Five Types of Shock The major types of shock are: Hypovolaemic 2) Cardiogenic -Distributive shock (Vasogenic) 3) Anaphylactic 4) Septic 5) Neurogenic 1) Shock In 1852, shock was defined as “a rude unhinging of the machinery of life.” Probably no better definition exists to describe the devastating effects of this process on a patient, but a more recent definition calls shock “the collapse and progressive failure of the cardiovascular system.” Shock left untreated may be fatal. It must be recognized and treated immediately, or the patient can die. Definition of Shock Shock is an acute state in which tissue perfusion is inadequate to maintain the supply of oxygen and nutrients necessary for normal cell function (Alexander et al 1994), resulting in widespread hypoxia. The main cause is circulatory failure, which produces a fall in blood pressure and cardiac output. This leads to a lack of blood perfusion of the key organs (brain, lungs, kidneys and heart). Hypovolemic Shock Hypovolemic shock refers to a medical or surgical condition resulting in rapid fluid loss and multiple organ failure due to inadequate circulating volume and subsequent inadequate tissue perfusion. Hypovolemic shock is often secondary to rapid blood loss (hemorrhagic shock). Hypovolemic shock Hemorrhage Burns Diarrhea Vomiting Trauma Hypovolemic Shock Non- hemorrhagic Vomiting Diarrhea Bowel Obstruction Burns Neglect, Environmental with dehydration Hypovolemic Shock Hemorrhagic GI Bleed Trauma Massive Hemoptysis Abdominal Aortic Aneurysm Rupture Ectopic Pregnancy Post-partum bleeding Compensatory MechanismsHypovolemic Shock 1) 2) 3) 4) The human body responds by activating the following major physiologic systems: Hematologic Cardiovascular Renal Neuro-endocrine systems Hematologic System The hematologic system responds to severe blood loss by activating the coagulation cascade and contracting bleeding vessels (by means of local thromboxane A2 release). Platelet activation (by means of local thromboxane A2 release) to form an immature clot on bleeding source. Hematologic System Damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of clot. Approximately 24 hours are needed for complete clot fibrination and mature formation. Cardiovascular system Initial responses of cardiovascular system to hypovolemic shock are ; increasing heart rate increasing myocardial contractility constricting peripheral blood vessels. Cardiovascular system These responses occur secondary to an increased release of nor-epinephrine and decreased 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. The renal system The renal system responds by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main effects, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium re-absorption and subsequent water conservation. The neuro-endocrine system The neuro-endocrine system responds by causing an increase in circulating anti-diuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baro-receptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased re-absorption of water and salt (NaCl) by the distal tubule, collecting ducts, and the loop of Henle. Without Oxygen Without oxygen, cells start to perform anaerobic metabolism, which the production of lactic and pyruvic acids causes the body to develop systemic metabolic acidosis. Anaerobic metabolism is far less efficient than the normal aerobic metabolism, which uses oxygen. Eventually, lactic acid builds up as waste product of anaerobic metabolism. This is harmful to cells and needs to be removed by blood and subsequently broken down in the liver; however, this process requires oxygen. Compensation- Oxygen Delivery Increasing oxygen delivery to cells through: stimulation of sympathetic nervous system to cause bronchodilation, increased respirations, and tidal volume. This is as a result of metabolic acidosis. Hypovolemic Shock SIGNS AND SYMPTOMS OF hypovolemic SHOCK Early Stage (compensated shock): Compensatory mechanisms are able to maintain perfusion of vital organsHeart Rate: mild tachycardia; bounding pulse Level of Consciousness: lethargy, confusion, combativeness Skin: delayed capillary refill; cool and clammy Blood Pressure: normal or slightly lowered Respirations: rapid and shallow Middle Stage (uncompensated shock) Compensatory mechanisms are unable to maintain perfusion Heart Rate: moderate tachycardia; weak and thready pulse Level of Consciousness: confusion or unconsciousness Skin: delayed capillary refill; cold, clammy, and cyanosed Blood Pressure: decreased Respirations: rapid and shallow Late Shock Heart Rate: bradycardia; severe dysrhythmias Level of Consciousness: coma Skin: pale, cold, marked diaphoresis Blood Pressure: marked hypotension Respirations: decreased rate and tidal volume Septic Shock Sepsis is an invasion of the body by some form of bacteria which causes an immune response. Sepsis attributed to bacteremia, presence of bacteria in the blood. The body’s response to bacteria in the blood include fever, increased respiratory rate, and lastly septic shock which is sepsis plus hypotension in spite of fluid resuscitation. Septic Shock The result is that tissue perfusion is impaired, and the cycle of shock begins at the cellular level. The classic example of septic shock is TSS or toxic shock syndrome which is an invasion of the body by a toxin producing gram-positive bacteria. Once the type of shock is understood, treatment becomes imperative. Pathogenesis of Sepsis Cardiogenic Shock Cardiogenic shock results from impaired ability of the heart to pump. The usual cause is myocardial infarction. There are some non-coronary causes such as cardio-myopathy, valvular heart abnormalities, cardiac tamponade, or cardiac arrhythmias. These patients would generally have poor cardiac output. Cardiogenic Shock Acute hypo-perfusion of the tissues and organs, usually with associated hypotension, due to a primary failure of the pump action of the heart, where the circulating blood volume is adequate. Commonest cause is myocardial death/stunning after infarction or critical ischemia. Ongoing myocardial ischemia causes further deterioration in cardiac function and coronary hypo-perfusion, leading to worsening ischemia. Cardiogenic Shock Risk factors Likely to develop in the elderly and diabetics. Anterior and rightventricular infarction are associated with an increased risk. History of previous infarction, peripheral vascular disease and cerebrovascular disease increase the likelihood of the development of cardiogenic shock. Cardiogenic Shock Presentation -Shock is due to an inability to adequately perfuse vital organs and tissues. The skin, brain, heart and kidneys are usually most severely affected. The symptoms and signs can present abruptly or develop insidiously over the course of many hours. Signs of Cardiogenic shock Chest pain Nausea and vomiting Dyspnoea Profuse sweating Confusion/disorientation Palpitations Faintness/syncope Anaphylactic shock Anaphylactic shock is when the body’s antibody-antigen response is triggered by an allergen. It can happen upon first exposure or after several exposures to a substance. Pathophysiology -anaphylactic shock 1) The antibody-antigen response is triggered, they in turn trigger release of biochemical mediators. These mediators have a two-fold effect. 1)Vasoconstriction of the airways occurs making it hard to breath. A decrease in available oxygen to the lungs causes a decrease in available oxygen to the rest of the body. Anaphylactic shock 2) Vasodilatation of peripheral vessels-This causes a decrease in preload volume to the heart. Decreased preload to the causes a decreased stroke volume which causes a decreased cardiac output. A decrease in cardiac out put ultimately causes a decrease in cellular oxygenation which will compound the cellular death cycle. Anaphylactic Shock Neurogenic Shock Neurogenic shock is caused by decreased sympathetic control of blood vessel tone due to a defect in the vasomotor center in the brain stem or the sympathetic outflow to the blood vessels. The term spinal shock describes the neurogenic shock that occurs in persons with spinal cord injury. Neurogenic Shock Output from the vasomotor center can be interrupted by brain injury, depressant action of drugs, general anesthesia and hypoxia. Type of Neurogenic shock - Psychogenic Shock Also known as “fainting spells or syncope” due to physiological and emotional causes Caused by sudden dilation of blood vessel resulting in gravitational pooling of blood as person stands up, leading to temporarily halting of blood flow to the brain Neurogenic Shock Varied factors, including increased fluid loss, central nervous system trauma, or emotional shock, can override the autonomic nervous system control. The veins and arteries immediately dilate, drastically expanding the volume of the circulatory system, with a corresponding reduction of blood pressure. Neurogenic Shock Many general anesthetic agents can cause a neurogenic shock reaction, especially during induction due to interference with sympathetic nervous system function. In contrast to other shock states due to the loss of blood volume or impaired cardiac function, the heart rate in neurogenic shock is slower than normal (bradycardia), the skin is dry. Neurogenic Shock Triad of i) hypotension ii) bradycardia iii) hypothermia More commonly in injuries above T6 Secondary to disruption of sympathetic outflow from T1 – L2 Neurogenic Shock
