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Shock
Mike Clark, M.D.
Definition of Shock
“The collapse and progressive failure of the
cardiovascular system leading to an inadequate
perfusion of the tissues.”
• However -shock does not always require an overall
drop in systemic blood pressure one can suffer from
shock of an individual organ – like if a pulmonary
embolus blocked blood supply to the lung (shock lung)
or an embolus blocked blood supply to the stomach
(shock stomach)
• Shock can be caused by some outside (extrinsic)
traumatic insult to the body (like getting stabbed) or
some (intrinsic) problem with the organs/systems that
control blood pressure (like heart failure)
Shock is caused by some traumatic insult to the body
or some problem with the organs/systems that control
blood pressure
MAP = CO x SVR
• CO = HR x SV
• SV = EDV – ESV
• (EDV concerned with blood volume and ESV
concerned more with inotropic effect)
• SVR = ∑R₁ + R₂ + 1/R₃ + 1/R₄ …..
• R = 8ŋL/∏r⁴
• In order to live – the body compensates by
increasing the actions of the organs not
affected (homeostasis – negative feedback)
Control of Blood Pressure
• Local Immediate Control – myogenic tone,
paracrine/autocrine, metabolites
• Widespread Long term Control – neurologic
and endocrine
• Heart – rate and inotropic
• Blood Volume
• Blood Vessel vasoconstriction and vasodilation
Stages of Shock
Reversible (cells can regenerate)
Stage I Compensated (body itself compensates) negative
feedback compensation
Stage II Uncompensated (need medical care to survive)
Positive feedback spiralling to destruction
Stage III Nonreversible– even if adequate perfusion to
tissue is re-established – still some nonreversible cell
damage (does not necessarily mean death)
Symptoms of Shock
• Lethargy
• Weakness
• Dizziness
Soft Signs of Shock
• Skin changes (cool, pale or damp)
• Altered Sensorium (depressed or
apprehensive)
• Thirst
• Vein changes
• Hyperventilation
• Obvious or occult blood loss
• Dilated pupils
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Definitive Measurable Signs
Blood pressure changes ↑ or ↓
Pulse rate ↑ or ↓
Hemoglobin / hematocrit ↓ or NL
Urine output ↓
Electrocardiogram
Arterial blood gas
**Pulmonary artery wedge
Pressure
**Cardiac output
**Cardiac index
** Central venous pressure
Types of Shock
• Hypovolemic – loss of fluid volume
• Cardiogenic – inadequate heart activity
• Vasogenic – extensive inappropriate
vasodilation
Septic Shock (Gram negative shock)
Neurogenic Shock (Vasomotor center
dysfunction)
Anaphylactic Shock
Psychogenic Shock
• Obstructive
Hypovolemic shock
• Some causes are
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Hemorrhage
Burns
Diarrhea
Vomiting
Peritonitis
Hypovolemic Shock
Hypovolemic shock refers to a medical
or surgical condition in which rapid fluid
loss results in multiple organ failure due
to inadequate perfusion.
Some causes are:
• Trauma
• Hemorrhage
• Vomiting / diarrhea
• Burns
Hypovolemic Shock
• If the hypovolemic shock is due to acute
hemorrhage then the human body responds by
activating 4 major physiologic systems if caused by
another reason then 3 major systems:
• the hematologic system (activated only in
hemorrhagic shock – the clotting system used)
• the cardiovascular system
• the renal system
• the neuroendocrine system
Hypovolemic Shock:
• Cardiovascular System Compensation
• Increases the heart rate, increasing myocardial
contractility, and constricting peripheral blood
vessels.
• This response occurs secondary to an increase in
release of norepinephrine and a decrease in baseline
vagal tone (regulated by the baroreceptors in the
carotid arch, aortic arch, left atrium, and pulmonary
vessels).
• The cardiovascular system also responds by
redistributing blood to the brain, heart, and
kidneys and away from skin, muscle, and GI
tract.
Hypovolemic Shock: Renal System Compensation
• The kidneys respond to hemorrhagic shock by
stimulating an increase in renin secretion from
the juxtaglomerular apparatus which
subsequently causes an increase in Angiotensin II.
• Angiotensin II has 2 main effects, both of which
help reverse hypovolemic shock, vasoconstriction
of arteriolar smooth muscle and stimulation of
aldosterone secretion by the adrenal cortex.
Hypovolemic Shock:
Neuroendocrine System Compensation
• Causes an increase in circulating antidiuretic
• hormone (ADH)
• ADH is released from the posterior pituitary gland
in response to a decrease in blood pressure (as
detected by baroreceptors) and a decrease in
sodium concentration.
• ADH indirectly leads to an increase in
reabsorption of water and salt (NaCl) by the
distal tubule, the collecting ducts, and the loop of
Henle.
Cardiogenic Shock
Cardiogenic shock is characterized by a decreased
pumping ability of the heart causing a shock-like
state with inadequate perfusion to the tissues.
It occurs most commonly in association with, and as
a direct result of, acute ischemic damage to the
myocardium.
Cardiogenic Shock
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Intrinsic Types
Myocardial injury
Tachycardia
Bradycardia
Valvular defect
Extrinsic Types
Pericardial tamponade
Tension pneumothorax
Large pulmonary embolus
Cardiogenic Shock
• The human body responds to Cardiogenic shock by
activating 2 major physiologic systems:
• the renal system (Renin and its actions)
• the neuroendocrine system (ADH)
Vasogenic Shock
extensive inappropriate vasodilation
Septic Shock (Gram negative shock)
Toxic Shock
Neurogenic Shock (Vasomotor center
dysfunction)
Psychogenic Shock
Anaphylactic Shock
Psychogenic Shock
Cortical and limbic system override of the
vasomotor center
• Also known as fainting spells or syncopal spells
• Caused by sudden dilation of blood vessels
which temporarily halts blood flow to the
brain
Neurogenic Shock
• Failure of the nervous system (Vasomotor
Center) to control diameter of blood vessels
• Causes pooling of blood and there is
generally no actual blood loss
• Classic signs of shock may not be present
• Compensation mechanisms
• Local Control mechanisms plus widespread
control mechanisms (hormones and heart)
Anaphylactic Shock
• Overall increase in histamine production
causing massive vasodilation – drop in
systemic vascular resistance
• Compensation mechanisms
• Local Control mechanisms plus widespread
control mechanisms (hormones and heart)
Septic Shock (Gram negative Shock)
• All cells have a cell membrane however almost all bacteria
have semirigid cell wall outside the cell membrane. This
cell wall is made up of some peptidoglycans, also called
murein. The cell wall can fix a stain called a gram stain –
thus making them Gram positive bacteria – Staphylococcus
and Streptococcus.
• Some bacteria have a membrane outside the cell wall (thus
they have a cell membrane, cell wall and outer membrane).
The outer membrane is made up of Lipopolysaccharides.
This does not fix the gram stain thus making them Gram
negative – like E-coli and Bacteroides. When the outer cell
membrane of a gram negative bacteria breaks apart it can
act as an endotoxin causing massive vasodilation.
Toll Like Receptors
• Macrophages (and cells of certain boundary
tissues such as epithelial cells lining the GI tract
and respiratory tracts) bear surface membrane
receptors termed “Toll Like Receptors.” These
serve to trigger the immune system. There are
11 so far identified, each recognizing a specific
class of attacking microbes. Some recognize TB
others recognize gram-negative bacteria. Once
activated, TLR triggers the release of chemical
cytokines – thus initiating massive inflammation
leading to massive vasodilation.
Toxic Shock Syndrome
• In both TSS (caused by S. aureus) and TSLS (caused by S.
pyogenes), disease progression stems from a superantigen
toxin that allows the non-specific binding of MHC II with T
cell receptors, resulting in polyclonal T cell activation. In
typical T cell recognition, an antigen is taken up by an
antigen-presenting cell, processed, expressed on the cell
surface in complex with class II major histocompatibility
complex (MHC) in a groove formed by the alpha and beta
chains of class II MHC, and recognized by an antigenspecific T cell receptor. By contrast, super-antigens do not
require processing by antigen-presenting cells but instead
interact directly with the invariant region of the class II
MHC molecule. In patients with TSS, up to 20% of the
body's T cells can be activated at one time. This polyclonal
T-cell population causes a cytokine storm, followed by a
multisystem disease. The toxin in S. aureus infections is
Toxic Shock Syndrome Toxin-1, or TSST-1.
Compensation for Vasogenic Shock
• Heart Action
• Neuroendocrine Action
• Local Control