2Definition 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)
3Shock is caused by some traumatic insult to the body or some problem with the organs/systems that control blood pressureMAP = CO x SVRCO = HR x SVSV = EDV – ESV(EDV concerned with blood volume and ESV concerned more with inotropic effect)SVR = ∑R₁ + R₂ + 1/R₃ + 1/R₄ …..R = 8ŋL/∏r⁴In order to live – the body compensates by increasing the actions of the organs not affected (homeostasis – negative feedback)
4Control of Blood Pressure Local Immediate Control – myogenic tone, paracrine/autocrine, metabolitesWidespread Long term Control – neurologic and endocrineHeart – rate and inotropicBlood VolumeBlood Vessel vasoconstriction and vasodilation
5Stages of Shock Reversible (cells can regenerate) Stage I Compensated (body itself compensates) negative feedback compensationStage II Uncompensated (need medical care to survive) Positive feedback spiralling to destructionStage III Nonreversible– even if adequate perfusion to tissue is re-established – still some nonreversible cell damage (does not necessarily mean death)
11Hypovolemic ShockHypovolemic shock refers to a medicalor surgical condition in which rapid fluidloss results in multiple organ failure dueto inadequate perfusion.Some causes are:TraumaHemorrhageVomiting / diarrheaBurns
12Hypovolemic ShockIf 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 systemthe renal systemthe neuroendocrine system
13Hypovolemic Shock:Cardiovascular System CompensationIncreases the heart rate, increasing myocardialcontractility, and constricting peripheral bloodvessels.This response occurs secondary to an increase inrelease 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 byredistributing blood to the brain, heart, andkidneys and away from skin, muscle, and GItract.
14Hypovolemic 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.
15Hypovolemic Shock:Neuroendocrine System CompensationCauses an increase in circulating antidiuretichormone (ADH)ADH is released from the posterior pituitary glandin response to a decrease in blood pressure (asdetected by baroreceptors) and a decrease insodium concentration.ADH indirectly leads to an increase inreabsorption of water and salt (NaCl) by thedistal tubule, the collecting ducts, and the loop ofHenle.
16Cardiogenic ShockCardiogenic 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.
20Psychogenic ShockCortical and limbic system override of the vasomotor centerAlso known as fainting spells or syncopal spellsCaused by sudden dilation of blood vesselswhich temporarily halts blood flow to thebrain
22Neurogenic ShockFailure of the nervous system (Vasomotor Center) to control diameter of blood vesselsCauses pooling of blood and there isgenerally no actual blood lossClassic signs of shock may not be presentCompensation mechanismsLocal Control mechanisms plus widespread control mechanisms (hormones and heart)
23Anaphylactic ShockOverall increase in histamine production causing massive vasodilation – drop in systemic vascular resistanceCompensation mechanismsLocal Control mechanisms plus widespread control mechanisms (hormones and heart)
24Septic 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.
25Toll Like ReceptorsMacrophages (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.
26Toxic Shock SyndromeIn 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.
27Compensation for Vasogenic Shock Heart ActionNeuroendocrine ActionLocal Control