Shock
MAP
CO x SVR
myocardial infarction
congestive heart failure
pulmonary embolism
cardiac tamponade
massive hemorrhage
severe dehydration
Distributive
Cardiogenic
Obstructive
Hypovolemic
sepsis
anaphylacic
Rx
oxygen delivery
tissue perfusion
venous saturation
lactate
end-organ function
SvO2 / CvO2
decreased urine output, increase Cr
decreased mentation
increased LFTs
decreased gut perfusion
inflammation
SVR
VASODILATION


MYOCARDIAL DEPRESSION
wall motion abnormalities
decreased ejection fraction
valvular disease
congestive heart failure
decreased outflow
decreased ejection fraction
decreased volume
decreased hemoglobin
CHF
cardiac output
Goal
cardiac output
cardiac output
cardiac output
causes not symptoms
SVR
infection
fluids
abx
source control
surgical debridement
+/- steroids
+/- APC
remove antigen
fluids
steroids
supportive care
improve oxygen delivery
anaphylaxis
CO
preload
afterload
contractility
fluids
IABP
remove obstruction
valve replacement
embolectomy
positive pressure ventilation
inotropes
crystalloid

colloid (hetastarch/albumin)

blood products
Hemodynamic Monitoring
USE AS A GUIDE
arterial line
central venous catheter
pulmonary artery catheter
pulse pressure

waveform analysis
respiratory variation
dichrotic notch
monitor central venous pressure

follow:
trends
response to therapy
monitor PCWP

measure CI/CO

follow:
trends
response to therapy
how much?
10-20cc/kg is a good start
monitor response to therapy (cvp, pcwp, HR)
cost
infection
transfusion reactions
TRALI
too much fluid?
congestive heart failure
pulmonay edema
fluid overload
when to transfuse
if active bleeding and hypotensive
signs of decreased oxygen delivery
Hb > 9 usually no need for transfusion
Hb 7-9 consider transfusion if:
NO TRANSFUSION TRIGGER
signs
low CVP, low PCWP
high HR
low CI/CO
<60 mmHg
Flow Matters ...
Not Pressure !
goal directed therapy
end organ function
cardiac output
CO is a measure of flow 
NOT pressure
mentation
urine output / Cr
enzyme function
lactate
mixed venous oxygenation
central venous oxygenation
base deficit
tissue perfusion
Mean Arterial Pressure
as an endpoint
pressure dependent organ systems
kidney
brain
heart
Vasopressors
norepinephrine
neosynephrine
dopamine
epinephrine
vasopressin
predominant alpha, some beta effects
drug of choice in septic shock
favorable gut perfusion
pure alpha effect
BAD for the gut
may have a role in temporizing

dose dependent effect
alpha, beta-1, beta-2, DA
NO role for renal dose DA
arrhythmogenic
use for bradycardic shock
all alpha and beta receptors
potent vasoconstriction - SPARES NONE
potent ino-/chronotrope
role in CPR and Anaphylactic Shock
V1 and V2 receptors
NOT TITRATABLE
role in septic shock - relative insufficiency
may be harmful in cardiogenic shock
part of ACLS algorhythm
focus on volume and CO first!
what fluid?
signs
low/high SVR
low/high PVR
dopamine
dobutamine
PDE inhibitors (milrinone)
dopexamine
levosimendan
NO BENEFIT
supranormal CO
catecholamine
dose dependent Beta effect
B1:   contractility &   chronotropy
B2:   vascular tone
use after fluid status optimized
inodilator (cAMP/cGMP)
PVR and SVR
good for RHF
can cause signifcant hypotension
heart rate
tachycardia
bradycardia
ACLS
cardioversion
anti-arrythmic
chronotropic agents
pacemaker
isoproterenol
dopamine
GOAL is to   afterload
vasodilators
snp
ntg/nitrates
ace-i
hydralazine
arterial tone
short T1/2
cyanide / thiocyanate toxicity
arterial and venous tone
titratable
rx for MI esp with CHF
arterial tone
long T1/2
iatrogenic lupus
arterial tone
oral administration
angiotensin II and bradykinin
management of the
critically ill patient
shiva birdi m.d.
anesthesiology resident lecture series
what you need to know
balance
supply
demand
product
carrier
consumer
transport
oxygen delivery
Hb x SpO2 x 1.34 x CO
oxygen consumption
CaO2 - CvO2   x   cardiac output
extraction
critical point
Ohm's Law
V = I x R
MAP = CO x SVR
CO = HR x SV