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Digestive System Physiology

Your Heart & Circulatory System
Video of the Day. The thin walls of the capillaries are what allow your circulatory system to make its deliveries! Platelets form in the red bone marrow from large megakaryocyte cells that periodically rupture and release thousands of pieces of membrane that become the platelets. The circulatory system includes the lymphatic system , which circulates lymph. Accelerated idioventricular rhythm Catecholaminergic polymorphic Torsades de pointes.

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The Circulatory System

The septum separates the right-hand and left-hand side of the heart. The tricuspid valve is located between the right atrium and right ventricle and opens due to a build-up of pressure in the right atrium. The bicuspid valve is located between the left atrium and left ventricle and likewise opens due to a build-up of pressure, this time in the left atrium. The semilunar valves stop the back flow of blood into the heart.

There is a semilunar valve where the aorta leaves the left ventricle and another where the pulmonary artery leaves the right ventricle. There are four main blood vessels that take blood into and out of the heart. The aorta is the largest artery in the body. It carries oxygenated blood away from the left ventricle to the body. The vena cava is the largest vein in the body. It carries deoxygenated blood from the body back to the heart. The pulmonary artery carries deoxygenated blood away from the right ventricle to the lungs.

The pulmonary vein returns oxygenated blood from the lungs to the heart. Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell.

Based on endocrine disturbances such as:. There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.

One of the key dangers of shock is that it progresses by a positive feedback mechanism. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. This is normally very useful to match up blood supply level with tissue demand for nutrients. However, if enough tissue causes this, it will deprive vital nutrients from other parts of the body. Additionally, the ability of the circulatory system to meet this increase in demand causes saturation, and this is a major result, of which other parts of the body begin to respond in a similar way; thus, exacerbating the problem.

Due to this chain of events, immediate treatment of shock is critical for survival. During this stage, the state of hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor in the electron transport chain, is not abundant, this slows down entry of pyruvate into the Krebs cycle , resulting in its accumulation.

Accumulating pyruvate is converted to lactate by lactate dehydrogenase and hence lactate accumulates causing lactic acidosis. This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition.

As a result of the acidosis , the person will begin to hyperventilate in order to rid the body of carbon dioxide CO 2. CO 2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension , and cause the release of epinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate , whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure.

The renin—angiotensin axis is activated, and arginine vasopressin Anti-diuretic hormone ; ADH is released to conserve fluid via the kidneys. These hormones cause the vasoconstriction of the kidneys , gastrointestinal tract , and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production.

However the effects of the renin—angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock. Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries.

As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. At this stage, the vital organs have failed and the shock can no longer be reversed.

Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix.

Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation , and then is transformed into uric acid. The first change seen in shock is an increased cardiac output followed by a decrease in mixed venous oxygen saturation SmvO2 as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation ScvO2 as measured via a central line correlates well with SmvO2 and are easier to acquire.

If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed there is no test that either makes or excludes the diagnosis.

A chest X-ray or emergency department ultrasound may be useful to determine volume state. The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas. Oxygen supplementation, intravenous fluids, passive leg raising not Trendelenburg position should be started and blood transfusions added if blood loss is severe.

Aggressive intravenous fluids are recommended in most types of shock e. For those with haemorrhagic shock the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist known as permissive hypotension.

Vasopressors may be used if blood pressure does not improve with fluids. There is no evidence of substantial superiority of one vasopressor over another; however, using dopamine leads to an increased risk of arrythmia when compared with norepinephrine.

The goal of treatment is to achieve a urine output of greater than 0. In trauma the goal is to stop the bleeding which in many cases requires surgical interventions. The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. In Hinshaw and Cox suggested the classification system for shock which is still used today.

From Wikipedia, the free encyclopedia. For the psychological condition, see Acute stress reaction. American College of Surgeons. Circulatory Shock and Physiology of Its Treatment". Textbook of Medical Physiology 11th ed. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis" PDF.

General features of circulation