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Clinical Approach to Case of PPH
Published in Gowri Dorairajan, Management of Normal and High Risk Labour During Childbirth, 2022
The goal of resuscitation is to prevent morbidity and mortality. It is prudent to call for help. One should call the senior most of the team on-site and the consultant, if needed, early in the management. One should alert the nursing and other staff, the blood bank, and the anaesthetist. The classification of hypovolemic shock as laid down by the advanced trauma [1] life support should guide in recognizing the severity. There is a 40%–50% increase in plasma volume throughout pregnancy. One must remember that the pulse and blood pressure may show a change only when immense blood loss has happened. So, one should be alert about the visual quantification of blood loss and act accordingly. Shock index (Pulse rate/systolic blood pressure) is helpful to assess the volume loss clinically. The shock index should always be less than 1.
Trauma of the Brain and Spinal Cord
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Fernando D. Goldenberg, Ali Mansour
In high cervical lesions, patients can develop respiratory compromise due to phrenic nerve injury and diaphragmatic paralysis. The sphincter tone may be lost and sacral functions compromised. Spinal shock results in hypotension and bradycardia due to loss of sympathetic tone. In comparison, hypovolemic shock presents with hypotension and tachycardia. Shock in patients with TSCI can be due to a mixed expression of loss of sympathetic tone, loss of muscle tone due to paralysis, and blood loss.
The Cardiovascular System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Hypovolemic shock is caused by a reduced blood volume, which may be hemorrhagic (caused by bleeding, whether external as in traumatic injury or internal such as from a perforated ulcer or a ruptured aneurysm) or nonhemorrhagic. Diarrhea, vomiting, unreplaced excess perspiration, or diabetes mellitus can cause severe dehydration, which can reduce blood volume sufficiently to result in nonhemorrhagic hypovolemic shock. Similarly, severe burns result in volume depletion, and ascites or any other conditions that sequester large volumes of fluid outside the vasculature will cause hypovolemia in the vessels and reduce tissue perfusion.
Echocardiography in a critical care unit: a contemporary review
Published in Expert Review of Cardiovascular Therapy, 2022
Muhammad Mohsin, Muhammad Umar Farooq, Waheed Akhtar, Waqar Mustafa, Tanzeel Ur Rehman, Jahanzeb Malik, Taimoor Zahid
Hypovolemic shock is the presence of inadequate organ perfusion caused by intravascular volume loss in acute settings [2,53]. This causes a drop in preload and cardiac output and reduces micro- and macrocirculation, leading to negative tissue metabolism and an inflammatory reaction [2,54]. Assessment of intravascular volume, although pertinent in all types of circulatory shock, is particularly used as a starting point in hypovolemic shock [55]. In contemporary practice, a clinician can assess volume status on 2D and M-mode echocardiography. LV collapse at the end of systole implies severe hypovolemia and a fixed bowing of atrial septum toward the right chambers means adequate fluid resuscitation was given [56]. However, these signs are not specific to intravascular fluid status.
The lethal effects and determinants of microcystin-LR on heart: a mini review
Published in Toxin Reviews, 2021
Muwaffak Alosman, Linghui Cao, Isaac Yaw Massey, Fei Yang
Researchers such as Milutinovic et al. (2006) considered that the outcome of hypovolemic shock as extensive and may cause tissue damage that ultimately leads to death as a result of MC intoxication. The production of high levels of MC leads to an intensive amount of protein in blood capillaries hence necessitating a significant increase in peripheral pressure. An increase in blood pressure is responsible for the increase of glomerular pressure which consequently affects the health of human and animals. Interference in blood flow is as a result of toxin-treated group. Therefore, there is an increase in vascular permeability due to capillary injuries that are caused by increased blood flow. Direct permeability is caused by endothelial injury and the alteration in blood flow (Best et al. 2001). An experimental study done by Qiu et al. (2009) indicated that rats exposed to MC-LR at a lethal dose experienced a decrease in blood pressure, which suggested a basic dysfunction of the normal compensatory responses vasculature and heart to hypotension. In the meantime, the observed decrease in both stroke volume and cardiac output in the rats exposed to lethal doses of MC-LR pointed at the proposition that MCs impede the heart's blood pumping role.
Modified ‘sandwich’ injection with or without ligation for variceal bleeding in patients with both esophageal and gastric varices: a retrospective cohort study
Published in Scandinavian Journal of Gastroenterology, 2020
Tingting Hu, Simon Stock, Wandong Hong, Yongping Chen
Failure to control bleeding was based on Baveno V consensus. It required that the time frame for the acute bleeding episode should be 120 h (5 days) and defined failure as death or the need to change therapy according to one of the following criteria: (1) Fresh hematemesis or nasogastric aspiration of ≥100 mL of fresh blood ≥2 h after the start of a specific drug treatment or therapeutic endoscopy. (2) Development of hypovolemic shock. (3) A 3 g drop in Hb (equivalent to a 9% drop in hematocrit) within any 24 h period if no blood transfusion is administered [19]. Rebleeding was defined as occurrence of one or more times clinically significant rebleeding (example: melena or/and hematemesis) from portal hypertensive sources after day 5 [20]. As proposed by Baveno VI consensus, 6 weeks should be the primary endpoint for studies for treatment of acute variceal bleeding. Therefore, we analyzed 6-week rebleeding rate [4]. The 1-year rebleeding rate was defined as cumulative rebleeding rate within 1-year after day 5.