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Clinical Workflows Supported by Patient Care Device Data
Published in John R. Zaleski, Clinical Surveillance, 2020
Shock can be caused by many things, but it is subdivided into four distinct groups: [117, 118] Hypovolemic shock: shock resulting from low blood volume as a result of blood loss or due to fluid loss (dehydration). The net result is hypoperfusion. Distributive shock: shock resulting from loss of blood vessel (i.e., smooth muscle) tone, causing hypoperfusion to result. Example causes can be anaphylaxis. Bacterial or viral infections can cause the body to respond by dilating blood vessels to facilitate white blood cell transport. The effect is hypoperfusion. Because of the systemic nature of the infection, however, the dilation becomes body wide. When blood vessels dilate, blood pressure goes down. Yet, the brain responds to the need for homeostasis and the heart rate increases in order to maintain cardiac output. This is why the shock index can be a good indicator of sepsis onset, as hypoperfusion is a chief indicator. Cardiogenic shock: shock induced when the heart fails in its ability to circulate blood adequately. This can occur as a result of myocardial infarction, causing injury to the heart muscle, or in cases of physical trauma. Hypoperfusion also results. Obstructive shock: blood is physically prevented from flowing. An example is pulmonary embolism. Blood is prevented from reaching essential organs, like portions of the lung, which results in hypoxia and necrosis.
EkoSonic® endovascular system and other catheter-directed treatment reperfusion strategies for acute pulmonary embolism: overview of efficacy and safety outcomes
Published in Expert Review of Medical Devices, 2020
Lukas Hobohm, Karsten Keller, Thomas Münzel, Tommaso Gori, Stavros V. Konstantinides
Acute PE interferes both with the circulation and with gas exchange. Thus, the main manifestations of severe PE are acute right ventricular (RV) failure and hypoxia. RV failure due to pressure overload is considered the primary cause of death in intermediate and severe PE [17]. Studies dating back to the 1970’s showed that pulmonary artery pressure increases substantially if more than 30–50% of the total cross-sectional area of the pulmonary arterial bed is occluded by thromboembolic mass [18]. The abrupt increase in pulmonary vascular resistance results in RV dilation and initiates a cascade of pathophysiological abnormalities, which may ultimately results in obstructive shock and death [5].