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Flashcards in Shock Deck (57)
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1

What is shock?

Clinical syndrome characterized by deceased tissue perfusion leading to impaired cellular metabolism. Begins as an adaptive response to injury / insult then progresses to multi-system organ failure

2

What are the three major classifications of shock?

1) Hypovolemic (Loss of volume)
2) Cardiogenic (Decreased contractility)
3) Distributive (Vasodilatory) --> Neurogenic, anaphylactic, septic

3

What are the 4 stages of shock?

1) Initial
2) Compensatory
3) Progressive
4) Refractory

4

What happens in the initial stage?

Nonspecific cellular changes but no clinical manifestations

5

What happens in the compensatory stage?

Compensatory mechanisms shunt blood to vital organs.
1) Nervous system compensation
2) Hormonal compensation
3) Chemical compensation

6

What is nervous system compensation?

SNS compensation:

Heart: Baroreceptors in aortic arch and carotid sinus increase HR, FOC, SV to increase CO and BP

Lungs: Increase RR, bronchodilation

Blood vessels: Constrict in skin, GIT, kidneys. Dilate in coronary arteries, skeletal muscles

Pupils: Dilate
Sweat glands: Increase activity

7

What is hormonal compensation?

Kidneys --> Decrease blood flow stimulates RAAS, Angiotensin II causes peripheral vasoconstriction. Adrenal cortex stimulated to release aldosterone increasing Na and H2O reabsorption

Adrenal medulla --> Release epinephrine, norepinephrine

Adrenal cortex --> Release aldosterone and glucocorticoids

Liver --> Secrete ACTH, leads to production of glucocorticoids (increases BG from glycogenolysis)

8

What is chemical compensation?

Lungs --> Decreased blood flow causes deadspace units, triggers chemoreceptors to increase RR. Causes resp alkalosis and eventually combined acidosis

Neuro --> Hyperventilation decreases CO2 causes cerebral vessels to constrict, decrease O2 to brain

Capillary --> Decreased CO causes cells to extract more O2

9

What happens in the progressive stage?

Ongoing compensatory mechanisms work against the pt, vasoconstriction causes adverse effects

1) Cellular function
2) Capillary dynamics
3) Systemic circulation
4) Specific organ systems

10

How is cellular function affected in the progressive stage?

Arteriolar vasoconstriction --> Decreased BF, decreased O2 and decreased ATP production. Cells switch to anaerobic metabolism, lactic acid produced which decreases FOC.

--> Pt goes into metabolic acidosis.
--> Impaired cellular function releases toxic substances accumulating in tissues and altering local environment

11

How are capillary dynamics affected in the progressive stage?

Acidic tissue environments from impaired cellular function causes pre-capillary sphincters to relax but post-capillary sphincters constrict. Histamine release further increases capillary permeability.

--> Increased hydrostatic pressure, histamine, pt becomes edematous as fluid leads out of intra-vascular space, decrease CO, decrease CA perfusion, ischemia
--> Blood becomes more viscous, increasing afterload, capillary sludging causes coagulopathy

12

What happens when blood becomes more viscous?

As fluid is lost, increased viscosity leads to:

Increased afterload
Capillary sludging (aggregation of RBCs, platelets, large proteins) causing coagulopathy, DIC

13

How is the systemic circulation affected by the progressive stage?

Decreased perfusion to periphery causes distal ischemia of tissues. Pulses weaker, then absent, local ischemia progresses to necrosis and becomes infection risk

14

How are specific body organs affected by the progressive stage?

Damage due to acidosis and prolonged vasoconstriction:

Heart --> Increased O2 consumption with decreased perfusion, arrythmias

Brain --> Initially vasoconstriction due to SNS response, then SNS response is LOST leading to decreased HR and vasodilation

Kidneys --> Nephron hypoxia, acute kidney injury

GI --> Ischemia to interstitial lumen cells leads to hemorrhage and bacterial translocation

Liver --> Decrease in phagocytosis (Kuppfer cells) thus blood from GI tract cant get filtered. Impaired metabolism, detoxification, liver ischemia

Pancreas --> Release proteolytic enzymes and MYOCARDIAL DEPRESSANT FACTOR (increases splanchnic vasoconstriction, interferes with role of calcium?)

Lungs --> Pulmonary vasoconstriction increases CO2, acidosis leads to interstitial and alveolar pulm. edema, decreased surfactant production causes atelectasis and decreased compliance

15

What are the cycles of the refractory stage?

1) Cycle of cardiac failure
2) Cycle of acidosis
3) Cycle of cerebral ischemia
4) Cycle of blood clotting

16

What is the cycle of cardiac failure?

Decreased CO --> Decreased CA perfusion --> Ischemia --> Decreased FOC (worsened by acidosis and MDF) --> Arrythmias

17

What is the cycle of acidosis?

Decreased renal function --> Decreased resp function (increase CO2), decreased cellular function (Increase lactic acid) --> Mixed acidosis --> Decrease CO + Pre-capillary sphincters relax decrease circulating fluid

18

What is the cycle of blood clotting?

Decreased blood volume --> Clot formation --> Decreased blood flow + Sluggish capillary flow, DIC --> Cellular hypoxia --> Acidosis

19

What is the cycle of cerebral ischemia?

Decreased CO --> Cerebral ischemia --> Initially causes vasoconstriction due to SNS response, then SNS response is LOST leading to decreased HR and vasodilation --> BRAIN DEATH --> Cardiac arrest, resp arrest

20

How much volume needs to be lost for hypovolemic shock?

15-30%, 750 - 1500mls

21

What is the etiology of hypovolemic shock?

1) Internal losses (Third spacing, internal hemorrhage)
2) External losses (Whole blood loss, coagulation disorders, plasma, fluid loss)

22

What is pathophys of hypovolemic shock?

Decrease intravascular volume
Decrease venous return
Decrease filling pressures
Decrease SV
Decreased CO
Decreased tissue perfusion

23

What is pulsus parodoxus associated with?

Hypovolemia (decreased preload and left side, decreased BP on inspiration)

24

Treatment of hypovolemic shock?

Fluid replacement --> Crystalloid / colloid / blood, should be warmed if large amount.

Inotropes / vasopressors

25

What are crystalloids?

NS, RL
Use isotonic solutions first, increase extracellular volume without altering electrolyte concentration of plasma. RL most compatible.

26

What are colloids?

Plasma proteins (FFP clotting factors, abumin). FFP MUST BE GIVEN COLD

27

What are blood products?

RBCs (improve O2 carrying capacity of blood), Cryoprecipitate (contains fibrinogens and other clotting factors)

28

What is the etiology of cardiogenic shock?

1) Coronary cardiogenic shock --> After acute MI decrease FOC
2) CA are fine but myocardium is sick decreasing FOC. Can be caused by viral infections, myocarditis, cardiomyopathies

29

What is 3 main pathophys of cardiogenic shock?

Systolic dysfunction, impaired LV contracility
Decrease tissue perfusion --> RAAS INCREASES AFTERLOAD
***Further decrease CO

Inadequate systolic emptying of LV
***Pulm. edema intra alveolar edema

Diastolic dysfunction, impaired LV compliance
Decreased preload, decreased CO

30

How does systolic dysfunction result in cardiogenic shock?

Impaired LV contracility
Decrease SV, CO, BP
Decrease tissue perfusion --> RAAS INCREASES AFTERLOAD
Decrease CA perfusion
Ischemia
Decrease FOC
***Further decrease CO


Inadequate systolic emptying of LV
Increase LV filling pressures, increase LAP
Increase pulm. venous pressure
Increase pulm. capillary pressure
***Pulm. edema intra alveolar edema