Index
Module 15 • Shock & Hemodynamics
Shock Syndromes I
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Shock Syndromes I
Gretchen L. Sacha ~3 min read Module 15 of 20
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Shock Syndromes I

C.Epidemiology and Social Determinants of Health
1

Sepsis is common, with an annual incidence in the United States above 890,000, rising by about 13%

per year, and an associated cost exceeding $24 billion.

2In a European epidemiologic study, 37% of all ICU patients had sepsis.
3

Septic shock is the most common shock type, accounting for 62% of all cases of shock syndromes

requiring vasopressors.

4

In-hospital mortality associated with severe sepsis and septic shock (using previous definitions) is

around 18%–25%, whereas mortality at 2 years is around 45%.

5

In-hospital mortality of patients with septic shock defined according to the new definition was 35%–

54% in large retrospective data sets.

6

Many disparities exist with sepsis incidence, complications, and mortality in at-risk, minority, and

underserved communities and populations.

American Indians and Alaskan Natives are 1.6 times more likely to die from sepsis than all other

races in the United States.

Asian and Pacific Islander patients are 16% more likely to die from sepsis than White patients.

Black patients are 1.7 times more likely to develop severe sepsis than White patients.

d.Hispanic patients are 10% more likely to develop severe sepsis than White patients.
D.Pathophysiology
1

Sepsis and septic shock involve complex interactions between an infecting pathogen and the host

inflammatory, immune, and coagulation response.

2Hypotension develops through the inappropriate activation of vasodilatory mechanisms (increased nitric

oxide synthesis) and the failure of vasoconstrictive pathways (activation of ATP-dependent potassium

channels in vascular smooth muscle cells and vasopressin deficiency), resulting in a vasodilatory

shock. In addition, blood flow is inappropriately dispersed at the organ level or in the microcirculation

(shunting), leading to distributive shock.

3

Vascular endothelial cell injury leads to capillary fluid leak and a resultant decrease in preload. Venous

dilation further exacerbates the decrease in cardiac preload.

4

Tissue Do2 may further be impaired by a decrease in CO, inadequate Cao2 (low hemoglobin concentration

or saturation), or impaired oxygen unloading from hemoglobin. These multifactorial hemodynamic

abnormalities lead to decreased effective tissue perfusion, in which Vo2 exceeds Do2 and cellular injury

results. This further compounds the proinflammatory and procoagulant state, precipitating multiple

organ dysfunction and possibly death.

E.Diagnosis
1

There is no specific diagnostic test for sepsis or septic shock, and the diagnosis is typically based on the

definitions noted earlier.

2Recognizing that pneumonia is the most common site of infection (in about 45% of cases), followed

by intra-abdominal infection (about 30%) and urinary tract infection (about 11%), microbial cultures

should be sent from all suspected infectious sites as soon as possible.

3

All microbial cultures are negative in more than 25% of cases, and only 30% of patients have positive

blood cultures. The most commonly isolated pathogens in ICU patients are gram-negative bacteria

(62%), gram-positive bacteria (47%), and fungi (19%).

4

Cultures should be obtained before antimicrobial therapy is initiated unless doing so would significantly

delay (greater than 45 minutes) therapy.

F.

Treatment of Sepsis and Septic Shock

1

The pharmacologic-related 2021 SSC recommendations can be found in Box 1

HD Video Explanation — Synchronized with PDF
Starts at: minute 31 Open on YouTube