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Shock: acute circulatory failure which arises when the tissues receive insufficient supply of
oxygen
Symptoms:
o Hypotension - BP < 90 mmHg, MAP < 70 mmHg
o AMS
o Cool skin, decreased capillary refill, cold/clammy skin
o AKI/Reduced UOP
o Hyperlactatemia (> 2 mmol/L)
Lactate is produced by lactate dehydroxenase in anaerobic conditions
Cleared by the liver --> increased in liver failure
Diagnosis: SIRS, qSOFA/SOFA
Hemodynamic Monitoring:
o DO2 = oxygen delivery
o VO2 = oxygen consumption
o DO2/VO2 = oxygen extraction ratio
25% at rest in a normal patient
o SCVO2 = hemoglobin saturation of venous blood from a central vein
Normally >70%
<40% = critical low, anaerobic metabolism starts to occur
>80% = inadequate end-organ O2 extraction
o SVO2 = hemoglobin saturation of venous blood from the pulmoary artery
Normal SCVO2 is 2-3% lower than SVO2
In shock – SCVO2 exceeds SVO2 by 5-8%
o Arterial Line – just as accurate as BP cuff
o Central Venous Line – measures SCVO2, low SCVO in the setting of
o Pulmonary arterial catheter (AKA Swan-Ganz, R heart cath) – measures SCVO 2, allows
administration of high volume fluid
Can measure CO via calculation
Calculates SVR
Measures Preload wia PCWP – catheter sensor rests in the pulm artery capillary
and measures pressure at the end of diastole (when valves are open, so the
entire connection of lungs to left side of the heart is one giant circuit)
Indicative of Preload
Only situations it’s regularly used – R heart cath, Pulmonary HTN
o Passive Leg Raise – if patient’s CO improves during this, they will be fluid responders
o Collapsible IVC = patient will be fluid responsive
Fluid Resuscitation
o Crystalloids are noninferior to albumin – preferred first line
Resuscitation Endpoints:
o BP
Goal MAP >65 mmHg oe SBP > 90 mmHg (usually MAP preferred -> true marker
of end-organ perfusion)
o Markers of End-Organ Perfusion:
Resolution of AMS
UOP > 0.5 mL/kg/hr
o Fluid Response
Defined as 10-15% increase in CO after fluid administration
Better predicted by dynamic markers (SVV, SPV, PPV, IVC collapsibility) of fluid
response rather than static markers (CVP, PCWP)
Vasopressors
o Increase SVR
o Norepinephrine preferred to dopamine --> safer and more effective
Inotropes
o Increase CO
o Dobutamine – B1 agonist that increases SV and CO
o Milrinone – PDE-3 inhibitor (potentiates cyclic AMP, leading to increased contractility
and vasodilation)
Hypovolemic Shock
o Common in trauma, GI bleeding, surgical, etc
o Clinical features: hypotension, tachycardia, diaphoresis, AMS, decreased UOP
o Treatment:
LR and NS are recommended (increased mortality with colloids like albumin)
PRBCs if estimated blood loss is >30% of total blood volume
Goal Hgb >10 g/dL
Pressors only recommended after hypovolemia is corrected or if cardiac arrest is
imminent
Goals: SBP >90, UOP >30 mL/hr
o Burn resuscitation: burn injury triggers third spacing
Resuscitate to goal UOP 0.5 mL/kg/hr
LR is recommended
Colloid use is controversial
Obstructive Shock
o Occurs as a result of extracardiac obstruction to flow in the CV system
Sources: cardiac tamponade, tension pneumothorax, PE, pulmonary HTN, aortic
dissection
o Characterized by decreased CO
o Treatment
Fluids, Pressors
Treat the underlying cause
Massive PE – possible thrombolytics
Distributive/Vasodilatory Shock – most common type of shock!!
o Vasodilatory shock: Tissue hypoperfusion secondary to decreased SVR
Distributive shock: a subset of vasodilatory shock that describes maldistribution
of blood flow (shunting at the organ level)
o Most Common Causes: septic shock, anaphylactic shock, and neurogenic shock
Neurogenic: decrease in sympathetic outflow from CNS (commonly spinal cord
injuries)
o Treatment:
Fluids, Pressors
In spinal cord injury: MAP goal >85
In neurogenic shock: agents with vasopressor + inotropic effects
preferred (norepi, epi, dopamine)
Sepsis door to antibiotic time – 60 minutes
Fluids recommended 30 mL/kg within first 3 hrs
Cardiogenic Shock
o Wet vs dry, cold vs warm --> see AHA guidelines