Hemodynamics & Shock

Question 1

Define shock

Answer 1

A potentially fatal reaction from conditions including infection, injury, hemorrhage, dehydration or HF (a state of acute circulatory failure (heart or perfusion failure))

Cellular dysoxia (less circulation/oxygen delivery to tissues = anaerobic metabolism), causes END ORGAN DYSFUNCTION

Question 2

In states of SHOCK, what happens to the BP and MAP? Provide cutoff values.

Answer 2

Systolic BP < 90 mmHg OR↓by 40 mmHg from baseline
MAP < 65 mmHg

Question 3

What are some signs of hypoperfusion in shock?

Answer 3

Cold, clammy, mottled skin
Scvo2 <65% OR Svo2 <60%
Lactate >2 mmol/L

Question 4

What are signs of organ dysfunction in shock?

Answer 4

Encephalopathy, lethargy, confusion
Liver dysfunction
Urine output <0.5 mL/kg/hr

Question 5

What is the equation for calculating MAP?

Answer 5

1/3 SBP + 2/3 DBP

Question 6

What THREE stages are included in Stroke Volume?

Answer 6

Preload
Intrinsic contractility
After load

Question 7

What is the equation for cardiac output (CO)?

Answer 7

HR x SV (stroke volume)

Question 8

What two hemodynamic parameters multiply to make MAP?

Answer 8

CO (cardiac output) x SVR (systemic vascular resistance)

Question 9

What value can be obtained from a central venous catheter? What can be administered through a CVC?

Answer 9

Measure central venous O2 (Scvo2)
Administer:
- fluids
- vasopressors
- antimicrobials
- TPN

Question 10

What is another name for pulmonary artery catheters? What can be measured? Why is it not commonly used?

Answer 10

aka Swan Ganz

Measures: preload, CO, Svo2, systemic vascular resistance

Not used commonly d/t major complications and high level of invasiveness

Question 11

The Frank-Starling curve compares stroke volume to preload. If the patient is fluid-responsive, what does this affect?

Answer 11

Fluid responsive = increased cardiac output

Question 12

Review: what are the GOALS in patients with shock?

Answer 12

MAP: > 65 mmHg
HR: < 100 BPM
CVP = 8 – 12 mmHg (uncommon)
PCWP = 12 - 15 mmHg
Cardiac Index: > 2.2 L/min/m2

Hg: 7 - 9 gm/dl
Arterial saturation: > 88-92%
SVO2 or SCVO2: > 65 % or 70 %

Lactate clearance: < 2 mmol/L
Urine output: > 0.5 ml/kg/hour

Question 13

What are the four types of shock syndrome?

Answer 13

Hypovolemic
Distributive
Cardiogenic
Obstructive

Question 14

For HYPOVOLEMIC shock, what are the changes in pulmonary capillary wedge pressure (preload), cardiac output (pump fx), systemic vascular resistance (afterload) and Svo2 (tissue perfusion)?

Answer 14

PCWP = decreased
CO = decreased
SVR = increased
Svo2 = decreased

(Decreased volume/preload = low CO = compensatory increase in SVR)

Question 15

For CARDIOGENIC shock, what are the changes in pulmonary capillary wedge pressure (preload), cardiac output (pump fx), systemic vascular resistance (afterload) and Svo2 (tissue perfusion)?

Answer 15

PCWP = increased
CO = decreased
SVR = increased
Svo2 = decreased

Same volume but valve doesn’t work = increased preload pressure BUT decreased output (CO), compensatory increase in SVR

Question 16

For DISTRIBUTIVE shock, what are the changes in pulmonary capillary wedge pressure (preload), cardiac output (pump fx), systemic vascular resistance (afterload) and Svo2 (tissue perfusion)?

Answer 16

PCWP = decreased
CO = variable
SVR = decreased
Svo2 = variable

Characterized by vasodilation = less SVR (resistance)
Less blood return to heart = less preload
HR increases to maintain CO

Question 17

For OBSTRUCTIVE shock, what are the changes in pulmonary capillary wedge pressure (preload), cardiac output (pump fx), systemic vascular resistance (afterload) and Svo2 (tissue perfusion)?

Answer 17

PCWP = increased
CO = decreased
SVR = increased
Svo2 = decreased

Obstruction = decrease in LV stroke volume, therefore decreased CO and perfusion (Svo2). Obstruction will increase resistance/afterload

Question 18

What is hypovolemic shock? What are some causes?

Answer 18

Low and sudden loss of intravascular volume

Causes:
- hemorrhage
- GI losses
- severe dehydration
- third spacing (fluid moves to interstitium)
- Burns

(#1 cause of death in those <45 yo)

Question 19

How do you treat hemorrhage hypovolemic shock? How do you treat GI loss/burn/third spacing hypovolemic shock?

Answer 19

Hemorrhage = replace blood w/ packed RBC, anticoagulant reversal
GI/burn/third spacing = replace fluids (LR, NS)

Question 20

What is cardiogenic shock? What are some causes?

Answer 20

Failure of left ventricle to deliver blood d/t impaired stroke volume or heart rate (“pump failure”)

Causes:
Acute MI
Arrhythmias
ESHF
Valve failure/disease

Question 21

What is distributive shock? What is a classic example?

Answer 21

Shock caused by extreme vasodilation
SEPTIC SHOCK = classic example
Other causes: anaphylaxis, neurogenic, coma, adrenal/hepatic insufficiency

Question 22

What is obstructive shock? What causes obstructive shock?

Answer 22

Comes from significant decrease in LV stroke volume OR increase in LV obstruction

Causes: pulmonary embolism, pneumothorax, tamponade

Question 23

When giving fluid therapy for shock, what is the preferred agent/dose?

Answer 23

Crystalloid (NS, LR) 30 mL/kg over 15-30 mins
+ 10 mL/kg boluses prn

Question 24

After fluid administration during shock, if the MAP is ____(1)____ mmHg then ____(2)____ should be administered

Answer 24

1. 65 mmHg
2. vasopressors

Question 25

What is the first line vasopressor for shock?

Answer 25

Norepinephrine

Question 26

What is the MOA for norepinephrine?

Answer 26

Potent alpha-adrenergic AGONIST - increases MAP by peripheral vasoconstriction - has a little beta-1 agonist, no effect at low doses [dont memorize dosing, pumps are automatically programmed for admin]

Question 27

What is the MOA of vasopressor epinephrine? Is its activity dose-dependent? What makes it a secondary choice (after NE + vasopressin) for sepsis?

Answer 27

MOA = potent alpha+beta agonist, DOSE DEPENDENT! Secondary choice for sepsis because it increases *aerobic* lactate production AEs limit clinical utility, NE still 1st line

Question 28

Dopamine is a precursor to NE and epi. If so, why is it rarely used in practice? What population may it be most beneficial?

Answer 28

Dose-dependent effects but has ceiling effect, no actual morbidity benefits. MOST beneficial in hypotensive pts with depressed cardiac function

Question 29

What are two major AEs of dopamine, preventing it from being used in shock?

Answer 29

Tahcycardia Arrhythmogenesis

Question 30

Phenylephrine is a _______ agonist, but this causes what AE?

Answer 30

Selective alpha-1 agonist Causes reflex bradycardia

Question 31

In what TYPE of shock is phenylephrine not recommended? What is the one exception where it can be used?

Answer 31

Distributive shock/sepsis May be used if CO is high and BP is low

Question 32

What is the MOA of dobutamine? How is it utilized in shock?

Answer 32

MOA = inotropic action by beta-1 agonism Adjunctive to other pressors when CO or SvO2/ScvO2 goals have not been achieved

Question 33

Vasopressors with more ALPHA agonism (epi, NE, phenylephrine) cause an increase in ____, which are better agents for what types of shock?

Answer 33

alpha agonism = increased SVR (afterload) Beneficial in: distributive shock (excluding phenylephrine), hypovolemic shock

Question 34

Vasopressors with more BETA agonism (dobutamine, isoproterenol) cause an increase in ____, which are better agents for what types of shock?

Answer 34

Beta agonism = increased CO Beneficial in: cardiogenic shock, cardiomyopathy

Question 35

Vassopressin is added to vasopressor therapy in what situation?

Answer 35

If we want to reduce current vasopressor doses (adjunctive only!) Additional benefit includes reduces need for ventilation, but at high doses may cause cardiac ischemia/severe vasoconstriction

Question 36

What is angiotensin II (Giapeza) used for? What is a major obstacle of long-term use?

Answer 36

Indicated for septic shock For ACUTE use only due to *high thromboembolism risk!*