Shock
Dr. Yogin Parikh
Definition
Circulatory insufficiency that creates
an imbalance between tissue oxygen
supply and demand causing cell
hypoxia
Pathophysiology
Normally the tissue consumes about
25% of the oxygen carried on
hemoglobin for cellular respiration
Venous blood returning to the right
heart is approximately 75%
saturated. (central venous oxygen
saturation)
70 kg adult has about 5 liters of
blood (2 L plasma plus 3 L RBC)
Pathophysiology
Tissue perfusion is determined by
Mean Arterial pressure (MAP)
MAP = CO X SVR
CO = Cardiac Output
SVR = Systemic vascular resistance
CO = Heart rate X Stroke volume
Stroke volume is dependent on
preload, afterload and contractility of
the heart
Pathophysiology
Preload dependent on intravascular volume.
Central venous pressure(CVP) measures
Preload (CVP = 8-12 mm of Hg)
Because the venous return in the rt ven, is what is
called as preload. And the laod to push the blood
out is afterload (measured by MAP)
Afterload determines tissue perfusion. MAP
measures Afterload (MAP = 60-90 mm of Hg)
Contractility of heart. Central venous oxygen
saturation used as a surrogate measure (75%)
How do we measure cell
hypoxia?
Shock = Cell hypoxia
Cell hypoxia measured by
(a)Venous oxygen saturation
(b)Serum Lactate: Increase in lactate
due to
-Decreased O2 --> aerobic metabolism
switches over to anaerobic -->
byproduct = lactate
-Decreased hepatic clearance of
lactate
Response to Shock
Arterial vasoconstriction
Increase in heart rate and contractility
increases cardiac output
Constriction of venous capacitance increases
venous return (press the veins, the blood is
pushed back up the veins-likewise running.)
Release of vasoactive hormones epinephrine,
norepinephrine, dopamine, and cortisol
increases arterial and venous tone
Response to Shock
Release of ADH and activation of
renin angiotensin axis enhances
sodium and water absorption
Cell hypoxia leads to ATP depletion
leading to ion - pump dysfunction
(influx of sodium and efflux of
potassium) leading to cell membrane
instability and cell dysfunction
Types of Shock
Hypovolemic
Cardiogenic
Distributive
Obstructive
Types of Shock
Hypovolemic Shock
Non-hemorrhagic:
Vomiting, Diarrhea
Bowel obstruction, Pancreatitis
Burns
Hemorrhagic:
GI bleed
Trauma
Massive hemoptysis
Ruptured aortic aneurysm
Ruptured ectopic pregnancy, post-partum
bleeding
Types of Shock
Cardiogenic Shock
Decreased contractility: myocardial infarction,
myocarditis, cardiomyopathy (restrictive, dilated,
hypertorphic cardiomyopathy)
Mechanical dysfunction: papillary muscle rupture
post MI, severe aortic stenosis, rupture of
ventricular aneurysm
Arrhythmia: heart block, ventricular tachycardia,
SVT, atrial fibrillation
Cardiotoxicity: B blocker and calcium channel
blocker overdose
Types of Shock
Distributive Shock
Septic
Neurogenic C spine or upper thoracic cord injuries
Anaphylactic
Adrenal crisis
Sepsis:
(a)Two or more of the systemic inflammatory response
syndrome (SIRS) criteria must be met.
Temperature >38 or < 36 C
HR > 90
RR > 20
WBC > 12000 or < 4000
(b) Presumed existence of infection
(c) BP can be normal!
Types of Shock
Obstructive Shock
Massive Pulmonary embolism
Aortic dissection
Cardiac tamponade
Tension Pneumothorax
Constrictive pericarditis
Summary of types of
shock
Summary of types of
shock
Management of shock
Management of Shock
Early intervention
Establish the ABCDE tenets of shock
resuscitation
Optimize hemodynamic endpoints by
algorithmic approach
Achieving End Points of
Resuscitation
Urine output >.5cc/kg/hr
CVP 8-12
MAP 65-90
Venous oxygen sat >70%
Role of serum lactate in
shock
Increased in shock
Predictor of mortality
Used as a guide to resuscitation
Since there is shift or change from
areobic to anerobic metabolism where
the end product is lactate, which is
increased in shock.
Role of serum bicarbonate in
shock
Bicarbonate worsens intracellular
acidosis
Bicarbonate shifts oxygen
dissociation curve to the right,
thereby impairing tissue unloading of
oxygen
Only give bicarbonate if severe
acidosis and withheld once the pH is
7.25 or greater
