Pharmacology of Shock
Shock: Definitions and Classification
Clinical syndrome characterized by acute disruption of circulatory function and tissue perfusion resulting in
inadequate provision of oxygenation/nutrients to meet the metabolic demands of tissues.
Patients can be in shock and still have
normal
blood pressure!
Abnormalities in circulatory function: blood volume, cardiac function, vascular tone
Microcirculatory dysfunction ex: Septic Shock
Abnormalities in cellular metabolic function
Classifications of Shock
:
(1) Hypovolemic
(2) Distributive
alterations of vascular tone leads to shunting of blood away from some organ beds
(3) Cardiogenic
primary problem is
pump failure
for any reason
(4) Obstructive
heart works normally but there is obstruction to ventricular outflow (injury, PE, etc)
(5) Dissociative
O
2
not released from hemoglobin
3 Stages of Shock
:
(1) Compensated
normal physiological mechanisms compensate for lack of O
2
(2) Uncompensated
above fail, acidosis beings
(3) Irreversible
no matter what you do patient will die
Management of Shock
:
Cardiovascular support is the cornerstone of therapy of shock
ALWAYS START TREATING SHOCK WITH FLUID, UNLESS THE PATIENT IS VOLUME OVERLOADED (PULMONARY EDEMA)
Blood Pressure
= Cardiac Output x SVR
Heart rate x
Stroke Volume
Preload >> Contractility >> Afterload
these are 3 interdependent factors, change in one will change the others
While a normal heart is sensitive to pre-load conditions, a failing heart is insensitive to the pre-load conditions
Shock Management
Fluid Resuscitation
= OPTIMIZE PRELOAD
Crystalloids
(Na as osmotically active solute) normal saline, lactated ringers, hypertonic saline
Colloids
(large molecules confined to plasma, therefore can use less volume) human serum albumin
Indications for stopping giving fluid
: attain desired effect, evidence of pulmonary edema, 60-80 ml/kg administered without improvement, CVP > 10 or PAOP > 15 mmHg without improvement (aka preload conditions optimized)
Pharmacotherapy
fluid refractory shock = CONTRACTILITY, AFTERLOAD
increased contractility positive inotropic agents
"Pure" inotropes
(
dont increase afterload
): Dobutamine, Digitalis, Calcium
Other inotropes
(increase afterload)
: Epinephrine, Norepinephrine, Dopamine
Other inotropes (decrease afterload)
: Isoproterenol, Amrinone (dose dependent thrombocytopenia), Milrinone (no side effects). Both amrinone and milrinone dont increase myocardial O
2
demand, this unlike catecholamines.
decrease afterload
Selection of appropriate drugs
: Determine physiological goals of therapy: increase contractility, decrease afterload, etc