10. Shock

Question 1

Shock

Answer 1

State of cellular and tissue hypoxia

Question 2

Classifications of shock

Answer 2

Distributive - septic, nonseptic

Cardiogenic - cardiomyopathies, arrythmogenic, mechanical

Hypovolemic - hemhorragic, non-hemhorragic

Obstructive - pulmonary vasculature, mechanical

Mixed/unknown

Question 3

Shock physiology

Answer 3

Hypoxia: HT and shock not enough perfusion to tissues

Cardiac output decrease
Systemic vascular resistance decrease

Question 4

Mechanisms of shock

Answer 4

Cellular hypoxia - progresses to systemic level - acidosis and endothelial dysfunction - further reduction in tissue per fusion

Reduced tissue perfusion and oxygen delivery
Increase oxygen consumption
Inadequate oxygen utilization

In turn causes:
Cellular membrane ion pump dysfunction
Intracellular edema
Inadequate regulation of internal pH

Clinical pearl: elevated serum lactate levels have been used as surrogates for hypoperfusion and tissue hypoxia

Question 5

Stages of shock

Answer 5

In shock there is a decrease in CO and resistance

1 initial nonprogressive phase (pre-shock) - compensatory responses ot reduced tissue perfusion, want to increase CO, resistance HT to offset hypotension

2. Progressive stage (shock) - compensatory mechanisms becomes overwhelmed and signs and symptoms of organ dysfunction appear
3. Irreversible stage (end-organ dysfunction) - irreversible organ damage, multiple organ failure and death

Question 6

Septic shock

Answer 6

Dysregulated host response to infection resulting in life threatening organ dysfunction

Question 7

Continuum of severity

Answer 7

Septic shock: response to infection becomes generalized and involves normal tissues remote from site of injury

Systemic inflammatory response syndrome (SIRS) - syndrome characterized by a robust inflammatory response, can be infectious or non infectious (atherosclerosis, embolism, thrombosis)

Question 8

Pathogenesis of septic shock

Answer 8

Inflammatory and counter inflammatory responses: complement activation (anaphytoxins C3a and C5a)

Endothelial activation and injury - widespread vascular leakage and tissue edema

Induction of a procoagulant state - produce complication in DIC, decrease thrombomodulin and protein C

Organ dysfunction - in kidneys, liver, lungs and heart - death