Shock Flashcards

(34 cards)

1
Q

Definition of shock?

A

Acute generalized failure of the circulatory system resulting from blood volume that is too low to fill the vascular system or insufficient cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

General characterization of shock?

A

Hypotension + Hypoperfusion –> Impaired perfusion+Hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

BP =

A

CO X Peripheral Resisitance (PR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Three causes of shock?

A

Decreased Cardiac Fxn
Decreased Blood Volume
Decreased Peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of decreased peripheral resistance

A

Systemic inflammation (Septic Shock)
Systemic mast cell activation (Anaphylaxis)
Systemic loss of vascular tone (Neurogenic shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

End result of shock

A

Cellular Hypoxia
Failure to transport CO2, Toxic substances away from cells
Cell Death/Tissue Dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Five types of shock

A
Cardiogenic
Hypovolemic/Hemorrhagic
Spetic
Anaphylactic
Neurogenic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of cardiogenic shock

A

Myocardial infarction
Ventricular arrythmias
Cardiac tamponade
Saddle Embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of hypovolemic shock?

A

Hemorrhage, Burns, Dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is septic shock?

A

Systemic inflammatory reaction from bacteremia with an organism expressing LPS or LOS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Systemic Inflammatory Response Syndrome (SIRS)?

A

LPS activation of macrophages, endothelial cells. Overproduction of inflammatory cytokines and mediators. Decreased PR, BV loss throughout the peripheral.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most common cause of mortality in ICU

A

Septic Shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Central feature of Septic Shock

A

LPS activation of inflammation

Activated endothelial cells, monocytes, macrophages, and compliment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do activated endothelial cells in septic shock do? (Molecular)

A

Decrease production of tissue factor pathway inhibitor (TFPI) and thrombomodulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does LPS activate Monocytes/Macrophages?

A

LPS/LPS BP complex binds CD14 on cell surface.
Signalling mediated thru TLR4, NFkB transcription
Cytokine storm
Triggers NO release and systemic inflammatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effects of Endothelial cell activation?

A

Increased vascular permeability, adhesion molecule expression. Inhibition of anti-coagulation properties. Switch to pro-coagulation phenotype.

17
Q

Describe initial stages of sepsis.

A

Widespread systemic inflammatory response
systemic vasodilation, diminished contractility.
Widespread adhesion + capillary damage.
Coagulation and DIC

18
Q

Describe the later stages of sepsis.

A

Burned out inflammatory and immune responses.

Immune hypo-reactiveness and immune paralysis

19
Q

What happens in the non-progressive stage of shock?

A

Compensatory mechanisms maintain cardiac output and blood pressure, perfusion of vital organs.

20
Q

Examples of compensatory mechanisms that play a role in the non-progressive stage of shock

A
Baroreflexes
Sympathetic NS, Catecholamine release
Renin-Angiotensin Axis
ADH
Tachy, Peripheral Vasoconstriction, Pallor
H2O Conservation
21
Q

What happens in the progressive phase

A

Anerobic Glycolysis –> Metabolic Acidosis –> low pH retards vasomotor response –> arterial dilation –> blood pooling in microvasculature –> decreased CO

22
Q

What happens in the irreversible phase of sepsis?

A

Survival not possible
Lysosomal Enzyme release
NO synthesis causes low myocardial contractility
Ischemic bowel and release of gut bacteria into bloodstream

23
Q

Most commonly seen symptoms of hypovolemic and cardiogenic shock

A

Hypotension
Weak, Rapid Pulse
Tachypnea
Cool, Clammy, Cyanotic Skin

24
Q

Most commonly seen symptoms of septic shock

A

Warm, Flush skin from peripheral vasodilation

25
Most commonly seen symptoms of anaphylaxis
Bronchoconstriction and Edema | Urticaria
26
Which two kinds of shock are most reversible?
Hypovolemic and Anaphylactic
27
Which is least reversible?
Cardiogenic
28
What is DIC?
Sudden or insidious development of numerous fibrin thrombi within the microvasculature. Consumption of clotting components later leads to widespread hemorrhaging.
29
Mechanism of DIC
Rapid consumption of platelets, prothrombinen, f, actors V, VIII, X, platelets and fibrin. Fibrin --> Anoxia/Hypoxia --> Coagulation Necrosis No platelets --> Hemorrhage
30
Synonym for DIC
Consumption Coagulopathy
31
Pathologic findings of DIC
Widespread Fibrin Thrombi Diffuse Circulatory Insufficiency Brain, Lungs, heart, Kidneys Inc. D Dimer and Hemorrhage
32
Difference between Septic Shock vs. DIC
- Degree of Activation of Endothelial Cells - Degree of activation of coagulation cascade - Severe septic shock --> DIC
33
Clinical Settings to look for Shock in.
Sepsis, Trauma, Malignancy, Obstetric calamities, vascular abnormalities, hepatic failure, severe toxic or immunologic reactions
34
Severe toxic or immunologic reactions associated with shock
Snake Bites Transfusion reactions Recreational drugs