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Management of the Critically Ill Patient

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by

Shiva Birdi

on 4 April 2014

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Transcript of Management of the Critically Ill Patient

Shock
MAP
CO x SVR
myocardial infarction
congestive heart failure
pulmonary embolism
cardiac tamponade
massive hemorrhage
severe dehydration
intravascular depletion
"third-spacing"
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
massive inflammation
SVR
HR
VASODILATION
wall motion abnormalities
decreased ejection fraction
valvular disease (AS/MS, TR/MR)
myocardial depression
congestive heart failure
decreased outflow
decreased ejection fraction
decreased volume
decreased hemoglobin
CHF
Goal
cardiac output
cardiac output
cardiac output
causes not symptoms
SVR
infection
fluids
antibiotics
source control
surgical debridement
+/- steroids
no role for APC
remove antigen
fluids
steroids, H2 antagonists
supportive care
improve oxygen delivery
anaphylaxis
CO
preload
afterload
contractility
fluids
remove obstruction
valve replacement
embolectomy
positive pressure ventilation
inotropes
crystalloid

colloid (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
how much?
20cc/kg is a good start
cost
infection
transfusion reactions
TRALI
too much fluid?
congestive heart failure
pulmonay edema
hypoxemia
fluid overload
when to transfuse
Hb > 9 usually not indicated
Hb 7-9 consider transfusion if:
if active bleeding and hypotensive
signs of decreased oxygen delivery
Hb <7 may benefit from transfusion
if decreased oxygen delivery
NO TRANSFUSION TRIGGER
signs
low CVP
high HR
collapse IVC >50%
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
Outflow obstruction
severe AS
pulmonary embolism

dopamine
dobutamine
PDE inhibitors (milrinone)
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/nitrates
ace-i
hydralazine
milrinone
management of the
critically ill patient
Shiva Birdi M.D.
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 = SV x HR
dry membranes
orthostasis
slow capillary refill
point of care ultrasound
RWMA
LV size and function
RV size and funcion
IVC collapse/dilation
pericardial fluid
cool, clammy
tachycardia
AMS
orthostasis
decrease cardiac work
improve cardiac output
Full transcript