Arteries pulmonary

Diuretics have become the cornerstone of all treatment regimens of CHF (III—II3). They can reheve symptoms of pulmonary and peripheral edema. In mild CHF, the thia2ide-type diuretics are adequate unless the GFR falls below 30 ml,/min, as compared to 120 ml,/min in normal subjects. Diuretics improve left ventricular function in CHF due in part to decrease of preload. Indapamide has been shown to cause reduction of pulmonary arterial pressure and pulmonary wedge pressure. 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

AHF acute heart failure, CHF chronic heart failure, CRF chronic renal failure, NEP neutral endopeptidase, ECE endothelin converting enzyme, PAH pulmonary arterial hypertension. 

Primary pulmonary hypertension is a disease of unclear etiology that is characterized by abnormally high mean pulmonary arterial pressures, in the absence of a demonstrable cause. A wide variety of pulmonary and cardiac diseases can lead to secondary pulmonary hypertension. 

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. 

Stock UA, Sakamoto T, Hatsuoka S, Martin DP, Nagashima M, Moran AM, Moses MA, Khalil PN, Schoen FJ, Vacanti JP, and Mayer JE Jr. Patch augmentation of the pulmonary artery with bioabsorbable polymers and autologous cell seeding. J Thorac Cardiovasc Surg, 2000, 20, 1158-1168. 

Phon, S.H., Gannon, D.E., Varan, J., Ryan, V.S. and Ward, P.A. (1989). Xanthine oxidase activity in rat pulmonary artery endothelial cells and its alteration by activated neutrophils. Am. J. Path. 134, 1201-1211. 

Utilize a central line +/- pulmonary artery catheter ° 10 mg/kg IV over 30 min followed by 5 mg/kg/h continuous IV infusion for 3 h (total loading dose is 25 mg/kg)... 

Invasive hemodynamic monitoring in patients with HF entails placement of a right heart or pulmonary artery catheter (PAC). The catheter is inserted percutaneously through a central vein and advanced through the right side of the heart to the... 

V/Q scan and CT scans are the most commonly used tests to diagnose PE. A V/Q scan measures the distribution of blood and air flow in the lungs. When there is a large mismatch between blood and air flow in one area of the lung, there is a high probability that the patient has a PE. Spiral CT scans can detect emboli in the pulmonary arteries. 

Pulmonary angiography is the gold standard for the diagnosis of PE. However, it is an invasive test that involves injection of radiopaque contrast dye into the pulmonary artery. The test is expensive and associated with a significant risk of mortality. 

In patients with acute PE, the use of thrombolytics provides short-term benefits such as restoring pulmonary artery patency and hemodynamic stability.8,26 A recent meta-analysis of nine small randomized clinical trials showed a slightly lower risk... 

Pulmonary artery catheter measurements decreased CO, decreased SV, increased SVR, low PAOP (pulmonary artery occlusion pressure)... 

FIGURE 10-4. Treatment algorithm for the management of moderate to severe hypovolemia. BP, blood pressure CVP, central venous pressure ECG, electrocardiogram MAP, mean arterial pressure PA, pulmonary artery PAOP, pulmonary artery occlusion pressure PRBCs, packed red blood cells SBP, systolic blood pressure. 

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... 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

Preload The stretched condition of the heart muscle at the end of diastole just before contraction volume in the left ventricle at the end of diastole estimated by the pulmonary artery occlusion pressure (also known as the pulmonary artery wedge pressure or pulmonary capillary wedge pressure). 

Pulmonary artery catheter An invasive device used to measure hemodynamic parameters directly, including cardiac output and pulmonary artery occlusion pressure calculated parameters include stroke volume and systemic vascular resistance. 

Pulmonary embolism A disorder of thrombus formation causing obstruction of a pulmonary artery or one of its branches may result in pulmonary infarction. 

C26. Curzen, N. P., Mitchell, J. A., Jourdan, K. B Griffiths, M. J. D., and Evans T. W., Endothelin-1-induced contraction of pulmonary arteries from endotoxemic rats is attenuated by the endo-helin-A receptor antagonist, BQ123. Crit. Care Med. 24,2007-2013 (1996). 

MDCK (Madin-Darby canine kidney) cells are derived from distal tubules, whereas LLC-PKi are from proximal tubes. b BMEC (brain microvessel endothelial cells) are isolated from capillaries. BPAEC (bovine pulmonary artery endothelial cells), BAEC (bovine aortic endothelial cells), and HUVEC (human umbilical vein endothelial cells) are large vessel endothelia. 

The semilunar valves separate the ventricles from their associated arteries. The pulmonary valve is found between the right ventricle and the pulmonary artery and the aortic valve is found between the left ventricle and the aorta. These valves prevent backward flow of blood from the pulmonary artery or the aorta into their preceding ventricles when the ventricles relax. The semilunar valves also have three cusps. There are no valves between the venae cavae or the pulmonary veins and the atria into which they deliver blood. The closure of the valves causes the "lub-dub" associated with the heart beat. Tire first heart sound, or the "lub," occurs when the ventricles contract and the AV valves close. The second heart sound, or the "dub," occurs when the ventricles relax and the semilunar valves close. 

Low-pressure receptors. The low-pressure receptors are located in the walls of the atria and the pulmonary arteries. Similar to baroreceptors, low-pressure receptors are also stretch receptors however, stimulation of these receptors is caused by changes in blood volume in these low-pressure areas. An overall increase in blood volume results in an increase in venous return an increase in the blood volume in the atria and the pulmonary arteries and stimulation of the low-pressure receptors. These receptors then elicit reflexes by way of the vasomotor center that parallel those of baroreceptors. Because an increase in blood volume will initially increase MAP, sympathetic discharge decreases and parasympathetic discharge increases so that MAP decreases toward its normal value. The simultaneous activity of baroreceptors and low-pressure receptors makes the total reflex system more effective in the control of MAP. 

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