomonas aeruginosa.

Back 7

Immunocompromised patient, Neutropenic patient, Higher mortality rate, Special consideration for antimicrobials (very resistant).

*pseudomonas seen a lot in burn victims, hospitalized pts, cystic fibrosis, hot tub infections as well.

Front 8

What skin lesion is seen (albeit rarely) due to pseudomonas?

Back 8

Ecthyma gangrenosum lesion. Blackened in the center, raised rim around it. Necrosis due to infection of the blood vessels and the skin, causing erosion.

Front 9

List some Cardiovascular and Hemodynamic changes during septic shock.

Back 9

1. Initial vasodilation and capillary leakage result in decreased SVR; compensatory cardiac output
2. Marked hypotension initially reSeptic shock is not caused directly by the invading pathogen. Rather, it results from an overwhelming host mediator response that induces pathologic changes.
sponsive to volume replacement; later becomes refractory
3. Generalized CV insufficiency due to vascular and myocardial abnormalities, from maldistribution of blood, endothelial damage, and HYPOPERFUSION
4. Coagulation abnormalities with organ damage

Front 10

Describe the dynamic of the three major factors during sepsis.

Back 10

as the balance of homeostasis is upset, there is an increase of coagulation, increase inflammation, and decrease in fibrinolysis

Front 11

How does the host recognize the infection that's going on?

Back 11

Innate cells of the body (neutrophils, monocytes, macrophages, dendritic cells) have receptors that recognize some of the microbial products (LPS, gram +/-... treigger host inflammation response)

Front 12

What is the likely role of the Patern Recognition Receptors?

Back 12

They recognize the microbial products (such as LPS) and starts the inflammatory cascade to try and get rid of the microorganisms. Once the cells are activated, they will release inflammatory mediators (TNF, IL-1, HMGB-1) which will then cause the endothelial cells to be more active (express more adhesion molecules, inflamm. cells, tissue factor)

Front 13

What does tissue factor do?

Back 13

starts the coagulation cascade. this can be started by either intrinsic or extrinsic pathways.

Front 14

What does Protein C do (in terms of coagulation)?

Back 14

it's an anti-coagulant (stops coagulation). Inhibits the plasminogen activator inhibitor. This will lead to a decrease in fibrinolysis. So Protein C's normal function is an anti-coagulant and on fibrinolysis. In septic patients, there's a significant decrease in protein C, which lets the coagulation cascade go unchecked, there's increased coagulation, and intervascular thrombosis.

Front 15

TNF and IL-1 are

Back 15

proinflammatory mediators, acting on the vasculature to increase cell adhesion molecules. increase expression of acute phase proteins, act on the hypothalamus to induce the fever response.

Front 16

Can you name a pattern recognition receptor?

Back 16

TLR-4 (toll-like receptor 4). it's found on the surface of cells like neutrophils, macrophages and is part of the recognition process to recognize the bacterial infection and start the whole inflammatory cascade. TLR4 binds to LPS endotoxin

Front 17

Nitric oxide bradykinin (a kinin)

Back 17

vasodilator to decrease vascular tone, leading to hypotension. Common for patients with sepsis.

Front 18

What is Early Goal Directed Therapy?

Back 18

For shock/organ failure, you want to: Stabilize and reverse CV and metabolic problems, Aggressive Fluid replacement, Vaso/cardioactive drugs.

Antimicrobial therapy: keep in mind that you need several blood samples taken to try to detect the organisms. Need to guess which organisms are most likely causing the infection.

Invasive Procedures: Drain abscess, debride necrotic tissues, remove colonized prostheses or catheters.

Front 19

what are the most important considerations and patient management steps needed to increase the likelihood of a positive outcome?

Back 19

1. Prevention
2. Early detection and recognition
3. Aggressive volume replacement
4. Early goal-directed therapy
5. Appropriate anti-microbial therapy
6. Eliminate infection source

Front 20

Nursing Home bacterial agents

Back 20

Listeria, s. pneumoniae

Front 21

ICU bacterial agents

Back 21

pseudomonas, staph aureus,

Front 22

Deep tissue wound bacterial agents

Back 22

coag - staph, pseudomonas (burn victims), bacteroides, clostridium spp. (anaerobes)

Front 23

postpartum bacterial agents

Back 23

group B strep

Front 24

UTI bacterial agents

Back 24

E Coli,
Enterococcus,
other gram negatives