Hemodynamics & Shock Flashcards
Define shock
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
In states of SHOCK, what happens to the BP and MAP? Provide cutoff values.
Systolic BP < 90 mmHg OR↓by 40 mmHg from baseline
MAP < 65 mmHg
What are some signs of hypoperfusion in shock?
Cold, clammy, mottled skin
Scvo2 <65% OR Svo2 <60%
Lactate >2 mmol/L
What are signs of organ dysfunction in shock?
Encephalopathy, lethargy, confusion
Liver dysfunction
Urine output <0.5 mL/kg/hr
What is the equation for calculating MAP?
1/3 SBP + 2/3 DBP
What THREE stages are included in Stroke Volume?
Preload
Intrinsic contractility
After load
What is the equation for cardiac output (CO)?
HR x SV (stroke volume)
What two hemodynamic parameters multiply to make MAP?
CO (cardiac output) x SVR (systemic vascular resistance)
What value can be obtained from a central venous catheter? What can be administered through a CVC?
Measure central venous O2 (Scvo2)
Administer:
- fluids
- vasopressors
- antimicrobials
- TPN
What is another name for pulmonary artery catheters? What can be measured? Why is it not commonly used?
aka Swan Ganz
Measures: preload, CO, Svo2, systemic vascular resistance
Not used commonly d/t major complications and high level of invasiveness
The Frank-Starling curve compares stroke volume to preload. If the patient is fluid-responsive, what does this affect?
Fluid responsive = increased cardiac output
Review: what are the GOALS in patients with shock?
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
What are the four types of shock syndrome?
Hypovolemic
Distributive
Cardiogenic
Obstructive
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)?
PCWP = decreased
CO = decreased
SVR = increased
Svo2 = decreased
(Decreased volume/preload = low CO = compensatory increase in SVR)
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)?
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
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)?
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
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)?
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
What is hypovolemic shock? What are some causes?
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)
How do you treat hemorrhage hypovolemic shock? How do you treat GI loss/burn/third spacing hypovolemic shock?
Hemorrhage = replace blood w/ packed RBC, anticoagulant reversal
GI/burn/third spacing = replace fluids (LR, NS)
What is cardiogenic shock? What are some causes?
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
What is distributive shock? What is a classic example?
Shock caused by extreme vasodilation
SEPTIC SHOCK = classic example
Other causes: anaphylaxis, neurogenic, coma, adrenal/hepatic insufficiency
What is obstructive shock? What causes obstructive shock?
Comes from significant decrease in LV stroke volume OR increase in LV obstruction
Causes: pulmonary embolism, pneumothorax, tamponade
When giving fluid therapy for shock, what is the preferred agent/dose?
Crystalloid (NS, LR) 30 mL/kg over 15-30 mins
+ 10 mL/kg boluses prn
After fluid administration during shock, if the MAP is ____(1)____ mmHg then ____(2)____ should be administered
- 65 mmHg
- vasopressors
What is the first line vasopressor for shock?
Norepinephrine
What is the MOA for norepinephrine?
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]
What is the MOA of vasopressor epinephrine? Is its activity dose-dependent?
What makes it a secondary choice (after NE + vasopressin) for sepsis?
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
Dopamine is a precursor to NE and epi. If so, why is it rarely used in practice? What population may it be most beneficial?
Dose-dependent effects but has ceiling effect, no actual morbidity benefits.
MOST beneficial in hypotensive pts with depressed cardiac function
What are two major AEs of dopamine, preventing it from being used in shock?
Tahcycardia
Arrhythmogenesis
Phenylephrine is a _______ agonist, but this causes what AE?
Selective alpha-1 agonist
Causes reflex bradycardia
In what TYPE of shock is phenylephrine not recommended? What is the one exception where it can be used?
Distributive shock/sepsis
May be used if CO is high and BP is low
What is the MOA of dobutamine? How is it utilized in shock?
MOA = inotropic action by beta-1 agonism
Adjunctive to other pressors when CO or SvO2/ScvO2 goals have not been achieved
Vasopressors with more ALPHA agonism (epi, NE, phenylephrine) cause an increase in ____, which are better agents for what types of shock?
alpha agonism = increased SVR (afterload)
Beneficial in: distributive shock (excluding phenylephrine), hypovolemic shock
Vasopressors with more BETA agonism (dobutamine, isoproterenol) cause an increase in ____, which are better agents for what types of shock?
Beta agonism = increased CO
Beneficial in: cardiogenic shock, cardiomyopathy
Vassopressin is added to vasopressor therapy in what situation?
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
What is angiotensin II (Giapeza) used for? What is a major obstacle of long-term use?
Indicated for septic shock
For ACUTE use only due to high thromboembolism risk!
