Shock blood pressure

A base, formed by the bacterial degradation of histidine, and present in ergot and in many animal tissues, where it is liberated in response to injury and to antigen-antibody reactions. If injected it causes a condition of shock with dilatation of many blood vessels, loss of plasma from the capillaries to the tissues and a rapid fall in blood pressure. It is normally prepared from protein degradation products. 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

Anaphylactic shock. A systemic hypersensitivity response resulting in dramatic decrease in blood pressure. 

Circulation Leakage of fluid from the vasculature into the surrounding tissue causes edema, drop in blood pressure and finally hemodynamic shock. 

The human histamine Hi-receptor is a 487 amino acid protein that is widely distributed within the body. Histamine potently stimulates smooth muscle contraction via Hi-receptors in blood vessels, airways and in the gastrointestinal tract. In vascular endothelial cells, Hi-receptor activation increases vascular permeability and the synthesis and release of prostacyclin, plateletactivating factor, Von Willebrand factor and nitric oxide thus causing inflammation and the characteristic wheal response observed in the skin. Circulating histamine in the bloodstream (from, e.g. exposure to antigens or allergens) can, via the Hi-receptor, release sufficient nitric oxide from endothelial cells to cause a profound vasodilatation and drop in blood pressure (septic and anaphylactic shock). Activation of... 

According to Merck (Ref 5), ... isopropyl nitrite can cause vasodilation with fall in blood pressure, tachycardia, headache. Large doses can cause methemoglobinuria with cyanosis. Severe poisoning results in shock which can end fatally. . 

All or only some of these symptoms may be present. Anaphylactic shock can be fatal if the symptoms are not identified and treated immediately. Treatment is to raise the blood pressure improve breathing, restore cardiac function, and treat other symptoms as they occur. 

The nurse should administer each IV dose of vancomycin over 60 minutes Too rapid an infusion may result in a sudden and profound fall in blood pressure and shock. When giving the drug IV, the nurse closely monitors the infusion rate and the patient s blood pressure. The nurse reports any decrease in blood pressure or reports of throbbing neck or back pain. These symptoms could indicate a severe adverse reaction referred to as "red neck or "red man syndrome. 9/mptoms of this syndrome include a sudden and profound fall in blood pressure, fever, chills paresthesias and erythema (redness) of the neck and badk. 

The adrenergic dragp are important in the care and treatment of patients in shock. Shock is defined as a life-threatening condition of inadequate perfusion. In shock, there is an inadequate supply of arterial blood flow and oxygen delivery to the cells and tissues. The body initiates compensatory mechanisms to counteract the symptoms of shock (eg, the release of epinephrine and norepinephrine), hi some situations, the body is able to compensate and blood pressure is maintained. However, if shock is untreated and compensatory mechanisms of the body fail, irreversible shock occurs and... 

When a patient is to receive an adrenergic agent for shock, the nurse obtains the blood pressure, pulse rate and quality, and respiratory rate and rhythm. The nurse assesses the patient s symptoms, problems, or needs before administering the drug and records any subjective or objective data on the patient s chart. In emergencies, the nurse must make assessments quickly and accurately. This information provides an important database that is used during treatment. 

MAINTAINING ADEQUATE TISSUE PERFUSION. When a patient is in shock and experiencing ineffective tissue perfusion tiiere is a decrease in oxygen resulting in an inability of die body to nourish its cells at die capillary level. If die patient has marked hypotension die administration of a vasopressor (a drug diat raises die blood pressure because of its ability to constrict blood vessels) is required. The primary health care provider determines die cause of die hypotension and then selects the best mediod of treatment. Some hypotensive episodes require die use of a less potent vasopressor, such as metaraminol, whereas at other times a more potent vasopressor, such as dobutamine (Dobutrex), dopamine (Intropin), or norepinephrine (Levoplied) is necessary. 

Monitoring the patient in shock requires vigilance on the part of the nurse The patient s heart rate, blood pressure, and ECG are monitored continuously. The urinary output is measured often (usually hourly), and an accurate intake and output is taken. Monitoring of central venous pressure via a central venous catheter will provide an estimation of the patient s fluid status. Sometimes additional hemodynamic monitoring is necessary with a pulmonary artery catheter. The use of a pulmonary artery catheter allows the nurse to monitor a number of parameters, such as cardiac output and peripheral vascular resistance The nurse adjusts therapy according to the primary health care provider s instructions. 

Solutions used to manage body fluids are often administered IV. Before administering an IV solution, the nurse assesses the patient s general status, reviews recent laboratory test results (when appropriate), weighs the patient (when appropriate), and takes the vital signs. Blood pressure, pulse, and respiratory rate provide a baseline, which is especially important when the patient is receiving blood plasma, plasma expanders, or plasma protein fractions for shock or other serious disorders. 

Metabolic acidosis can also result when a person is severely burned. Blood plasma leaks from the circulatory system into the injured area, producing edema (swelling) and reducing the blood volume. If the burned area is large, this loss of blood volume may be sufficient to reduce blood flow and oxygen supply to all the body s tissues. Lack of oxygen, in turn, causes the tissues to produce an excessive amount of lactic acid and leads to metabolic acidosis. To minimize the decrease in pH, the injured person breathes harder to eliminate the excess C02. However, if blood volume drops below levels for which the body can compensate, a vicious circle ensues in which blood flow decreases still further, blood pressure falls, C02 excretion diminishes, and acidosis becomes more severe. People in this state are said to be in shock and will die if not treated promptly. 

The most frequent symptoms of anaphylaxis in patients with mastocytosis are decreased blood pressure and tachycardia. Also observed are dizziness, dyspnea, flushing, nausea and diarrhea [4]. Severe reactions are typical for patients with mastocytosis. In 55 patients with insect sting allergy and confirmed mastocytosis, 81% of patients experienced severe anaphylaxis with shock or cardiopulmonary arrest, whereas clinical reactions of this severity occurred in only 17% of 504 patients without evidence for mastocytosis and normal tryptase levels [29]. In another study in... 

In an anesthetized, ventilated canine model of anaphylactic shock defined as hypotension with blood pressure maintained at 50% of baseline, epinephrine infusion produces an improvement in blood pressure, associated with positive inotropy [21]. 

Dopamine is most commonly reserved for patients with low systolic blood pressures and those approaching cardiogenic shock. It may also be used in low doses (less than 3 mcg/kg per minute) to improve renal function in a patient with inadequate urine output despite high filling pressures and volume overload, although this indication is controversial. 

Termination of VT Hemodynamically unstable VT should be terminated immediately using synchronized DCC beginning with 100 J and increasing subsequent shocks to 200, 300, and 360 J.14 In the event that VT is present but the patient has no pulse (and therefore no blood pressure), asynchronous defibrillation should be performed, starting with 200 J and increasing to 300 and 360 J.14... 

Major treatment goals in hypovolemic shock following fluid resuscitation are as follows arterial systolic blood pressure greater than 90 mm Hg within 1 hour, organ dysfunction reversal, and normalization of laboratory measurements as rapidly as possible (less than 24 hours). 

Upon stabilization, placement of a pulmonary artery (PA) catheter may be indicated based on the need for more extensive cardiovascular monitoring than is available from non-invasive measurements such as vital signs, cardiac rhythm, and urine output.9,10 Key measured parameters that can be obtained from a PA catheter are the pulmonary artery occlusion pressure, which is a measure of preload, and CO. From these values and simultaneous measurement of HR and blood pressure (BP), one can calculate the left ventricular SV and SVR.10 Placement of a PA catheter should be reserved for patients at high risk of death due to the severity of shock or preexisting medical conditions such as heart failure.11 Use of PA catheters in broad populations of critically ill patients is somewhat controversial because clinical trials have not shown consistent benefits with their use.12-14 However, critically ill patients with a high severity of illness may have improved outcomes from PA catheter placement. It is not clear why this was... 

Successful treatment of hypovolemic shock is measured by the restoration of blood pressure to baseline values and reversal of associated organ dysfunction. The likelihood of a successful fluid resuscitation will be directly related to the expediency of treatment. Therapy goals include ... 

V. cholerae is a gram-negative bacillus. Vibrios pass through the stomach to colonize the upper small intestine. Vibrios have filamentous protein extensions that attach to receptors on the intestinal mucosa, and their motility assists with penetration of the mucus layer.2 The cholera enterotoxin consists of two subunits, one of which (subunit A) is transported into the cells and causes an increase in cyclic AMP, which leads to a deluge of fluid into the small intestine.20 This large volume of fluid results in the watery diarrhea that is characteristic of cholera. The stools are an electrolyte-rich isotonic fluid, the loss of which results in blood volume depletion followed by low blood pressure and shock.2 Of note, the diarrheal fluid is highly infectious. 

Norepinephrine is a potent a-adrenergic agent with less pronounced P-adrenergic activity. Doses of 0.01 to 3 mcg/kg per minute can reliably increase blood pressure with small changes in heart rate or cardiac index. Norepinephrine is a more potent agent than dopamine in refractory septic shock.24,27-28... 

Vasopressin levels are increased during hypotension to maintain blood pressure by vasoconstriction. However, there is a vasopressin deficiency in septic shock. Low doses of vasopressin increase MAP, leading to the discontinuation of vasopressors. However, routine use of vasopressin is not recommended because of lack of evidence of efficacy. Vasopressin is a direct vasoconstrictor without inotropic or chronotropic effects and may result in decreased cardiac output and hepatosplanchnic flow. Vasopressin use may be considered in patients with refractory shock despite adequate fluid resuscitation and high-dose vasopressors.24,27-28... 

Septic shock Sepsis with hypotension (a systolic blood pressure of <90 mm Hg or a reduction of <40 mm Hg from baseline), despite adequate fluid resuscitation, along with the presence of perfusion abnormalities as seen by severe sepsis. Patients who are receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured. 

First described in the 1980s as "endothelium-derived relaxing factor," nitric oxide (NO) is a vasodilator believed to play a role in regulation of blood pressure under physiologic and pathophysiological conditions. For example, inhibition of NO synthesis under normal conditions and during septic shock results in a significant elevation of blood pressure. 

The response varies, depending on the individual and the allergen. The worst case is that anaphylactic shock arises when gastrointestinal, cutaneous and respiratory symptoms occur in conjunction with a dramatic fall in blood pressure and cardiovascular complications. Death can occur within minutes of anaphylactic shock. Table 4 lists the other symptoms of IgE allergy. 

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