Hemodynamics & Shock Flashcards

1
Q

Define shock

A

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

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2
Q

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

A

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

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3
Q

What are some signs of hypoperfusion in shock?

A

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

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4
Q

What are signs of organ dysfunction in shock?

A

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

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5
Q

What is the equation for calculating MAP?

A

1/3 SBP + 2/3 DBP

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6
Q

What THREE stages are included in Stroke Volume?

A

Preload
Intrinsic contractility
After load

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7
Q

What is the equation for cardiac output (CO)?

A

HR x SV (stroke volume)

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8
Q

What two hemodynamic parameters multiply to make MAP?

A

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

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9
Q

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

A

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

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10
Q

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

A

aka Swan Ganz

Measures: preload, CO, Svo2, systemic vascular resistance

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

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11
Q

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

A

Fluid responsive = increased cardiac output

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12
Q

Review: what are the GOALS in patients with shock?

A

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

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13
Q

What are the four types of shock syndrome?

A

Hypovolemic
Distributive
Cardiogenic
Obstructive

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14
Q

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)?

A

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

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

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15
Q

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)?

A

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

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16
Q

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)?

A

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

17
Q

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)?

A

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

18
Q

What is hypovolemic shock? What are some causes?

A

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)

19
Q

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

A

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

20
Q

What is cardiogenic shock? What are some causes?

A

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

21
Q

What is distributive shock? What is a classic example?

A

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

22
Q

What is obstructive shock? What causes obstructive shock?

A

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

Causes: pulmonary embolism, pneumothorax, tamponade

23
Q

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

A

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

24
Q

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

A
  1. 65 mmHg
  2. vasopressors
25
Q

What is the first line vasopressor for shock?

A

Norepinephrine

26
Q

What is the MOA for norepinephrine?

A

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]

27
Q

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

A

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

28
Q

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

A

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

29
Q

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

A

Tahcycardia
Arrhythmogenesis

30
Q

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

A

Selective alpha-1 agonist
Causes reflex bradycardia

31
Q

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

A

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

32
Q

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

A

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

33
Q

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

A

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

34
Q

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

A

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

35
Q

Vassopressin is added to vasopressor therapy in what situation?

A

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

36
Q

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

A

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