1. Shock Mike Clark, M.D.

2. 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)

3. 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)

4. 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

5. 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)

6. Symptoms of Shock
Lethargy
Weakness
Dizziness

7. 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

8. 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

9. 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

10. Hypovolemic shock
Some causes are
Hemorrhage
Burns
Diarrhea
Vomiting
Peritonitis

11. 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

12. 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

13. 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.

14. 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.

15. 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.

16. 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.

17. Cardiogenic Shock Intrinsic Types Myocardial injury Tachycardia
Bradycardia
Valvular defect
Extrinsic Types
Pericardial tamponade
Tension pneumothorax
Large pulmonary embolus

18. 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)

19. Vasogenic Shock extensive inappropriate vasodilation
Septic Shock (Gram negative shock)
Toxic Shock
Neurogenic Shock (Vasomotor center dysfunction)
Psychogenic Shock
Anaphylactic Shock

20. 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

22. 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)

23. 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)

24. 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.

25. 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.

26. 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 antigen-specific 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.

27. Compensation for Vasogenic Shock
Heart Action
Neuroendocrine Action
Local Control