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

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 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 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 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.

Compensation for Vasogenic Shock Heart Action Neuroendocrine Action Local Control