1
Q
Shock
A
- a state of reduced end-organ perfusion/oxygenation
2
Q
Shock occurs at what vascular level?
A
- the capillary level
3
Q
What homeostatic mechanisms kick in to try and compensate in shock?
A
- heart contractions increase in both force and frequency
- blood flow to non-vital organs gets reduced
- vasoconstriction to maintain perfusion of vital organs
4
Q
What is the mortality rate from shock?
A
- 35 - 70%
5
Q
4 Major Types of Shock
A
- hypovalemic, cardiogenic, obstructive, and distributive
6
Q
In shock, why do patients commonly have acidic blood?
A
- because not enough oxygen is being supplied to the tissues for normal respiration, so glycolysis (anaerobic respiration) kicks in
- lactic acid builds up as a result = lactic acidosis
7
Q
Mechanism behind Hypovalemic Shock
A
- large loss of blood/fluid results in a decreased cardiac preload, leading to decreased and insufficient cardiac output
- (trauma, ectopic pregnancy, severe dehydration)
8
Q
Mechanism behind Cardiogenic Shock
A
- dysfunction of the heart pump leads to decreased cardiac output
- (MI, heart failure, arrhythmia, etc.)
9
Q
Mechanism behind Obstructive Shock
A
- obstruction to cardiac flow or filling results in decreased cardiac output
- (PE, pulmonary HTN, cardiac tamponade, pneumothorax)
10
Q
Mechanism behind Distributive Shock
A
- systemic vasodilation, leads to massive drop in TPR, resulting in decreased preload
- (septic shock)
11
Q
Distributive Shock is HIGH/LOW output failure, while the other three types are HIGH/LOW output failure. (Include whether TPR, CO, and venous return are increased or decreased.)
A
- distributive: high output failure (TPR decreases, CO increases, venous return increases)
- other three: low output failure (TPR increases, CO decreases, venous return decreases)
12
Q
What are the three classic symptoms of shock?
A
- pallor, sweating, rapid & weak pulse
Cardiovascular
flashcards
Decks in class (11)
# Cards
