SEPTIC SHOCK &

CARDIOGENIC
SHOCK
Fiddy Firmansyah
17-777-013
SEPTIC SHOCK
In the setting of suspected or documented
infection, septic shock is typically defined in
a clinical setting by low systolic (≤90 mm
Hg) or mean arterial blood pressure (≤65
mm Hg) accompanied by signs of
hypoperfusion (eg, oliguria, hyperlactemia,
poor peripheral perfusion, or altered mental
status).
TREATMENT OF
SEPTIC SHOCK
INITIAL RESUSCITATION
INFECTION ISSUES
Initial resuscitation
• Central venous pressure (CVP) 8-12 mm Hg
• Mean atrial pressure (MAP) ≥ 65 mm Hg
• Urine output ≥ 0.5 ml/kg/hr
• Central venous (superior vena cava) or mixed
venous oxygen saturation 70% or 65%,
respectively
• In patients with elevated lactate levels targeting
resuscitations to normazile lactate
SCREENING FOR SEPSIS AND
PERFOMACE IMPROVEMENT
Routine screening of potentially infected
seriously ill patients for severe sepsis to
allow earlier implementation of therapy
(grade 1C). Hospital–based performance
improvement efforts in severe sepsis (UG).
DIAGNOSIS
To optimize identification of causative organisms,
we recommend at least two blood cultures be
obtained before antimicrobial therapy is
administered as long as such cultures do not cause
significant delay (>45 minutes) in antimicrobial
administration, with at least one drawn
percutaneously and one drawn through each
vascular access device, unless the device was
recently (<48 hr.) inserted (Grade 1C).
ANTIMICROBIAL THERAPHY
• Administration of effective intravenous
antimicrobials within the first hour of
recognition of septic shock (grade 1B) and
severe sepsis without septic shock (grade
1C) as the goal of therapy.
SOURCE CONTROL
• No randomized-controlled data
• Don’t be satisfied with a diagnosis of
sepsis and no source.
• If a source exists and is potentially
removable, get the ball rolling.
INFECTION PREVENTION
• Selective oral decontamination and selective digestive
decontamination should be introduced and investigated
as a method to reduce the incidence of ventilator-
associated pneumonia; this infection control measure
can then be instituted in health care settings and regions
where this methodology is found to be effective (grade
2B).
• Oral chlorhexidine gluconate be used as a form of
oropharyngeal decontamination to reduce the risk of
ventilator-associated pneumonia in ICU patients with
severe sepsis (grade 2B).
FLUID THERAPY
• Crystalloids (1B)
• Albumin (2C)
• Avoid HES (1B)
VASOPRESSOR
• We recommend norepinephrine as the first
choice vasopressor (Grade 1 B).
• We suggest epinephrine (added to and
potentially substituted for norepinephrine) when
an additional agent is needed to maintain blood
pressure (Grade 2B).
• Vasopressin .03 units/min can be added to
norepinephrine with the intent of raising MAP to
target or decreasing or decreasing
norepinephrine dosage. (UG)
INOTROPIC THERAPY
• A trial of dobutamine infusion up to 20
micrograms/kg/min be administered or added to
vasopressor (if in use) in the presence of (a)
myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output,
or (b) ongoing signs of hypoperfusion, despite
achieving adequate intravascular volume and
adequate MAP (grade 1C).
• Not using a strategy to increase cardiac index to
predetermined supranormal levels (grade 1B).
CORTICOSTEROIDS
• We suggest against using intravenous
hydrocortisone to treat septic shock
patients if adequate fluid resuscitation and
vasopressor therapy are able to restore
hemodynamic stability. If this is not
achievable, we suggest intravenous
hydrocortisone at a dose of 200 mg per
day.
CARDIOGENIC SHOCK
CARDIOGENIC SHOCK
The clinical definition of cardiogenic shock is
decreased cardiac output and evidence of tissue
hypoxia in the presence of adequate
intravascular volume. Cardiogenic shock is the
leading cause of death in acute myocardial
infarction (MI), with mortality rates as high as
70-90% in the absence of aggressive, highly
experienced technical care.
TREATMENT OF
CARDIOGENIC SHOCK
THERAPY/TREATMENT
• ACC Guidelines

• Vasopressors and Inotropes

• Diuretics

• Cardiac Catheterization

• Intra-aortic balloon pumps (IABPs)

• Left Ventricular Assist Devices (LVADs)

THERAPY/TREATMENT: ACC
GUIDELINES
Class I
1. Intra-aortic balloon counterpulsation is recommended for STEMI
patients when cardiogenic shock is not quickly reversed with
pharmacological therapy. The IABP is a stabilizing measure for
angiography and prompt revascularization. (Level of Evidence: B)

2. Intra-arterial monitoring is recommended for the management of

STEMI patients with cardiogenic shock. (Level of Evidence: C)

3. Early revascularization, either PCI or CABG, is recommended for

patients less than 75 years old with ST elevation or LBBB who
develop shock within 36 hours of MI and who are suitable for
revascularization that can be performed within 18 hours of shock
unless further support is futile because of the patient’s wishes or
contraindications/unsuitability for further invasive care. (Level of
Evidence: A)
THERAPY/TREATMENT: ACC
GUIDELINES
4. Fibrinolytic therapy should be administered to STEMI patients
with cardiogenic shock who are unsuitable for further invasive
care and do not have contraindications to fibrinolysis. (Level of
Evidence: B)

5. Echocardiography should be used to evaluate mechanical

complications unless these are assessed by invasive measures.
(Level of Evidence: C)
VASOPRESSORS AND
INOTROPES
• Goal: optimize perfusion while minimizing toxicity

• Close monitoring of mixed venous saturation

• Invasive hemodynamic monitoring (arterial line, cardiac output

monitoring) to guide therapy

• Inotropes: shift Frank-starling curve to a higher plateau (increased

contractility)

• Low output syndrome without shock: start with an inotrope such as

dobutamine

• Low output syndrome with shock: start with dopamine or

norepinephrine
VASOPRESSORS AND
INOTROPES
VASOPRESSORS AND
INOTROPES
• Dobutamine: B1 and B2, inotropic but also causes peripheral
vasodilation
• Good for non-hypotensive cardiogenic shock
• Start with 5 ug/kg/min, don’t go higher than 20 ug/kg/min
• Dopamine: inotrope and vasopressor in hypotensive
cardiogenic shock
• Up to 3 ug/kg/min – vasodilation and increase blood flow to
tissue beds, but no good evidence for “renal-dose dopamine”
• Start at 5 ug/kg/min up to 15 ug/kg/min. Good inotropic and
chronotropic effect at doses between 3 and 10 ug/kg/min (B1)
• Mild peripheral vasoconstriction beyond 10 ug/kg/min (A1)
VASOPRESSORS AND
INOTROPES
• Norepinephrine: primarily vasoconstrictor, mild inotrope
• Increases SBP/DBP and pulse pressure
• Increases coronary flow
• Start 0.01 to 3 ug/kg/min
• Good for severe shock with profound hypotension
• Epinephrine: B1/2 effects at low doses, A1 effects at higher
doses
• Increases coronary blood flow (increases time in diastole)
• Prolonged exposure -> myocyte damage
VASOPRESSORS AND
INOTROPES
• Milrinone: phosphodiesterase inhibitor, decreases rate of
intracellcular cAMP degradation -> increases cytosolic calcium
• Increases cardiac contractility at expense of increase myocardial
oxygen consumption
• More vasodilation than dobutamine
• Can be combined with dobutamine to increases inotropy
• Start bolus 25 ug/kg (if pt is not hypotensive) over 10-20 min then
0.25-0.75 ug/kg/min
• May be proarrythmic, questionable in setting of acute MI
VASOPRESSORS AND
INOTROPES
• Vasopressin: causes vasoconstriction, glyconeogenesis,
platelet aggregation and ACTH release
• Neutral or depressant effect on cardiac output
• Dose-dependent increase in PVR with resultant increase in
reflexive vagal tone
• Increases vascular sensitivity to norepinephrine
• Good for norepinephrine-resistant shock
DIURETICS
• Mainstay of therapy to treat pulmonary edema and augment
urine output

• No good data regarding optimal diuretic protocol or whether

diuretics improve outcome in renal failure

• Lower doses of lasix are needed to maintain urine output

when continuous infusions are used
• Start at 5 mg/hr, can increase up to 20 mg/hr
CARDIAC CATHETERIZATION IN
CARDIOGENIC SHOCK
• ACC Guidelines: emergent coronary revascularization is the
standard of care for CS due to pump failure (acute MI and
shock)
• Most often demonstrates multi-vessel disease:
• Left main disease 23%
• 3-vessel disease 64%
• 2-vessel disease 22%
• 1-vessel disease 14%
• Compensatory hyperkinesis: favorable prognostic factor
INTRA-AORTIC BALLOON COUNTERPULSATION

Arterial Pressure

Standby Counterpulsation
Inflation
Deflation Inflation
Systole Diastole

SMH #619 2008

INTRA-AORTIC BALLOON COUNTERPULSATION

• Reduces afterload and augments diastolic perfusion

pressure

• Beneficial effects occur without increase in oxygen

demand

• No improvement in blood flow distal to critical coronary

stenosis

• No improvement in survival when used alone

• May be essential support mechanism to allow for

definitive therapy
REFENSI
• GUIDELINES AND APPLICATION TO SEPSIS MANAGEMENT. (MICHAEL
H. HOOPER, MD, MSc Assistant Professor of Medicine Eastern
Virginia medical School)
• The New Surviving Sepsis Bundles: From Time Zero to Tomorrow. (R.
Phillip Dellinger, MD, MCCM. Mitchell M. Levy, MD, FCCM)
• Professor of Medicine Cooper Medical School of Rowan University
(R. Phillip Dellinger, MD, MCCM, FCCP)
• JAMA. 2015 August 18; 314(7): 708–717.
doi:10.1001/jama.2015.7885.
• https://www.slideshare.net/ShashankAgrawal17/septic-shock-
management-1
• Cardiogenic Shock (Nitasha Sarswat, MD Cardiology Fellow)