Shock and Other Inadequate States

Question 1

What’s the simplest definition of shock?

Answer 1

Acute inadequate oxygen delivery to tissues.

it doesn’t have a 1:1 relationship with pressure etc.

Question 2

3 main determinants of tissue perfusion?

Main driving force?

Answer 2

CO
Overall SVR
Distribution of blood flow
Main driving force is blood pressure.

Question 3

How does a flow directed PA catheter work? What does it measure?

Answer 3

It’s threader through RA -> RV -> PA, then occludes of the branch of the PA (like a pulmonary embolism).
Once occluded, the pressure recorded is a pretty good approximation of LA pressure / a good measure of preload / LVEDP.
(this is also called PA wedge pressure - PAWP)
- the same catheter can be used to measure RA and RV and RA pressures.

Question 4

4 types of shock? (note that multiple types can be happening at the same time)

Answer 4

Hypovolemic (e.g. bleeding out)
Cardiogenic (e.g. acute MI)
Distributive (e.g. sepsis)
Obstructive (e.g. PE)

Question 5

Primary pathophysiologic derangement in hypovolemic shock? (How do you measure it?)

Answer 5

Decreased preload (measured with PAWP) -> decreased SV and CO.

Question 6

How does the body compensate for hypovolemic shock?

Answer 6

Symps -> increased HR, contractility, SVR.

Question 7

4 symptomatic stages of hypovolemia? At about what % volume loss does each occur?

Answer 7

15% loss: resting tachycardia.
20-25% loss: orthostatic hypotension
30-40% loss: hypotension and oliguria
>40% loss: obtundation and circulatory collapse
(probably more important to know symptoms vs. the exact percentages. Note that hypotension occurs later, so you shouldn’t wait until you see that to make your Dx)

Question 8

Primary pathophysiologic derangement in distributive shock?

Answer 8

SVR way too low due to vasodilation with maldistribution -> wastefully increased CO, but not pressure.

Question 9

2 phases of distributive shock?

Answer 9

Early: Decreased SVR, increased CO
Late: Heart fails, leading to decreased CO and increased SVR.

Question 10

Causes of distributive shock?

Answer 10

Sepsis is the prototype, but other inflammatory (e.g. anaphylaxis) / endocrine (e.g. Addisonian crisis) conditions can cause it.

Question 11

Mediators of sepsis?

Answer 11

Endotoxin (LPS from gram neg bacteria in bloodstream)

Interleukins and TNF.

Question 12

What’s the primary pathophysiologic derangement in cardiogenic shock?

Answer 12

Reduction in CO due to heart failure (myocytes can’t contract) -> elevated filling pressures and compensatory increase in SVR (to keep pressure up).

Question 13

Common causes of cardiogenic shock?

Answer 13

Massive MI with >40% loss of LV myocardium.
Acute valvular disease (e.g. ruptured papillary muscle or endocarditis)
Acute interventricular septal defect
etc.

Question 14

How does cardiogenic shock produce a vicious cycle of damage?

Answer 14

decreased CO -> decreased perfusion of heart -> further heart failure -> further decreased CO

Question 15

How does the PAWP look in cardiogenic shock?

Answer 15

It’s increased - there is increased preload / LA pressure because LV can’t contract to eject.

Question 16

Treatment for cardiogenic shock?

Answer 16

Relieve the ischemia.

as with all of these, you must treat the underlying cause to save the pt

Question 17

What’s the primary physiologic derangement in obstructive shock?
What will the RA and RV pressure look like?

Answer 17

“Obstruction” to right heart flow, reducing LV preload.
From perspective of the LV, this looks like hypovolemic shock (reduces preload, SV, CO with compensatory increase in SVR), but RA and RV pressure will be increased.

Question 18

What’s the problem in pericardial tamponade?

Answer 18

Impaired diastolic filling due to external force (blood / fluid in pericardium) opposing relaxation.

(not to be confused with cardiac tapenade)

Question 19

Why is acute tamponade worse than chronic tamponade?

Answer 19

In chronic, the heart has time to increase compliance / otherwise adapt.

Question 20

What is pulsus paradoxus?

Why does it happen?

Answer 20

Inspiratory drop in systolic BP (a small change is normal, a large change indicates tamponade)
Normally with inspiration, there is an increase in RV filling -> more right preload, but LV has a small drop in preload -> less SV and pressure.

In tamponade, increased RV filling with inspiration makes the RV push on the LV, decreasing LV filling and thus SV and systolic BP.
(note that PP isn’t specific for tamponade)

Question 21

What must be the pressure drop to meet the definition of pulsus paradoxus?

Answer 21

> 10 mmHg

Question 22

What do you see on echo of pericardial tamponade?

Answer 22

A shadow of pericardial effusion (“echo free space”).

Collapse of the RV during diastole.

Question 23

For hypovolemic shock, what are the RA/RV pressure, PAWP, CO, and SVR?
(low, normal, or increased/high)

Answer 23

RA/RV pressure: Low
PAWP pressure: Low
CO: Low
SVR: Increased (compensatory)

Question 24

For distributive shock, what are the RA/RV pressure, PAWP, CO, and SVR?
(low, normal, or increased/high)

Answer 24

RA/RV pressure: Normal
PAWP pressure: Normal
CO: Increased (compensatory, but ineffective)
SVR: Low

Question 25

For cardiogenic shock, what are the RA/RV pressure, PAWP, CO, and SVR?
(low, normal, or increased/high)

Answer 25

RA/RV pressure: High
PAWP pressure: High
CO: Low
SVR: High (compensatory)

Question 26

For obstructive shock, what are the RA/RV pressure, PAWP, CO, and SVR?
(low, normal, or increased/high)

Answer 26

RA/RV pressure: High
PAWP pressure: Low
CO: Low
SVR: High (compensatory)

Question 27

How does the SVR change in each form of shock?

Answer 27

SVR is always increased as a compensatory mechanism for low CO, unless SVR being too low is itself the source of the shock - as it is in distributive shock.

Question 28

What happens to metabolism when tissues are hypoxic?

Answer 28

They use glycolysis and make lactate…. but then die.

Ion pumps don’t work, mitochondria damaged, lysozymes burst, complement activates, etc. etc.

Question 29

What’s the cell death called / first thing to go when hypoxic in each skeletal muscle, GI tract, kidneys, lungs, liver, and heart? (not that important for now, probably)

Answer 29

Skeletal muscle: rhabdomyolysis
GI: mucosal damage
Kidneys: acute renal tubular necrosis
Lungs: alveolar damage, capillary injury, ARDS
Liver: impaired detoxification
Heart: myocardial depression

Question 30

3 changes in “pre-shock”?

What notably doesn’t change at first?

Answer 30

Sympathetic activation leads to...
Tachycardia
Increased contractility
Vasoconstriction.
Initially blood pressure and CO are maintained. (shock does not equal low blood pressure)

Question 31

What happens in “frank shock”?

Answer 31

Fall in cardiac index.
Organs begin to fail.
Tachypnea, tachycardia, low bp, oliguria.

Question 32

What’s the last stage of shock?

Answer 32

End-organ failure:
Renal failure
Altered mental state
Lactic acidosis
Multi-system organ failure (MSOF)
Death

Question 33

Treatment for hypovolemic shock?

Answer 33

Replace fluids (give blood, saline, crystalloid, whatever)
Treat underlying cause (stop bleeding, diarrhea, treat burns)

Question 34

Treatment for distributive shock?

Answer 34

Correct underlying cause.

Supportive: pressors, esp. dopamine (covered in adrenergic agonists lecture)

Question 35

What’s a post-heart mechanical support device for cardiogenic shock?

Answer 35

Intra-aortic balloon pump.

Increases BP and decreases afterload.

Question 36

I think all the technologies for mechanically assisting cardiogenic shock will come up again if relevant.

Answer 36

okay.