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Shock/Hypotension
Clinical Presentation and
Pharmacological Treatment
of Shock/Hypotension
5/23/2017
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Introduction
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Review the current view on clinical
presentation and management of
shock with emphasis on
pharmacotherapy.
O. D. Polk, Jr., M.D.
Assistant Professor of Medicine
Pulmonary Critical Care
Medicine
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Topics of Discussion
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Clinical Presentation
Types of Circulatory Shock
Management of Shock
Inotropic Agents
 Vasodilators
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Shock
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Term “choc” – French for “push” or
impact was first published in 1743
by the physician LeDran
Belief – symptoms arose from fear
or some other form of altered
cerebral function
Crile in 1899 showed that
replacement of blood volume
decreased mortality experimentally
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SHOCK - DEFINITION
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A profound and widespread
reduction in the effective delivery
of oxygen and other nutrients to
tissues leads first to reversible and
then, if prolonged, to irreversible
cellular injury.
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SHOCK-NEW CONCEPTS
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Shock is probably the most common and
important problem in critical care medicine.
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Cardiogenic shock represents one of the most
important complications of IHD, the number one
cause of mortality in the US.
Hypovolemic and/or extracardiac obstructive shock
are major contributors to trauma-associated
morbidity and mortality.
Septic shock is the 13th most frequent cause of
death in the US.
Shock causes or contributes to multiple
organ dysfunction syndrome (MODS), organ
failure, and death.
Parillo JE 1999
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MORTALITY FROM SHOCK
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Septic Shock
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Cardiogenic Shock
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60 to 90%
Hypovolemic Shock
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35 to 40% within one month
Highly variable
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STAGES OF SHOCK
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Preshock
Shock
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End-organ dysfunction
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20 to 25 reduction of EBV
Fall in CI to <2.5
Activation of mediators
Urine output decline
Restlessness evolves into agitation,
obtundation, and coma
Acidosis further decreases CO and alters
cellular metabolic processes
Multiple organ system failure proceeds to
cause the demise of the patient
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Determinants of Shock
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Inadequate tissue perfusion
Sustained loss of effective circulatory
blood volume
Breakdown of cellular metabolism and
microcirculatory homeostasis
Hypoperfusion of peripheral tissue
that leads to a diminutive
transcapillary exchange function
Disproportion between VO2 and DO2
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Pathophysiology of
Shock
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Shock develops with inadequate
capillary perfusion by decreased
Cardiac Output following heart
attack (cardiogenic shock) or
blood/volume loss (hypovolemic
shock)
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Mediators of Shock
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Toxins
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Oligo- and polypeptides
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Arachidonic acid metabolites
Varia
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Complement Factors
Opiods
TNF, Interleukins
Fatty Acid Derivatives
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Endotoxins
Calcium
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Main Classes of Shock
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Hypovolemic Shock
Distributive Shock
Cardiogenic Shock
Obstructive Shock
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Hypovolemic Shock
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Hemorrhagic/Traumatic
Dehydrative
Burn
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Distributive Shock
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Septic
Anaphylactic/
Anaphylactoid
Neurogenic
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Cardiogenic Shock
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Myopathies
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Arrhythmias
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Atrial fibrillation/flutter
Ventricular fibrillation
Bradyarrhythmias/Heart Block
Mechanical abnormalities
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Infarction involving >40% of LV
Dilated cardiomyopathies
Myocardial depression of sepsis
Valvular defects
Ventricular aneurysm
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Obstructive Shock
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Pulmonary Embolism
Cardiac Tamponade
Pneumothorax
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Common Features of Shock
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Hypotension
Systolic BP <90 mmHg
 Drop systolic BP >40 mmHg
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Cool, clammy skin
Oliguria
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Objective measure of intravascular
volume depletion
Change in Mental Status
Metabolic acidosis
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Other Signs of Hypovolemia
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Tachycardia
Orthostatic hypotension
Poor skin turgor
Absent axillary sweat
Dry mucous membranes
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Management of Shock
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Shock begins when DO2 (delivery
of oxygen) to the cells is
inadequate to meet metabolic
demand
The major therapeutic goals in
shock therefore are sufficient
tissue perfusion and oxygenation
Early diagnosis remains a major
problem
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Shock
Initial Diagnostic Steps
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History and Physical
Laboratory
CBC
 Coags
 ABG’s
 Biochemical profile
 Lactate
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EKG
Chest x-ray
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Shock
Initial Management
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Venous access
Central venous catheter
Arterial catheter
EKG monitoring
Pulse oximetry
Hemodynamic support (MAP<60 mmHg)
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Fluid Challenge
Vasopressors for patients unresponsive
to fluids
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Complicated Shock
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Pulmonary Artery Catheterization
done to measure
Cardiac output
 Filling pressures
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Echocardiography done to look at
Pericardial fluid
 Cardiac function (non-invasively)
 Valve or shunt abnormalities
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Hemodynamic Characteristics in
Different Types of Shock
Type
Preload
CO
PVR
SVR
Hemmorrhagic
Anaphylactic
/
Cardiogenic
Septic
(Hyperdynamic)
Septic
(Hypodynamic)
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Inotropic Agents and
Vasodilators
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Vasoactive drugs are an important
pharmacologic defense in the
treatment of shock.
May be required to support BP in the
early stages of shock.
These agents may be needed to:
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Enhance CO through the use of inotropic
agents
Increase SVR through the use of
vasopressors
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Effects of Inotropic
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Agents and Vasodilators
Drug
Epinephrine
Receptor
CO
, b1, (b2)
Norepinephrine , b1
SVR
Dose Range
2-10 µg/min
0-
2-20 µg/min
Dopamine
b1, DR, ()
1 - 30
Dobutamine
b1, b2
2 - 20
Phenylphrine
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Vasopressin
Angiotensin III
Amrinone
PDI
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0
0-
20-200µg/min
5 - 20
2 -15
(mg/kg/min)
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Effects of Inotropic
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Agents and Vasodilators
Drug
CO
SVR
Dose Range
Nifedipine
0-
0.5 - 10
Nitroglycerin
0-
3-5
Nitroprusside
0-
0.5 - 5
Prostacyclin
10 - 40
(mg/kg/min)
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Dopamine
An endogenous precursor of norepinephrine with
multiple dose-related effects
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Low Dose (0.5 - 3 µg/kg/min)
Predominantly dopaminergic (DR)
effects
 Enhanced blood flow to renal and
splanchnic beds
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Moderate Dose (5 -10 µg/kg/min)
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High Dose (>10 µg/kg/min)
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Positive inotropic effects (b1)
-actions (vasoconstriction)
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Indications for Selected
Vasoactive Drugs
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DRUG
Common Uses
Phenylephrine
Septic Shock,
neurogenic shock, PAIH
Norepinephrine
Septic shock
Epinephrine
Anaphylaxis, ACLS,
septic shock
Dopamine
Renal Insufficeny, septic
shock, cardiogenic shock
Dobutamine
Cardiogenic shock (CS)
Isoproterenol
CS with bradycardia due
to heartblock, effects HR
Milrinone
Cardiogenic shock- in
those who don’t respond29
Complications:
Vasopressors and Inotropic Agents
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Hypoperfusion
Dysrhythmias
Myocardial ischemia
Local effects
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Hyperglycemia
Unique drug
interactions/contraindications
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Skin necrosis
Pheochromocytoma
Avoid dobutamine in the setting of IHSS
Patients receiving MAO Inhibitors
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Reference
Pharmacotherapy of Shock. In: The Pharmacologic
Approach to the Critically Ill Patient, 3rd ed. Williams
& Wilkins,1994, pp 1104 – 1121.
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