Vasospasm as a major complication after SAH which can lead to Delayed Cerebral Ischemia (DCI)Raised intracranial pressure due to intracranial hematoma is the most important complication in TBIMyocardial dysfunction (e.g. Especially in SAH patients with considerable volume shifts, fluid balance goals should constantly be assessed for the prevention of vasospasm and DCI(3).
Manage Myocardial Dysfunction and Perfusion Pressures with the Right Dosage of Vasopressors and Inotropes. Acute pulmonary edema (APE) is a medical emergency caused by leakage of water from the blood vessels into the lung tissue, making breathing difficult.
The edema of the lung has the same pathophysiologic mechanism as any swelling in the body, occurring whenever there is water leakage from blood vessels into a tissue. Contrary to what one might imagine, our blood vessels tubes are not waterproof, they do have pores that allow the entry and exit of cells, bacteria, proteins and water.
When the left side of the heart becomes weak, it finds it difficult to adequately pump blood to the rest of the body.
In heart failure pulmonary edema develops slowly unless there is some factor triggering an acute worsening of heart function.
The acute myocardial infarction, commonly known as a heart attack, can be caused by pulmonary edema if there is a large area of the heart muscle on the left side of the heart, leading to sudden heart failure. The increase in pressure tends to be a frequent cause of acute pulmonary edema, especially in patients who already have some degree of heart failure. In normal situations the patient's heart with moderate heart failure may still be able to pump blood properly. Renal failure leads to accumulation of water and salt in the body, causing an increase in the volume of liquid within the vessels. Some lung infections, particularly those of viral origin, may cause a frame of intense pulmonary inflammation, leading to increased permeability of vessels and subsequent leakage of fluid into the lung. The use of some drugs, such as heroin or cocaine, can cause severe pulmonary inflammation, leading to increased permeability of vessels and subsequent pulmonary edema.
Some patients with severe neurological injury, such as head trauma, brain surgery, convulsions, cerebral hemorrhage, etc.
Depending on the cause, the picture of pulmonary edema may develop slowly or suddenly, the latter called acute pulmonary edema. In patients accumulating fluid in the lungs slowly and gradually, the symptoms of pulmonary edema begin with intolerance to exertion, fatigue (even at rest), shortness of breath when lying down, no need to use at least two pillows to sleep, swelling in the feet and ankles and wheezing. If this same patient described above presents a factor of decompensation of their heart failure, such as a heart attack, a hypertensive crisis or even a serious infection, heart suddenly becomes unable to adequately pump blood to the body, and there is a framework of acute fluid retention in the lungs. The first step in the treatment of acute pulmonary edema is to provide oxygen to the patient.
If the patient does not urinate or does not respond adequately to diuretics, the option is the urgent hemodialysis, a method capable of removing up to a quart of water from the lungs in just 20-30 minutes. Instability Hypotension –most likely dry due to fluid shifts that have occurred –consider HCT - would PRBCs be appropriate? Bleeding Sudden decrease in CT output - be sure your tubes are not clotting, keep them in eyesight at all times.
Butler University was founded in 1855 by attorney and abolitionist Ovid Butler on a sprawling 290 acre plot in Indianapolis’ Butler-Tarkington neighborhood. Exceptionally talented artists Chris Blice (right) and Jon Edwards (left) have been gracing the communities in and around Indianapolis since 1993 with their decorative paintings, art and custom murals. Click on the video to watch an interview with Blice Edwards and see the sculptural mural unfold and come to life.
As we approach the middle of January, we are in the midst of creating the new home of Blice Edwards.


Anaesthesia for Patients with COPD Dr Sajith Damodaran University College of Medical Sciences & GTB Hospital, Delhi.
Chronic Obstructive Pulmonary Disease Definition: Disease state characterised by airflow limitation that is not fully reversible The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.
COPD Chronic Bronchitis: (Clinical Definition) Chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of productive chronic cough have been excluded. Increased Neutrophils, Lymphocytes & Macrophages Pathogenesis: Tobacco smoke & other noxious gases Inflammatory response in airways Tissue Destruction Impaired defense against tissue destruction Impaired repair mechanisms Tissue Destruction Impaired defense against tissue destruction Impaired repair mechanisms Proteinase & Antiproteinase imbalance Oxidative Stress Alpha 1 antitrypsin def. Effect of smoking and smoking cessation on Lung Function: Loss of lung function over 11 yrs in the Lung Health Study for continuous smokers (–––), intermittent quitters (–––) and sustained quitters (–––). Acute Respiratory Failure n Hypoxemia- inadequate O2 transfer PaO2 of 60mmHg or less when pt. Diffusion Limitations n Gas exchange is compromised by a process that thickens or destroys the membrane 1.
50 only one cause- hypoventilationonly one cause- hypoventilation *In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. Hypercapnia n Dyspnea to respiratory depression- if too high CO2 narcosis n Headache-vasodilation- Increases ICP n Papilledema n Tachycardia and inc. Drug Therapy n Relief of bronchospasm- bronchodilators alupent and albuterol-(Watch for what side effect?)alupent and albuterol-(Watch for what side effect?) n Reduction of airway inflammation- Corticosteroids by inhalation or IV or po n Reduction of pulmonary congestion-diuretics and nitroglycerine with heart failure- why HF with pulmonary problems?why HF with pulmonary problems? Whether hypervolemia (triple H concept) or normovolemia (hyperdynamic concept) is targeted a€“ PiCCO is your guide in hemodynamic management.GEDI is a reliable and validated parameter for preload.
When the pressure gets too high within the vessels of the lung, water blood tends to "turn into serum" through pores, accumulating within lung tissue, mainly in the alveoli, which are the structures that perform gas exchange. Some diseases, which will be explained below, cause an increase in the pores of blood vessels, making them more permeable, which facilitates the outflow of water. We describe simplified cardiopulmonary circulation for this mechanism so that it is easily understandable.
After nourishing all tissues, blood, now low in oxygen and high in carbon dioxide, it returns to the right side of the heart where it is immediately pumped toward the lungs. As the left side of the heart is responsible for pumping blood from the lungs and when the heart pump fails, there is a jam, causing an accumulation of blood in the pulmonary vessels. If much of the heart muscle dies, the heart becomes unable to pump blood properly, causing this retention in the lungs.
However, just a sudden elevation in blood pressure is enough for an increase in resistance to blood flow, requiring further work of the heart muscle. In some cases, especially if the patient does not urinate in appropriate volumes, the quantity of liquid trapped in the vessels becomes so large that it starts to overflow, causing edema and pulmonary edema. The cause is unknown, but it is believed that there are changes in the pulmonary microvasculature favoring fluid leakage at high altitudes. This frame is typical in patients with heart failure who have gradual worsening of heart function and progressive pulmonary congestion. In this case the symptoms of acute pulmonary edema are severe: shortness of breath, feeling of drowning, agitation, cough with frothy secretions, inability to lie down and tachycardia (racing heart). The acute pulmonary edema is a medical emergency and if not treated in time, will definitely lead to cardiac arrest. Usually the patient arrives at the emergency department in hypoxemia, or with low levels of blood oxygenation. Miller, RN, MN,CCRN-CSC, PCCN-CMC, CNRN, CEN, CMSRN, NP Education Specialist LRM Consulting Nashville, TN. As Butler states on their website, “the University emphasizes a liberal arts-based education with the goal of teaching clear and effective communication, appreciation of beauty, and a commitment to lifelong learning, community service and global awareness”.


Blice Edwards had the privilege of painting the fun, retro style murals both inside and out. FEV1: forced expiratory volume in one second (Anthonisen NR et al,Lung Health Study Research Group. Oxygen delivery methods include nasal continuous flow, reservoir cannulas and transtracheal catheter. Anatomic- passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect1.
Abnormalities of the airways and alveoli- air flow obstruction and air trapping Asthma, COPD, and cystic fibrosisAsthma, COPD, and cystic fibrosis 2. Abnormalities of the chest wall Flail chest, morbid obesity, kyphoscoliosisFlail chest, morbid obesity, kyphoscoliosis 4. It better predicts fluid responsiveness compared to CVP or PCWP(1)SVV provides information about volume responsiveness in ventilated neurosurgical patients. With its broad spectrum of parameters the PiCCO gives a clear picture which allows optimal titration, and frequently, minimization of the dosage of inotropes and vasopressors. In the lungs the blood is oxygenated again and returns to the left side of the heart, where it will be pumped into the rest of the body, restarting the process.
This congestion causes an increase in blood pressure in pulmonary vessels, favoring leakage of water. Some patients do not have a heart able to work against high blood pressure, which leads to pulmonary congestion. If the heart valve does not open properly, blood cannot be drained there through, causing congestion. The edema arises from changes in pulmonary hemodynamics, with increased pressure and permeability in the pulmonary vessels.
In some cases pulmonary edema is so severe and oxygenation is so low, that the patient needs to be intubated and connected to a mechanical ventilator to stay alive. Lowered blood pressure is also important to facilitate the work of the heart, so usually vasodilators are used. 3.Discuss treatment strategies for complications seen in the postoperative CV surgery patient. Physiological indications for oxygen include an arterial oxygen tension (PaO 2 ) 90% during rest, sleep and exertion.
Anatomic- passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect 2. According to studies a SVV value of 9.5% or more predicted a SV increase of at least 5%(4). ELWI is a unique lung water parameter which gives a more precise bedside assessment of pulmonary edema than chest X-Rays.
Intrapulmonary shunt- blood flows through pulmonary capillaries without participating in gas exchange ex: alveoli filled with fluid2.
The Pulmonary Vascular Permeability Index (PVPI) distinguishes between cardiogenic (PVPI 3).



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