Download Update on shock managment

Update on shock
management
Dr. Manal Al Maskati
Oct, 2011 - Kuwait
Objectives
 Briefing
about pathophysiology of shock.
 Initial steps of pt’s stabilization.
 Work-up in A/E.
 Some important procedures ,which
considered beneficial for shock
management.
 How ?When? and What ? medications are
important to know to manage any type of
shock.
Pathophysiology

Shock  inadequate delivery of
substrates and oxygen to meet the
metabolic needs of tissues.

Cell  anaerobic metabolic pathway
 accumulation of lactic acid.

Hypoxic-ischemic injury  widespread
cellular death  multiple system organ
failure  death.
Pathophysiology




DO2 (mL O2/min) =
CaO2 (mL O2/L blood)
X CO (L/min)
DO2 amount of oxygen delivered
to body tissues/ min.
CaO2 oxygen-carrying capacity
depends on:
 Hemoglobin (Hb) content
 Arterial oxygen saturation
(SaO2).
CO cardiac output depends on:
 stroke volume (SV)
 heart rate (HR).

CO = HR (beats/min)
X SV (mL/beat)

SV stroke volume depends
on:
 Preload
 Afterload
 Contractility

BP = CO X SVR
Treatment




ABC
Non-invasive monitors
Abx in septic shock with empiric coverage
 Neonates : combination of ampicillin and
gentamicin.
 Older infants and children: third-generation
cephalosporin,with vancomycin if indicated.
Baseline work-up
Treatment

Volume expansion
Children with hypovolemic shock receive appropriate aggressive
fluid resuscitation within the 1st hr of resuscitation  optimal
chance of survival and recovery.

Place 2 large-bore IV catheters or IO access.

Administer 20 mL/kg isotonic crystalloid infusion  re-evaluate
 administer additional 20 mL/kg if needed.

If > 2-3 of 20-mL/kg volumes crystalloid given to patient at risk for
hemorrhage  packed RBCs.

In study of survival in children with septic shock  children
received an average 65 mL/kg of volume in 1st hr had statistically
increased chance of survival compared with other groups
received < 40 mL/kg in 1st hr.

Exception to repetitive volume resuscitation  cardiogenic
shock.
Work-Up




CBC count
Hb
or
oxygen-carrying capacity.
white cell count
Thrombocytopenia
septic shock.
bleeding disorder or DIC.
Work-Up


Acid-base status
Shock produces lactic acid
with
metabolic acidosis
anion gap.

Diarrhea leads to direct bicarbonate loss.

Measurement of serum lactate level
distinguish
bicarbonate loss from lactic acidosis due to shock.
Work-Up


Complete metabolic panel
Hypernatremia
contraction



intravascular volume
hypovolemic shock.
serum carbon dioxide
Hypovolemia
liver enzymes
to liver.
metabolic acidosis.
BUN and creatine levels.
hypoxic-ischemic damage
Work-Up

B-type natriuretic peptide

BNP : hormone produced by ventricular myocytes in
response to myocardial wall stress.

Plasma BNP levels (adult and pediatric studies)
in
sepsis and congestive heart failure with cardiogenic
shock.

Elevated levels of BNP
myocardial stress, and
improvement in cardiac function
of BNP levels.
normalization
Work-Up

Imaging Studies
Never delay resuscitation of patient in shock
CXR

Cardiomegaly in cardiogenic shock.

Small heart size in hypovolemic shock .

ARDS from pneumonia and sepsis.
Work-Up

Other Tests

Near-infrared spectroscopy (NIRS)


Values correlate with venous oxygen saturations
noninvasive measurements of increased or
decreased tissue oxygen saturation (adequate
or inadequate DO2 ).
Cardiac index

CO divided by body surface area (BSA)

Normal CI is 3.5-5.5 L/min/m2

Cardiac index
invasive or noninvasive
measurements (Doppler echocardiography, or
classic pulmonary artery catheter).
Procedures

Mixed Venous Oxygen Saturation (SvO2)

Blood gas from central venous catheter or Swan-Ganz
catheter.

In patient with normal SaO2 (90-100%)  SvO2 70-80%.

Tissues extract 28-33% of oxygen delivered to them.

If oxygen extraction difference > 33%  poor tissue
perfusion  state of shock.

If oxygen extraction difference < 25%  oxygenated
blood shunting  distributive shock.
Procedures

Central venous pressure and pulmonary capillary
wedge pressure

Low CVP or PCWP  inadequate intravascular
volume.

Normal CVP  1-3 cm H2 O.

Pressures > 10 cm H2 O  volume overload or poor
right-sided heart function

PCWP of 12-18 cm H2o  good perfusion.
Medications

Dextrose administration often necessary

If glucose level low

Shock with documented hypocalcemia, or
caused by arrhythmias (hyperkalemia,
hypermagnesemia, or calcium channel blocker
toxicity)
calcium therapy.

Recommended dose is 10-20 mg/kg (0.1-0.2
mL/kg of calcium chloride 10%) IV at infusion rate
100 mg/min.
0.5-1 g/kg IV Dextrose.
Medications

Sodium bicarbonate use in treatment of shock is
controversial.

No better effect on

Ability to defibrillate

DO2

Survival rates in shock and cardiac arrest
Medications

In patients with persistent shock or ongoing
bicarbonate loss (eg, severe diarrhea)
careful
replacement of bicarbonate.
HCO3- (mEq) = Base deficit X patient's weight (in kg)
X 0.3

Half of calculated bicarbonate deficit administered
initially.
OR

0.5-1 mEq/kg/dose IV infused over 1-2 minutes.
Medications

Vasopressors/inotropic agents

Increase myocardial contractility + variable effects on
peripheral vascular resistance

Dopamine
o
1st inotrope
fluid-refractory septic shock .
o
Low dose (2-5 mcg/kg/min IV) vasodilatory effect
on end-organ perfusion .
o
Intermediate dose (5-10 mcg/kg/min IV) improves
myocardial contractility + CO + enhancing
conduction.
o
Higher dose (10-20 mcg/kg/min IV ) increases
peripheral vasoconstriction + BP.
Medications

Dobutamine
o
Good for cardiogenic shock.
o
Increases cardiac contractility + peripheral
vasodilation (afterload and improve tissue
perfusion).
o
Less likely to precipitate ventricular
dysrhythmias than epinephrine.
o
Dose begins with 5 mcg/kg/min IV , gradually
increased to 20 mcg/kg/min IV.
Medications

Epinephrine
o
For fluid refractory dopamine resistant, nonvasodilatory (cold) shock.
o
Increases myocardial contractility + peripheral
vasoconstriction.
o
Risk of ventricular dysrhythmias + extremities
ischemia
o
Dose : 0.1 mcg/kg/min IV , titrated upward
according to effect and adverse effects.
o
Severe cases
higher.
2-3 mcg/kg/min IV or
Medications

Norepinephrine
o
For fluid-refractory, dopamine-resistant vasodilatory
(warm) shock.
o
Increases peripheral vasoconstriction
o
Best pressor agent increases BP in shock persists after
adequate fluid replacement.
o
Dose : 0.1 mcg/kg/min IV ,titrated upward according
to effect and adverse effects.
BP.
Medications

Phosphodiesterase Enzyme Inhibitor

Inamrinone + milrinone
o
Useful for shock with adequate intravascular volume,
but need increased cardiac contractility and better
peripheral perfusion ( compensated shock with poor
peripheral perfusion).
o
Improve cardiac inotropy + peripheral vasodilation.
o
Phosphodiesterase inhibitor used together with
catecholamines
increase myocardial
contractility + reducing systemic vascular resistance
and afterload.
Medications

Inamrinone + milrinone
o
Inamrinone : loading dose of 0.75 mg/kg IV
over 2-3 minutes followed by continuous IV
infusion of 5-10 mcg/kg/min.
o
Milrinone : loading dose of 25-50 mcg/kg over
10 minutes, followed by continuous IV infusion of
0.375-0.75 mcg/kg/min.
o
Adverse effects: arrhythmias +
thrombocytopenia
Medications

Prostaglandin E1
o
Neonates with shock (large liver, enlarged cardiac
silhouette, or heart murmur)
obstructive
shock(PDA closure) .
o
PDA allow sufficient systemic blood flow to bypass
obstructive lesion.
o
PGE1 maintains patency of PDA.
o
Dose 0.05-0.1 mcg/kg/min IV as continuous
infusion.
o
Adverse effects : fever, apnea, or hypotension
due to vasodilation.
Medications

Corticosteroid
o
Use of corticosteroids in septic shock
controversial
o
Adrenocortical failure or infarction (WaterhouseFriderichsen syndrome)
cardiovascular failure
+ hyporesponsiveness to catecholamines.
o
Initiation of stress-dose hydrocortisone (50-100
mg/m2/d IV), may be lifesaving.
o
A serum cortisol level drawn prior to first dose of
corticosteroids
serum cortisol level low
replacement doses.
Medications

Corticosteroid
o
Study of adult patients with septic shock
survived 48 hours ,dependent on inotropic
agents showed some benefit when treated with
supraphysiologic doses of corticosteroids.
o
Patients developed adrenal insufficiency
1-2 mg/kg hydrocortisone IV every 6 hours OR
50 mg/kg bolus followed by same amount
infused over 24 hours.
o
Therapy continued for patients
baseline cortisol level < 20 mcg/dL.
absolute
Take Home Message

Initial steps of stabilization make tremendous
difference in pts survival.

In non-cardiogenic shock
fluid fluid fluid.

Early Abx improved survival in septic shock.

Arrange for ICU bed.

Don’t forget the Team-Work management.
Thank you
Discussion