document_title: Heart failure

question_text: what is the most common cause of right ventricular heart failure

question_tokens: what is the most common cause of right ventricular heart failure

text: Heart failure

text: Terminology[edit]

text: Heart failure is a physiological state in which cardiac output is insufficient to meet the needs of the body and lungs.[2] The term "congestive heart failure" is often used, as one of the common symptoms is congestion, or build-up of fluid in a person's tissues and veins in the lungs or other parts of the body.[2] Specifically, congestion takes the form of water retention and swelling (edema), both as peripheral edema (causing swollen limbs and feet) and as pulmonary edema (causing breathing difficulty), as well as ascites (swollen abdomen). This is a common problem in old age as a result of cardiovascular disease, but it can happen at any age, even in fetuses.

text: The term "acute" is used to mean rapid onset, and "chronic" refers to long duration. Chronic heart failure is a long-term condition, usually kept stable by the treatment of symptoms. Acute decompensated heart failure is a worsening of chronic heart failure symptoms which can result in acute respiratory distress.[20] High-output heart failure can occur when there is an increased cardiac output. The circulatory overload caused, can result in an increased left ventricular diastolic pressure which can develop into pulmonary congestion (pulmonary edema).[21]

text: Heart failure is divided into two types based on ejection fraction, which is the proportion of blood pumped out of the heart during a single contraction.[22] Ejection fraction is given as a percentage with the normal range being between 50 and 75%.[22] The two types are:

text: 1) Heart failure due to reduced ejection fraction. This type is also known as heart failure due to left ventricular systolic dysfunction or systolic heart failure. This type of heart failure occurs when the ejection fraction is less than 40%.[23]

text: 2) Heart failure with preserved ejection fraction (HFpEF). This type is also known as diastolic heart failure or heart failure with normal ejection fraction.[2][16] This type of heart failure occurs when the heart muscle contracts well but the ventricle does not fill with blood well in the relaxation phase.[2]

text: Signs and symptoms[edit]

text: Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation. However, heart failure is not exclusively backward failure (in the part of the circulation which drains to the ventricle).

text: There are several other exceptions to a simple left-right division of heart failure symptoms. Additionally, the most common cause of right-sided heart failure is left-sided heart failure.[24] The result is that patients commonly present with both sets of signs and symptoms.

text: Left-sided failure[edit]

text: The left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to the systemic circulation (the rest of the body except for the pulmonary circulation). Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood. Common respiratory signs are increased rate of breathing and increased work of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe low blood oxygen, is a late sign of extremely severe pulmonary edema.

text: Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

text: Backward failure of the left ventricle causes congestion of the lungs' blood vessels, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into the failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the patient may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea: a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise.

text: "Cardiac asthma" or wheezing may occur.

text: Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest.

text: Right-sided failure[edit]

text: Right-sided heart failure is often caused by pulmonary heart disease (cor pulmonale), which is usually caused by difficulties of the pulmonary circulation, such as pulmonary hypertension or pulmonic stenosis.

text: Physical examination may reveal pitting peripheral edema, ascites, and liver enlargement. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength.

text: Backward failure of the right ventricle leads to congestion of systemic capillaries. This generates excess fluid accumulation in the body. This causes swelling under the skin (termed peripheral edema or anasarca) and usually affects the dependent parts of the body first (causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down). Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and liver enlargement may develop. Significant liver congestion may result in impaired liver function (congestive hepatopathy), and jaundice and even coagulopathy (problems of decreased or increased blood clotting) may occur.

text: Biventricular failure[edit]

text: Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion (fluid collection between the lung and the chest wall). Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain into both the systemic and pulmonary venous systems. When unilateral, effusions are often right sided.

text: If a person with a failure of one ventricle lives long enough, it will tend to progress to failure of both ventricles. For example, left ventricular failure allows pulmonary edema and pulmonary hypertension to occur, which increase stress on the right ventricle. Right ventricular failure is not as deleterious to the other side, but neither is it harmless.

text: Causes[edit]

text: Congestive heart failure[edit]

text: Heart failure may also occur in situations of "high output" (termed "high-output heart failure"), where the amount of blood pumped is more than typical and the heart is unable to keep up.[21] This can occur in overload situations (blood or serum infusions), kidney diseases, chronic severe anemia, beriberi (vitamin B1/thiamine deficiency), hyperthyroidism, cirrhosis, Paget's disease, multiple myeloma, arteriovenous fistulae, or arteriovenous malformations.

text: Viral infections of the heart can lead to inflammation of the muscular layer of the heart and subsequently contribute to the development of heart failure. Heart damage can predispose a person to develop heart failure later in life and has many causes including systemic viral infections (e.g., HIV), chemotherapeutic agents such as daunorubicin, cyclophosphamide, and trastuzumab, and abuse of drugs such as alcohol, cocaine, and methamphetamine. An uncommon cause is exposure to certain toxins such as lead and cobalt. Additionally, infiltrative disorders such as amyloidosis and connective tissue diseases such as systemic lupus erythematosus have similar consequences. Obstructive sleep apnea (a condition of sleep wherein disordered breathing overlaps with obesity, hypertension, and/or diabetes) is regarded as an independent cause of heart failure.

text: Acute decompensation[edit]

text: Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as myocardial infarction (a heart attack), pneumonia), abnormal heart rhythms, uncontrolled hypertension, or a patient's failure to maintain a fluid restriction, diet, or medication.[25] Other well recognized factors that may worsen CHF include the following: anemia and hyperthyroidism which place additional strain on the heart muscle, excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones.[26] NSAIDs in general increase the risk twofold.[27]

text: Medications[edit]

text: A number of medications may cause or worsen the disease. This includes NSAIDS, a number of anesthetic agents such as ketamine, thiazolidinediones, a number of cancer medications, salbutamol, and tamsulosin among others.[28]

text: Pathophysiology[edit]

text: Heart failure is caused by any condition which reduces the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which misfolded proteins are deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself:

text: The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle. In a healthy heart, increased filling of the ventricle results in increased contraction force (by the Frank–Starling law of the heart) and thus a rise in cardiac output. In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.[29]

text: A reduced stroke volume may occur as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling; this occurs when the compliance of the ventricle falls (i.e. when the walls stiffen). As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand (e.g., exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve, or the ability of the heart to work harder during strenuous physical activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands of the body during exercise.

text: A common finding in those with heart failure is an increased heart rate, stimulated by increased sympathetic activity[30] in order to maintain an adequate cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal abnormal heart rhythms. An increase in the physical size of the heart's muscular layer may occur. This is caused by the terminally differentiated heart muscle fibers increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and thus decrease the ability to relax during diastole. Enlargement of the ventricles can also occur and contributes to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and inefficient contraction of the heart.[31]

text: The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to abnormal ventricular heart rhythms) and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process:

text:
Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch which link to the nucleus tractus solitarii. This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and makes contractions more forceful in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform.
Increased sympathetic stimulation also causes the posterior pituitary to secrete vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention at the kidneys. This increases the blood volume and blood pressure.
Heart failure also limits the kidneys' ability to dispose of sodium and water, which further increases edema.[32] Reduced blood flow to the kidneys stimulates the release of renin – an enzyme which catalyses the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasoconstriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys.
The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affect the myocardium directly, causing structural remodelling of the heart over the long term. Many of these remodelling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common downstream target of the signal transduction cascade initiated by catecholamines[33] and angiotensin II,[34] and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone[35]
Reduced perfusion of skeletal muscle causes atrophy of the muscle fibers. This can result in weakness, increased fatiguability and decreased peak strength – all contributing to exercise intolerance.[36]

text: The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts the balance of forces in favor of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in edema (fluid build-up) in the tissues. In right-sided heart failure, this commonly starts in the ankles where venous pressure is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral region.) It may also occur in the abdominal cavity, where the fluid buildup is called ascites. In left-sided heart failure edema can occur in the lungs – this is called cardiogenic pulmonary edema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. The consequences of this are dyspnea (shortness of breath), orthopnea and paroxysmal nocturnal dyspnea.

text: The symptoms of heart failure are largely determined by which side of the heart fails. The left side pumps blood into the systemic circulation, whilst the right side pumps blood into the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the systemic circulation, the initial symptoms often manifest due to effects on the pulmonary circulation. In systolic dysfunction, the ejection fraction is decreased, leaving an abnormally elevated volume of blood in the left ventricle. In diastolic dysfunction, the end-diastolic ventricular pressure will be high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and favors the flow of fluid from the capillaries to the lung parenchyma, causing pulmonary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with respiratory symptoms: shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea.

text: In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion become more apparent, and patients will manifest with cold and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and fainting.

text: The resultant low blood oxygen caused by pulmonary edema causes vasoconstriction in the pulmonary circulation, which results in pulmonary hypertension. Since the right ventricle generates far lower pressures than the left ventricle (approximately 20 mmHg versus around 120 mmHg, respectively, in the healthy individual) but nonetheless generates cardiac output exactly equal to the left ventricle, this means that a small increase in pulmonary vascular resistance causes a large increase in amount of work the right ventricle must perform. However, the main mechanism by which left-sided heart failure causes right-sided heart failure is actually not well understood. Some theories invoke mechanisms that are mediated by neurohormonal activation.[37] Mechanical effects may also contribute. As the left ventricle distends, the intraventricular septum bows into the right ventricle, decreasing the capacity of the right ventricle.

text: Systolic dysfunction[edit]

text: Heart failure caused by systolic dysfunction is more readily recognized. It can be simplistically described as a failure of the pump function of the heart. It is characterized by a decreased ejection fraction (less than 45%). The strength of ventricular contraction is attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate cardiac output. In general, this is caused by dysfunction or destruction of cardiac myocytes or their molecular components. In congenital diseases such as Duchenne muscular dystrophy, the molecular structure of individual myocytes is affected. Myocytes and their components can be damaged by inflammation (such as in myocarditis) or by infiltration (such as in amyloidosis). Toxins and pharmacological agents (such as ethanol, cocaine, doxorubicin, and amphetamines) cause intracellular damage and oxidative stress. The most common mechanism of damage is ischemia causing infarction and scar formation. After myocardial infarction, dead myocytes are replaced by scar tissue, deleteriously affecting the function of the myocardium. On echocardiogram, this is manifest by abnormal wall motion (hypokinesia) or absent wall motion (akinesia).

text: Because the ventricle is inadequately emptied, ventricular end-diastolic pressure and volumes increase. This is transmitted to the atrium. On the left side of the heart, the increased pressure is transmitted to the pulmonary vasculature, and the resultant hydrostatic pressure favors extravasation of fluid into the lung parenchyma, causing pulmonary edema. On the right side of the heart, the increased pressure is transmitted to the systemic venous circulation and systemic capillary beds, favoring extravasation of fluid into the tissues of target organs and extremities, resulting in dependent peripheral edema.

text: Diastolic dysfunction[edit]

text: Heart failure caused by diastolic dysfunction is generally described as the backward failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall. The "stiffness" and contractility of the ventricular walls in diastole was first described by Pierre-Simon Laplace. This causes inadequate filling of the ventricle and therefore results in an inadequate stroke volume (SV). SV is a mathematical term amenable to manipulation of many variables. The failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure, peripheral edema in right heart failure).

text: Diastolic dysfunction can be caused by processes similar to those that cause systolic dysfunction, particularly causes that affect cardiac remodeling.

text: Diastolic dysfunction may not manifest itself except in physiologic extremes if systolic function is preserved. The patient may be completely asymptomatic at rest. However, they are exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be caused simply by physiological responses to exertion, fever, or dehydration, or by pathological tachyarrhythmias such as atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema. Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is, therefore, of key importance to preventing acute decompensation.

text: Left ventricular diastolic function can be determined through echocardiography by measurement of various parameters such as the E/A ratio (early-to-atrial left ventricular filling ratio), the E (early left ventricular filling) deceleration time, and the isovolumic relaxation time.

text: Diagnosis[edit]

text: No system of diagnostic criteria has been agreed on as the gold standard for heart failure. The National Institute for Health and Care Excellence recommends measuring brain natriuretic peptide (BNP) followed by ultrasound of the heart if positive.[38] This is recommended in those with shortness of breath.[39] In those with heart failure who worsen both a BNP and a troponin are recommended to help determine likely outcomes.[39]

text: Ultrasound[edit]

text: Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction (EF). In pediatrics, the shortening fraction is the preferred measure of systolic function. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy. Echocardiography can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo.

text:
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Ultrasound showing severe systolic heart failure[40]

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Ultrasound showing severe systolic heart failure[40]

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Ultrasound showing severe systolic heart failure[40]

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Ultrasound showing severe systolic heart failure[40]

Ultrasound showing severe systolic heart failure[40]

text: Chest X-ray[edit]

text: Chest X-rays are frequently used to aid in the diagnosis of CHF. In a person who is compensated, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion" or "cephalization"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema. Ultrasound of the lung may also be able to detect Kerley lines.[41]

text: Electrophysiology[edit]

text: An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction.[42]

text: Blood tests[edit]

text: Blood tests routinely performed include electrolytes (sodium, potassium), measures of kidney function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

text: According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure.[43]

text: Angiography[edit]

text: Angiography is the X-ray imaging of blood vessels which is done by injecting contrast agents into the bloodstream through a thin plastic tube (catheter) which is placed directly in the blood vessel. X-ray images are called angiograms.[44] Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery.

text: Monitoring[edit]

text: Various measures are often used to assess the progress of patients being treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts).[45] Remote monitoring can be effective to reduce complications for people with heart failure.[46][47]

text: Classification[edit]

text: There are many different ways to categorize heart failure, including:

text:
the side of the heart involved (left heart failure versus right heart failure). Right heart failure compromises pulmonary flow to the lungs. Left heart failure compromises aortic flow to the body and brain. Mixed presentations are common; left heart failure often leads to right heart failure in the longer term.
whether the abnormality is due to insufficient contraction (systolic dysfunction), or due to insufficient relaxation of the heart (diastolic dysfunction), or to both.
whether the problem is primarily increased venous back pressure (preload), or failure to supply adequate arterial perfusion (afterload).
whether the abnormality is due to low cardiac output with high systemic vascular resistance or high cardiac output with low vascular resistance (low-output heart failure vs. high-output heart failure).
the degree of functional impairment conferred by the abnormality (as reflected in the New York Heart Association Functional Classification[48])
the degree of coexisting illness: i.e. heart failure/systemic hypertension, heart failure/pulmonary hypertension, heart failure/diabetes, heart failure/kidney failure, etc.

text: Functional classification generally relies on the New York Heart Association functional classification. The classes (I-IV) are:

text:
Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities.
Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion.
Class III: marked limitation of any activity; the patient is comfortable only at rest.
Class IV: any physical activity brings on discomfort and symptoms occur at rest.

text: This score documents the severity of symptoms and can be used to assess response to treatment. While its use is widespread, the NYHA score is not very reproducible and does not reliably predict the walking distance or exercise tolerance on formal testing.[49]

text: In its 2001 guidelines the American College of Cardiology/American Heart Association working group introduced four stages of heart failure:[50]

text:
Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder.
Stage B: a structural heart disorder but no symptoms at any stage.
Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment.
Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

text: The ACC staging system is useful in that Stage A encompasses "pre-heart failure" – a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC Stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV.

text: Algorithms[edit]

text: There are various algorithms for the diagnosis of heart failure. For example, the algorithm used by the Framingham Heart Study adds together criteria mainly from physical examination. In contrast, the more extensive algorithm by the European Society of Cardiology (ESC) weights the difference between supporting and opposing parameters from the medical history, physical examination, further medical tests as well as response to therapy.

text: Framingham criteria[edit]

text:
By the Framingham criteria, diagnosis of congestive heart failure (heart failure with impaired pumping capability)[51] requires the simultaneous presence of at least 2 of the following major criteria or 1 major criterion in conjunction with 2 of the following minor criteria. Major criteria include an enlarged heart on a chest x-ray, an S3 gallop (a third heart sound), acute pulmonary edema, episodes of waking up from sleep gasping for air, crackles on lung auscultation, central venous pressure of more than 16 cm H
2O at the right atrium, jugular vein distension, positive abdominojugular test, and weight loss of more than 4.5 kg in 5 days in response to treatment (sometimes[52] classified as a minor criterion).[53] Minor criteria include an abnormally fast heart rate of more than 120 beats per minute, nocturnal cough, difficulty breathing with physical activity, pleural effusion, a decrease in the vital capacity by one third from maximum recorded, liver enlargement, and bilateral ankle swelling.[53]

text: Minor criteria are acceptable only if they can not be attributed to another medical condition such as pulmonary hypertension, chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome.[53] The Framingham Heart Study criteria are 100% sensitive and 78% specific for identifying persons with definite congestive heart failure.[53]

text: ESC algorithm[edit]

text: The ESC algorithm weights the following parameters in establishing the diagnosis of heart failure:[54]

text:
Diagnostic assessments supporting the presence of heart failure

Assessment
Diagnosis of heart failure

Supports if present
Opposes if normal or absent

Compatible symptoms
++
++

Compatible signs
++
+

Cardiac dysfunction on echocardiography
+++
+++

Response of symptoms or signs to therapy
+++
++

ECG

Normal

++

Abnormal
++
+

Dysrhythmia
+++
+

Laboratory

Elevated BNP/NT-proBNP
+++
+

Low/normal BNP/NT-proBNP
+
+++

Low blood sodium
+
+

Kidney dysfunction
+
+

Mild elevations of troponin
+
+

Chest X-ray

Pulmonary congestion
+++
+

Reduced exercise capacity
+++
++

Abnormal pulmonary function tests
+
+

Abnormal hemodynamics at rest
+++
++

+ = some importance; ++ = intermediate importance; +++ = great importance.

text: Differential diagnosis[edit]

text: There are several terms which are closely related to heart failure and may be the cause of heart failure, but should not be confused with it. Cardiac arrest and asystole refer to situations in which there is no cardiac output at all. Without urgent treatment, these result in sudden death. Myocardial infarction ("Heart attack") refers to heart muscle damage due to insufficient blood supply, usually as a result of a blocked coronary artery. Cardiomyopathy refers specifically to problems within the heart muscle, and these problems can result in heart failure. Ischemic cardiomyopathy implies that the cause of muscle damage is coronary artery disease. Dilated cardiomyopathy implies that the muscle damage has resulted in enlargement of the heart. Hypertrophic cardiomyopathy involves enlargement and thickening of the heart muscle.

text: Prevention[edit]

text: This section needs expansion. You can help by adding to it. (September 2016)

text: A person's risk of developing heart failure is inversely related to their level of physical activity. Those who achieved at least 500 MET-minutes/week (the recommended minimum by U.S. guidelines) had lower heart failure risk than individuals who did not report exercising during their free time; the reduction in heart failure risk was even greater in those who engaged in higher levels of physical activity than the recommended minimum.[55]

text: Management[edit]

text: Treatment focuses on improving the symptoms and preventing the progression of the disease. Reversible causes of the heart failure also need to be addressed (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities, and occasionally various forms of device therapy and rarely cardiac transplantation.

text: Acute decompensation[edit]

text: In acute decompensated heart failure (ADHF), the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway, breathing, and circulation are adequate. Immediate treatments usually involve some combination of vasodilators such as nitroglycerin, diuretics such as furosemide, and possibly noninvasive positive pressure ventilation (NIPPV).

text: Chronic management[edit]

text: The goals of treatment for people with chronic heart failure are the prolongation of life, the prevention of acute decompensation and the reduction of symptoms, allowing for greater activity.

text: Heart failure can result from a variety of conditions. In considering therapeutic options, it is important to first exclude reversible causes, including thyroid disease, anemia, chronic tachycardia, alcohol abuse, hypertension and dysfunction of one or more heart valves. Treatment of the underlying cause is usually the first approach to treating heart failure. However, in the majority of cases, either no primary cause is found or treatment of the primary cause does not restore normal heart function. In these cases, behavioral, medical and device treatment strategies exist which can provide a significant improvement in outcomes, including the relief of symptoms, exercise tolerance, and a decrease in the likelihood of hospitalization or death. Breathlessness rehabilitation for chronic obstructive pulmonary disease (COPD) and heart failure has been proposed with exercise training as a core component. Rehabilitation should also include other interventions to address shortness of breath including psychological and education needs of patients and needs of carers.[56]

text: Lifestyle[edit]

text: Behavioral modification is a primary consideration in any chronic heart failure management program, with dietary guidelines regarding fluid and salt intake being of particular importance.[57]

text: Exercise should be encouraged and tailored to suit individual capabilities. The inclusion of regular physical conditioning as part of a cardiac rehabilitation program can significantly improve quality of life and reduce the risk of hospital admission for worsening symptoms; however, there is no evidence for a reduction in mortality rates as a result of exercise. Furthermore, it is not clear whether this evidence can be extended to people with heart failure with preserved ejection fraction (HFpEF) or to those whose exercise regimen takes place entirely at home.[58]

text: Home visits and regular monitoring at heart failure clinics reduce the need for hospitalization and improve life expectancy.[59]

text: Medication[edit]

text: First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme (ACE) inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) if the person develops a long term cough as a side effect of the ACE-I.[60] Use of medicines from this class is associated with improved survival and quality of life in people with heart failure.[61]

text: Beta-adrenergic blocking agents (beta blockers) also form part of the first line of treatment, adding to the improvement in symptoms and mortality provided by ACE-I/ARB.[61][62] The mortality benefits of beta blockers in people with systolic dysfunction who also have atrial fibrillation (AF) is more limited than in those who do not have AF.[63] If the ejection fraction is not diminished (HFpEF), the benefits of beta blockers are more modest; a decrease in mortality has been observed but reduction in hospital admission for uncontrolled symptoms has not been observed.[64]

text: In people who are intolerant of ACE-I and ARBs or who have significant kidney dysfunction, the use of combined hydralazine and a long-acting nitrate, such as isosorbide dinitrate, is an effective alternate strategy. This regimen has been shown to reduce mortality in people with moderate heart failure.[65] It is especially beneficial in African-Americans (AA).[65] In AAs who are symptomatic, hydralazine and isosorbide dinitrate (H+I) can be added to ACE-I or ARBs.

text: In people with markedly reduced ejection fraction, the use of an aldosterone antagonist, in addition to beta blockers and ACE-I, can improve symptoms and reduce mortality.[66][67]

text: Second-line medications for CHF do not confer a mortality benefit. Digoxin is one such medication. Its narrow therapeutic window, a high degree of toxicity, and the failure of multiple trials to show a mortality benefit have reduced its role in clinical practice. It is now used in only a small number of people with refractory symptoms, who are in atrial fibrillation and/or who have chronic low blood pressure.

text: Diuretics have been a mainstay of treatment for treatment of fluid accumulation, and include diuretics classes such as loop diuretics, thiazide-like diuretic, and potassium-sparing diuretic. Although widely used, evidence on their efficacy and safety is limited, with the exception of mineralocorticoid antagonists such as spironolactone.[66][68] Mineralocorticoid antagonists in those under 75 years old appear to decrease the risk of death.[69] A recent Cochrane review found that in small studies, the use of diuretics appeared to have improved mortality in individuals with heart failure.[70] However, the extent to which these results can be extrapolated to a general population is unclear due to the small number of participants in the cited studies.[68]

text: Anemia is an independent factor in mortality in people with chronic heart failure. The treatment of anemia significantly improves quality of life for those with heart failure, often with a reduction in severity of the NYHA classification, and also improves mortality rates.[71][72] The latest European guidelines (2012) recommend screening for iron-deficient anemia and treating with parenteral iron if anemia is found.[73]

text: The decision to anticoagulate people with HF, typically with left ventricular ejection fractions <35% is debated, but generally, people with coexisting atrial fibrillation, a prior embolic event, or conditions which increase the risk of an embolic event such as amyloidosis, left ventricular noncompaction, familial dilated cardiomyopathy, or a thromboembolic event in a first-degree relative.[74]

text: Minimally invasive therapies[edit]

text: In people with severe cardiomyopathy (left ventricular ejection fraction below 35%), or in those with recurrent VT or malignant arrhythmias, treatment with an automatic implantable cardioverter defibrillator (AICD) is indicated to reduce the risk of severe life-threatening arrhythmias. The AICD does not improve symptoms or reduce the incidence of malignant arrhythmias but does reduce mortality from those arrhythmias, often in conjunction with antiarrhythmic medications. In people with left ventricular ejection (LVEF) below 35%, the incidence of ventricular tachycardia (VT) or sudden cardiac death is high enough to warrant AICD placement. Its use is therefore recommended in AHA/ACC guidelines.[17]

text: Cardiac contractility modulation (CCM) is a treatment for people with moderate to severe left ventricular systolic heart failure (NYHA class II–IV) which enhances both the strength of ventricular contraction and the heart's pumping capacity. The CCM mechanism is based on stimulation of the cardiac muscle by non-excitatory electrical signals (NES), which are delivered by a pacemaker-like device. CCM is particularly suitable for the treatment of heart failure with normal QRS complex duration (120 ms or less) and has been demonstrated to improve the symptoms, quality of life and exercise tolerance.[18][75][76][77][78] CCM is approved for use in Europe, but not currently in North America.[79][80]

text: About one third of people with LVEF below 35% have markedly altered conduction to the ventricles, resulting in dyssynchronous depolarization of the right and left ventricles. This is especially problematic in people with left bundle branch block (blockage of one of the two primary conducting fiber bundles that originate at the base of the heart and carries depolarizing impulses to the left ventricle). Using a special pacing algorithm, biventricular cardiac resynchronization therapy (CRT) can initiate a normal sequence of ventricular depolarization. In people with LVEF below 35% and prolonged QRS duration on ECG (LBBB or QRS of 150 ms or more) there is an improvement in symptoms and mortality when CRT is added to standard medical therapy.[81] However, in the two-thirds of people without prolonged QRS duration, CRT may actually be harmful.[17][18][82]

text: Surgical therapies[edit]

text: People with the most severe heart failure may be candidates for ventricular assist devices (VAD). VADs have commonly been used as a bridge to heart transplantation, but have been used more recently as a destination treatment for advanced heart failure.[83]

text: In select cases, heart transplantation can be considered. While this may resolve the problems associated with heart failure, the person must generally remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides.[84] A major limitation of this treatment option is the scarcity of hearts available for transplantation.

text: Palliative care[edit]

text: People with CHF often have significant symptoms, such as shortness of breath and chest pain. Palliative care should be initiated early in the HF trajectory, and should not be an option of last resort.[85] Palliative care can not only provide symptom management, but also assist with advanced care planning, goals of care in the case of a significant decline, and making sure the patient has a medical power of attorney and discussed his or her wishes with this individual.[86] A 2016 and 2017 review found that palliative care is associated with improved outcomes, such as quality of life, symptom burden, and satisfaction with care.[87][85]

text: Without transplantation, heart failure may not be reversible and cardiac function typically deteriorates with time. The growing number of patients with Stage IV heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines.[86]

text: Prognosis[edit]

text: Prognosis in heart failure can be assessed in multiple ways including clinical prediction rules and cardiopulmonary exercise testing. Clinical prediction rules use a composite of clinical factors such as lab tests and blood pressure to estimate prognosis. Among several clinical prediction rules for prognosticating acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying patients and identifying those at low risk of death during hospitalization or within 30 days.[88] Easy methods for identifying low-risk patients are:

text:
ADHERE Tree rule indicates that patients with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications.
BWH rule indicates that patients with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or fewer breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications.

text: A very important method for assessing prognosis in advanced heart failure patients is cardiopulmonary exercise testing (CPX testing). CPX testing is usually required prior to heart transplantation as an indicator of prognosis. Cardiopulmonary exercise testing involves measurement of exhaled oxygen and carbon dioxide during exercise. The peak oxygen consumption (VO2 max) is used as an indicator of prognosis. As a general rule, a VO2 max less than 12–14 cc/kg/min indicates a poor survival and suggests that the patient may be a candidate for a heart transplant. Patients with a VO2 max<10 cc/kg/min have a clearly poorer prognosis. The most recent International Society for Heart and Lung Transplantation (ISHLT) guidelines[89] also suggest two other parameters that can be used for evaluation of prognosis in advanced heart failure, the heart failure survival score and the use of a criterion of VE/VCO2 slope > 35 from the CPX test. The heart failure survival score is a score calculated using a combination of clinical predictors and the VO2 max from the cardiopulmonary exercise test.

text: Heart failure is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life.[90][91] With the exception of heart failure caused by reversible conditions, the condition usually worsens with time. Although some people survive many years, progressive disease is associated with an overall annual mortality rate of 10%.[92]

text: Approximately 18 of every 1000 persons will experience an ischemic stroke during the first year after diagnosis of HF. As the duration of follow-up increases, the stroke rate rises to nearly 50 strokes per 1000 cases of HF by 5 years.[93]

text: Epidemiology[edit]

text: In 2015 heart failure affected about 40 million people globally.[7] Overall around 2% of adults have heart failure[19] and in those over the age of 65, this increases to 6–10%.[3][8] Above 75 years old rates are greater than 10%.[19]

text: Rates are predicted to increase.[19] Increasing rates are mostly because of increasing life span, but also because of increased risk factors (hypertension, diabetes, dyslipidemia, and obesity) and improved survival rates from other types of cardiovascular disease (myocardial infarction, valvular disease, and arrhythmias).[94][95] Heart failure is the leading cause of hospitalization in people older than 65.[96]

text: United States[edit]

text: In the United States, heart failure affects 5.8 million people, and each year 550,000 new cases are diagnosed.[97] In 2011, congestive heart failure was the most common reason for hospitalization for adults aged 85 years and older, and the second most common for adults aged 65–84 years.[98] It is estimated that one in five adults at age 40 will develop heart failure during their remaining lifetime and about half of people who develop heart failure die within 5 years of diagnosis.[99] Heart failure is much higher in African Americans, Hispanics, Native Americans and recent immigrants from the eastern bloc countries like Russia. This high prevalence in these ethnic minority populations has been linked to high incidence of diabetes and hypertension. In many new immigrants to the U.S., the high prevalence of heart failure has largely been attributed to lack of preventive health care or substandard treatment.[100] Nearly one out of every four patients (24.7%) hospitalized in the U.S. with congestive heart failure are readmitted within 30 days.[101] Additionally, more than 50% of people seek re-admission within 6 months after treatment and the average duration of hospital stay is 6 days.

text: Congestive heart failure is a leading cause of hospital readmissions in the U.S. People aged 65 and older were readmitted at a rate of 24.5 per 100 admissions in 2011. In the same year, Medicaid patients were readmitted at a rate of 30.4 per 100 admissions, and uninsured patients were readmitted at a rate of 16.8 per 100 admissions. These are the highest readmission rates for both patient categories. Notably, congestive heart failure was not among the top ten conditions with the most 30-day readmissions among the privately insured.[102]

text: United Kingdom[edit]

text: In the UK has despite moderate improvements in prevention, heart failure rates have increased due to population growth and ageing.[103] Overall heart failure rates are similar to the four most common causes of cancer (breast, lung, prostate and colon) combined.[103] People from deprived backgrounds are more likely to be diagnosed with heart failure and at a younger age.[103]

text: Developing world[edit]

text: In tropical countries, the most common cause of HF is valvular heart disease or some type of cardiomyopathy. As underdeveloped countries have become more affluent, there has also been an increase in the incidence of diabetes, hypertension and obesity, which have in turn raised the incidence of heart failure.[104]

text: Sex[edit]

text: Men have a higher incidence of heart failure, but the overall prevalence rate is similar in both sexes since women survive longer after the onset of heart failure.[105] Women tend to be older when diagnosed with heart failure (after menopause), they are more likely than men to have diastolic dysfunction, and seem to experience a lower overall quality of life than men after diagnosis.[105]

text: Economics[edit]

text: In 2011, non-hypertensive congestive heart failure was one of the ten most expensive conditions seen during inpatient hospitalizations in the U.S., with aggregate inpatient hospital costs of more than $10.5 billion.[106]

text: Heart failure is associated with a high health expenditure, mostly because of the cost of hospitalizations; costs have been estimated to amount to 2% of the total budget of the National Health Service in the United Kingdom, and more than $35 billion in the United States.[107][108]

text: Research[edit]

text: There is low-quality evidence that stem cell therapy may help.[109][needs update] Although this evidence positively indicated benefit, the evidence was of lower quality than other evidence that does not indicate benefit.[110]

text: A previous claim, which came from a 2012 article published by the British Journal Heart, stated that a low salt diet increased the risk of death in those with congestive heart failure. This claim has since been withdrawn. The paper was retracted by the journal in 2013 because two of the cited studies contained duplicate data that could not be verified, and the data have since been lost.[111][112][113]

text: A 2016 Cochrane review found tentative evidence of longer life expectancy and improved left ventricular ejection fraction in persons treated with bone marrow-derived stem cells.[114]


document_title: Manslaughter in English law

question_text: what are the four requirements to establish criminal liability for gross negligence manslaughter

root

text: Manslaughter in English law

text: Voluntary manslaughter[edit]

text: Voluntary manslaughter occurs when the defendant kills with mens rea (an intention to kill or cause grievous bodily harm), but one of those partial defences which reduce murder to manslaughter applies (these consist of mitigating circumstances which reduce the defendant's culpability). The original mitigating factors were provocation and chance medley which existed at common law, but the former has been abolished by statute, the latter has been held no longer to exist[1] and new defences have been created by statute.

tag: p

text: The Homicide Act 1957 now provides two defences which may be raised to allow the court to find the accused guilty of voluntary manslaughter: diminished responsibility and suicide pact. The Coroners and Justice Act 2009 creates the defence of "loss of control".

text: Diminished responsibility[edit]

text: Under section 2 of the Homicide Act 1957 there are three requirements for the defendant to raise the defence of diminished responsibility. The defendant must have suffered from an abnormality of mind at the time of the killing caused by one of the causes specified by the Act which substantially impaired the defendant’s mental responsibility for the killing. Under section 2(2) of the Act it is for the defendant to prove he suffered from such a condition on the balance of probabilities.

text: Abnormality of mind[edit]

text: An abnormality of mind has been defined by Lord Parker CJ "as state of mind so different from that of ordinary human beings that the reasonable man would term it abnormal".[2] In deciding whether this state of mind exists the jury should consider medical evidence, but also all other evidence including acts and statements of the accused and his demeanour. The jury does not have to accept the medical evidence if other material conflicts with and outweighs it.

text: Specified causes[edit]

text: The Homicide Act specifies three causes one of which must cause the abnormality; they are a condition of arrested or retarded development of mind, any inherent cause or a disease or injury. Whether the abnormality is caused by one of the specified causes is a matter for medical evidence alone.[2] Alcoholism is capable of being an abnormality of mind even if there is no physical damage to the brain.[3]

text: Substantial impairment of mental responsibility[edit]

text: Whether the abnormality substantially impaired the defendant’s mental responsibility for the killing is a question of degree for the jury. In R v Lloyd the Court of Appeal held that the lack of control must simply be ‘more than trivial’.[4]

text: Loss of control[edit]

text: See sections 54 and 55 of the Coroners and Justice Act 2009.

text: Suicide pacts[edit]

text: Section 4(1) of the Homicide Act 1957 introduced the defence of suicide pact. Parliament's intention was to show some compassion for those who had been involved in a suicide pact but failed to die. Section 4(3) defines a suicide pact as "a common agreement between two or more persons having for its object the death of all of them, whether or not each is to take his own life". Further the accused must have had a "settled intention of dying in pursuance of the pact" to avoid the accused entering into a supposed pact with the real intention of committing murder. The Law Commission has proposed abolishing the defence with deserving cases falling within diminished responsibility,[5] but feels it should be retained pending a review of a new partial defence of mercy killings.[6]

text: Involuntary manslaughter[edit]

text: Involuntary manslaughter arises where the accused did not intend to cause death or serious injury but caused the death of another through recklessness or criminal negligence. For these purposes, recklessness is defined as a blatant disregard for the dangers of a particular situation. An example of this would be dropping a brick off a bridge, landing on a person's head, killing him. Since the intent is not to kill the victim, but simply to drop the brick, the mens rea required for murder does not exist because the act is not aimed at any one person. But if in dropping the brick, there is a good chance of injuring someone, the person who drops it will be reckless. This form of manslaughter is also termed "unlawful act" or "constructive" manslaughter.

text: Manslaughter by gross negligence[edit]

text: Under English law, where a person owes a duty of care (either by statute or by the neighbour principle[7]) and is negligent to such a degree that consequently the law regards it as a crime[8] (namely the person has been grossly negligent) and that person causes the victim to die, he may be liable for gross negligence manslaughter.[9] The defendants in such cases are often people carrying out jobs that require special skills or care, such as doctors, teachers, police or prison officers, or electricians, who fail to meet the standard which could be expected from a reasonable person of the same profession.[10] In R v Bateman[11] the Court of Criminal Appeal held that gross negligence manslaughter involved the following elements:

text:
the defendant owed a duty to the deceased to take care;
the defendant breached this duty;
the breach caused the death of the deceased; and
the defendant's negligence was gross, that is, it showed such a disregard for the life and safety of others as to amount to a crime and deserve punishment.

tag: ol

text: The House of Lords in Seymour[12] sought to identify the mens rea for "motor manslaughter" (negligently causing death when driving a motor vehicle). Reference was made to R v Caldwell and R v Lawrence[13][14] which held that a person was reckless if:

text:
he did an act which in fact created an obvious and serious risk of injury to the person or substantial damage to property; and
when he did the act he either had not given any thought to the possibility of there being any such risk or had recognised that there was some risk involved and had nonetheless gone on to do it.

text: The conclusion was that for motor manslaughter (and, by implication, for all cases of gross negligence), it was more appropriate to adopt this definition of recklessness. Consequently, if the defendant created an obvious and serious risk of causing physical injury to someone, there could be liability whether there was simple inadvertence or conscious risk-taking. It was no longer a defence to argue that the negligence had not been gross.

text: In Adomako[15] an anaesthetist failed to notice that a tube had become disconnected from the ventilator and the patient died. Lord Mackay disapproved Seymour and held that the Bateman test of gross negligence was the appropriate test in manslaughter cases involving a breach of duty, allowing the jury to consider the accused's conduct in all the surrounding circumstances, and to convict only if the negligence was very serious. Individuals have a duty to act in the following situations:

text:
to care for certain defined classes of helpless relatives, e.g. spouses must take care of each other, and parents must look after their dependent children. In R v Stone and Dobinson[16] an elderly woman with anorexia nervosa, came to stay with her brother and his cohabitee, who were both of low intelligence, and subsequently starved herself to death. The Court of Appeal held that the question whether the couple owed a duty to care for the deceased was a question of fact for the jury, which was entitled to take into account the facts that she was a relative of one of the appellants, that she was occupying a room in his house, and that the other appellant had undertaken the duty to care for her by trying to wash her and taking food to her.
where there is a contract (even if the person injured was outside the contractual relationship and, in the civil law would be barred by privity from enforcing the contract). In R v Pittwood 1902 TLR 37, a railway crossing gatekeeper had opened the gate to let a cart pass and forgot to shut it again. Later a hay cart was struck by a train while crossing. He was convicted of manslaughter. It was argued on his behalf that he owed a duty only to his employers, the railway company, with whom he had contracted. Wright J, held, however, that the man was paid to keep the gate shut and protect the public so had a duty to act. In contracts relating both to employment and to the provision of services, R v Yaqoob[17] considered a partner in a taxi firm who was responsible for making all necessary arrangements for the inspection and maintenance of a minibus which had overturned after its tyre burst, killing one of its passengers. He was convicted of manslaughter because the failure properly to maintain the minibus was the direct cause of the accident and there was an implied duty owed both to other members of the partnership and to those renting the vehicle, to inspect and maintain beyond the standard required for an MOT test, council inspections, and other duties imposed by regulation. The jury was competent to assess whether the failure to discharge that implied duty was gross negligence without hearing any expert evidence; these were not technical issues and they did not need expert help. The sentence of four years imprisonment was within the sentencing band and not excessive.

tag: ul

text: In Attorney-General’s Reference (No 2 of 1999),[18] a case on corporate manslaughter that arose out of the Southall rail crash, the Court of Appeal decided the defendant's subjective state of mind (i.e. whether there was conscious risk-taking) is irrelevant and, therefore, so is the question of recklessness, leaving the objective test as the only test for liability. Rose LJ, said:

text: Although there may be cases where the defendant’s state of mind is relevant to the jury’s consideration when assessing the grossness and criminality of his conduct, evidence of his state of mind is not a pre-requisite to a conviction for manslaughter by gross negligence. The Adomako test is objective, but a defendant who is reckless as defined in Stone may well be the more readily found to be grossly negligent to a criminal degree. In our judgment unless an identified individual’s conduct, characterisable as gross criminal negligence, can be attributed to the company, the company is not, in the present state of the common law, liable for manslaughter.

text: Civil negligence rules are not apt to confer criminal liability…the identification principle remains the only basis in common law for corporate liability for gross negligence manslaughter. (see imputation). This was only persuasive authority for the law of manslaughter at large, but R v DPP, ex p Jones[19] which said that the test of negligent manslaughter is objective, confirmed Attorney General’s Reference (No 2 of 1999) as a correct general statement of law.

text: Death by dangerous driving[edit]

text: Because of a reluctance by juries to convict when the charge was manslaughter, a statutory offence of "causing death by dangerous driving" was introduced. Following the Road Traffic Law Review Committee (1988), the Road Traffic Act 1991 abandoned recklessness in favour of the pre-statutory objective test of "dangerousness", i.e. did the driving fall far below the standard of the competent and careful driver. The Committee also recommended that manslaughter should be an optional charge for the more serious driving cases. There is the possibility of charging an aggravated taking without consent for less seriously dangerous driving where death results. An equivalent, in many American states, to motor manslaughter, is vehicular homicide. An equivalent to causing death by dangerous driving in Canada under the Criminal Code is Causing death by criminal negligence.

text: Manslaughter by an unlawful and dangerous act[edit]

text: Under English law, according to R v Creamer,[20] a person is guilty of involuntary manslaughter when he or she intends an unlawful act that is likely to do harm to the person, and death results which was neither foreseen nor intended. The name for this crime is 'manslaughter by an unlawful and dangerous act' (MUDA). The term 'constructive manslaughter' is commonly and correctly used as a synonym. Although the accused did not intend to cause serious harm or foresee the risk of doing so, and although an objective observer would not necessarily have predicted that serious harm would result, the accused's responsibility for causing death is constructed from the fault in committing what might have been a minor criminal act.

text: The case of R v Goodfellow[21] laid out a four-part requirement which if satisfied could lead to liability for MUDA. The person's action must:

text:
Be intentional
Be unlawful
Lead the reasonable person to realise that some other person is at risk of physical harm
Be the cause of death

text: A number of authorities clarify the test from R v Goodfellow:

text:
As to (1): either did the person intend to bring about the commission of the offence,[22] or was the outcome a virtual certainty that the person knew was a virtual certainty?.[23] If the answer to either of these questions is yes then the person's action was intentional.
As to (2): a full 'base offence' must be established, or else there can be no liability for MUDA.[24]
As to (3): the test is one of objective reasonableness and is a question for the jury to determine (i.e. to answer the question: "Would a reasonable person realise that the defendant's act was bound to subject some other person to the risk of physical harm?")
As to (4): was the act a cause in fact and in law? (see Causation (law) for details)

text: In R v Dawson,[25] a petrol station attendant with a weak heart died of heart failure when the appellant attempted a robbery of the station. In judging whether this act was sufficiently dangerous, the Court of Appeal applied a test based on the "sober and reasonable" bystander who could be assumed to know that the use of a replica gun was likely to terrify people and so be a danger to those with a weak heart. Note the aggravated form of criminal damage with intent to endanger life under section 1(2) of the Criminal Damage Act 1971 which could provide the unlawful act if the damage actually causes death. But R v Carey, C and F[26] limits the scope of unlawful act manslaughter. An argument became violent and the first defendant punched and kicked one victim. The second defendant assaulted the deceased by pulling her hair back and punching her in the face. The third defendant assaulted another. The deceased was one of the first to run away, after which she felt faint, and later died of a heart condition (ventricular fibrillation or dysrhythmia) which was congenital but which had not been diagnosed before her death. The unlawful act was said to be the affray and the judge held that it was legitimate to aggregate the violence by the other defendants in order to decide whether the affray had subjected the deceased to the threat of at least some physical harm, and so had been a cause of death. On appeal, it was inappropriate to hold the defendants liable for the death. There must be an unlawful act that was dangerous in the sense that sober and reasonable persons would recognise that the act was such as to subject Y to the risk of physical harm. In turn, that act must cause the death. When deciding whether an act is dangerous, knowledge of the victim's characteristics may be relevant. In this case, no reasonable person would have been aware of the victim's heart condition which distinguishes this case from Dawson, and from R v Watson[27] in which the victim's approximate age (he was 87 years old) and frail state would have been obvious to a reasonable person. A sober and reasonable person would not have foreseen that an apparently healthy person of 15 years would suffer shock as a result of it. The court held that the deceased's death was not caused by injuries that were a foreseeable result of the affray. The assault by the second defendant was an unlawful act causing death. The other two defendants could have been convicted by virtue of common purpose given that the death was an accidental departure from the general plan of the affray. But the Crown did not elect to present the case in this way, but pleaded the case as a public order group activity. The result would be that if anyone died in a general disturbance amounting to an affray, all those who participated could be convicted of manslaughter which would be against public policy. Deaths in a general disturbance are too remote to be caused by all participants.

text: Thus, a punch which causes a person to fall will almost inevitably satisfy the test of dangerousness, and where the victim falls and suffers a fatal head injury the accused is guilty of manslaughter. It is foreseeable that the victim is at risk of suffering some physical harm (albeit not serious harm) from such a punch and that is sufficient. Physical harm includes shock. The reason why the death resulting from the attempted robbery of the 60-year-old petrol station attendant was not manslaughter was that the attempted robbery was not dangerous in the relevant sense. It was not foreseeable that an apparently healthy 60-year-old man would suffer shock and a heart attack as a result of such an attempted robbery. But the jury properly found that it was foreseeable that an obviously frail and very old man was at risk of suffering shock leading to a heart attack as a result of a burglary committed at his home late at night.

text: In R v Charles James Brown,[28] following the break-up of his relationship with his girlfriend, at about 3 pm., the defendant sent a text message to his mother saying that he did not want to live any more. He then drove his car against the flow of traffic along the hard shoulder of the A1(M) at high speed, before moving into the carriageway, still accelerating and straddling the centre line. He then crashed, head on, into an oncoming car, killing the passenger and injuring many others in the resulting consequential crashes. A sentence of 10 years' detention in a young offender institution was upheld because although the intentional focus might have been only on suicide, the defendant must have known from the way he was driving that he would kill or injure at least one other person (thus enforcing an objective standard on the defendant).

text: Unlawful (constructive) act manslaughter and the liability imposed on drug suppliers[edit]

text: The law on those who supply the (post) deceased with drugs had been uncertain until the case of R v Kennedy.[29] The defendant supplied heroin to a drug user that asked for something to help them sleep. An hour after administering the drug the victim died. Kennedy was found guilty of manslaughter and appealed on the grounds that there must be an unlawful act which caused the victim's death. In this case the defendant set up the drug and supplied it but did not administer it, therefore it was an act of the victim himself that caused his own death. Kennedy was acquitted of manslaughter. Prior to this House of Lords ruling, the lower courts (in particular the Court of Appeal) struggled to strike a balance between those suppliers considered to have administered the drug (in the subsequent cases, heroin) to the victim themselves, and those suppliers who simply "supply" the drug for the victim to then voluntarily administer themselves.[30]

text: Defence[edit]

text: Infanticide is a partial defence to manslaughter under the Infanticide Act 1938 (as amended by section 57 the Coroners and Justice Act 2009 to confirm the decision in R v Gore[31]) and reduces the manslaughter to the crime of infanticide.

text: Mode of trial and sentence[edit]

text: Manslaughter is an indictable-only offence.

text: A person guilty of manslaughter is liable to imprisonment for life or for any shorter term.[32]

text: For case law on sentencing see the Crown Prosecution Service sentencing manual:

text:
Involuntary manslaughter[33]
Manslaughter - diminished responsibility[34]
Manslaughter - provocation[35]
Manslaughter - suicide pact[36]

text: Attempt[edit]

text: In R v Creamer,[20] the court said obiter that attempted manslaughter is not an offence known to law.[37]

text: History[edit]

text: Voluntary manslaughter - former partial defence of provocation[edit]

text: Provocation in English law was abolished on 4 October 2010[38] by section 56(1) of the Coroners and Justice Act 2009,[39] but replaced by the similar partial defence of "loss of control".

text: Acts constituting provocation[edit]

text: At common law, acts of provocation had to be actual violence towards the defendant; words could not amount to provocation. The two exceptions to this rule were a husband discovering his wife committing adultery and a father finding someone buggering his son. There were two limbs to the defence, first the defendant had to have actually been provoked, and second the provocation had to be such as would have made the reasonable man act as the defendant did. The Homicide Act 1957 removed all limits on what could amount to provocation and allowed it to include provocation from someone other than the victim,[40] and aimed at someone other than the accused.[41] Further the defence was not defeated by the fact that the defendant induced the provocation.[42] Section 56[43] of the Coroners and Justice Act 2009 states that the common law defence of provocation is abolished and replaced by sections 54 and 55; and that section 3 of the Homicide Act 1957 is also abolished and replaced with sections 54 and 55.

text: Subjective limb: provocation in fact[edit]

text: This was a question of fact for the jury. The loss of control had to be sudden and temporary,[44] however it could be the result of slow burn; the final straw needed not be very bad as long as it led to an actual sudden and temporary loss of control. A delay between the act of provocation and the killing did not always defeat the defence, but often would.[45]

text: Objective limb: the reasonable man test[edit]

text: Under section 3 of the Homicide Act 1957 the second question to be answered by the jury in order for the defence to succeed was ‘whether the provocation was enough to make a reasonable man act as [the defendant] did?’. The reasonable man for the purposes of this test had the same sex and age as the defendant and shared such characteristics as affect the gravity of the provocation to the defendant, but characteristics irrelevant to the provocation such as unrelated mental disorders were not given to the reasonable man.[46] Finally, the reasonable man always had reasonable powers of self-control[47] and was never intoxicated.[48]


document_title: Pete's Dragon (2016 film)

question_text: where was the new pete's dragon filmed

question_tokens: where was the new pete 's dragon filmed

text: Pete's Dragon (2016 film)

text: Plot[edit]

text: In 1977, Pete Healy, a five-year-old boy, is on a road trip with his parents when their car flips off the road following a near-collision with a deer. Pete’s mom and dad are killed, but Pete survives the accident and is chased into the forest by a pack of wolves. He is rescued by a huge dragon with green fur, yellow eyes, and wings. The dragon quickly bonds with Pete and becomes protective of the boy. Pete names the dragon "Elliot" after the character of a lost puppy from his favorite book.

text: Six years later, Pete, now 11, spots a lumberjack crew chopping down trees near his home. Natalie, the daughter of the ethical site foreman Jack, spots and chases him. When Natalie accidentally falls from a tree, her screams attract her father Jack and his girlfriend, park ranger Grace Meacham. Pete tries to run away, but Gavin, Jack's pragmatic brother, accidentally knocks him unconscious. After realizing that Pete has vanished, Elliot stumbles around looking for him and ends up knocking over a tree near the lumber camp, leading Gavin to organize a hunting party to find him. Meanwhile, Pete wakes up in a local hospital, which he escapes in an effort to return to the forest. Before the police can catch the boy, Grace finds Pete and asks him to come to her home and promises to take him to the forest the next day.

text: Gavin and his men locate Pete and Elliot's treehouse, but when they try to search it, Elliot reveals himself and scares them away. He follows them to town trying to find Pete. After seeing Pete settling in with Grace's family, he leaves. After Pete gives Grace a drawing of Elliot, she shows her father, Mr. Meacham. He says that he discovered the same dragon as a young man. He advises her to trust Pete, and to find Elliot.

text: The next day, Pete, Grace, Natalie, and Mr. Meacham travel to the forest to meet Elliot. A group of hunters led by Gavin surprise Elliot and shoot him with tranquilizer darts, then lock him up in Jack's warehouse. Before the authorities can inspect the dragon, Pete and Natalie free him from his chains and escape on a lumber truck with Mr. Meacham.

text: Angered, Gavin sets up a roadblock at the bridge to stop them. When Elliot tries to fly, he crashes into the truck, damaging its brakes and it goes through the barricade. Confused and frightened, Elliot perches on top of the bridge and starts breathing fire at the police. The bridge begins to collapse under the intense heat, causing Grace and Jack's truck to fall through. Gavin tries to save the pair from falling to their deaths. Elliot emerges from the ravine with Grace and Jack riding safely on his back. With a firefighting helicopter approaching, Pete decides to flee with Elliot back to the woods.

text: Pete pleads with Elliot to let him stay so he can protect him from his attackers, just as Elliot protected him. However, Elliot concludes that as long as they stay close together, Pete will always be in danger. He points out Pete's book to encourage him to return to stay with Grace and Jack. Pete is reluctant & worried for Elliott's safety, but ultimately trusts the dragon's judgment. After a very tearful hug, Elliot returns to the mountains and Pete returns to live with Grace and Jack as his new family.

text: In the years that follow, Grace and Jack marry and adopt Pete as their son. Not only has Elliot slowly faded from the town's memory, but Gavin has learned to be more scrupulous and has moved on from the experience. Pete and his family eventually go on vacation, and see that Elliot is finally reunited with his fellow dragons.

text: Cast[edit]

text:
Bryce Dallas Howard as Grace Meacham, a forest ranger.
Oakes Fegley as Pete Healy, a young orphan who lives in the forest with Elliot the Dragon.
Levi Alexander as 5-year-old Pete
Wes Bentley as Jack Magary, a widowed lumber mill owner who is Natalie's father and Grace's boyfriend. He has a moral compass and tries to restrain his brother Gavin's more unethical tendencies.
Karl Urban as Gavin Magary, a hunter and lumberjack who is Jack's brother and Natalie's uncle. He is a pragmatic man who chafes under his brother's scruples.[5]
Oona Laurence as Natalie Magary, Jack's daughter and Gavin's niece.
Robert Redford as Mr. Meacham, Grace's father
Isiah Whitlock Jr. as Sheriff Gene Dentler
Marcus Henderson as Woodrow, a lumberjack
Aaron Jackson as Abner, a lumberjack
Phil Grieve as Bobby, a lumberjack
Jim McLarty as Ranger Wentworth
Ian Harcourt as Deputy West
Steve Barr as Deputy Smalls
John Kassir as the voice of Elliot the Dragon

text: Production[edit]

text: In March 2013, Walt Disney Pictures announced it would remake Pete's Dragon, as non-musical, dramatic film to be written by David Lowery and Toby Halbrooks, and directed by Lowery. Disney intended to rework the core story as a dramatic story, rather than a musical. It set the new work in the Pacific Northwest of the early 1980s, rather than the Northern New England of the early 1900s in the 1977 film.[6][7]

text: The film was shot in live-action using Panavision Panaflex cameras. The dragon, Elliot, was entirely animated by Weta Digital in CGI, instead of the original hand-drawn animation.[8][9]

text: On September 19, 2014, Disney cast Oakes Fegley and Oona Laurence to star as Pete and Natalie.[10] On October 2, Barrie M. Osborne was set to be the executive producer for the film.[11] On October 16, Robert Redford was in early talks to play a local storyteller who remembers seeing a dragon in the woods.[8] On November 20, Bryce Dallas Howard was in talks for the female lead role, a forest ranger who finds the boy and does not believe his stories about a dragon.[12] On January 7, 2015, Wes Bentley joined the cast of the film.[13] On January 9, Michael C. Hall was also added to the cast.[14] On January 29, Karl Urban replaced Hall.[15]

text: Principal photography commenced in January 2015 in New Zealand, with Lowery directing.[16] Rehearsals began early January 2015,[17] while news reported the beginning of the shooting on January 26, 2015, set to last through April.[8][18] Live-action filming locations included Bay of Plenty, Taupo and Wellington, while CGI was done at Stone Street Studios.[19] On February 10, 2015, a press release confirmed that principal photography had commenced.[9] Shooting took place in and around Wellington and Rotorua, before transferring to Tapanui, where the old Blue Mountain Lumber mill was used as the mill in the film, and the main street became Millhaven for two weeks.[20][21] Production concluded on April 30, 2015.[22]

text: Soundtrack[edit]

text:
Pete's Dragon (Original Motion Picture Soundtrack)Soundtrack album / Film score by Daniel HartReleased
August 12, 2016Recorded
2016Studio
Air StudiosBritish Grove StudiosGenre
Soundtrack, Film scoreLength
75:29Label
Walt DisneyProducer

Daniel Hart
Jake Jackson
David Lowery (exec.)
Jim Whitaker (exec.)
Adam Borba (exec.)
Daniel Hart film scores chronology

Lost in the Sun(2015)Lost in the Sun2015

Pete's Dragon(2016)

Half the Perfect World(2016)Half the Perfect World2016

tag: table

text:
Academy Award-winning composer Howard Shore was originally chosen to write the music for the film.
He was replaced during post-production by Daniel Hart, who had previously worked with director Lowery on other films, most notably Ain't Them Bodies Saints (2013).[23] The soundtrack was released on August 12, 2016 by Walt Disney Records.  Candle on the Water was the only original song to be featured on the 2016 soundtrack from the 1977 soundtrack.  Though the song was not used in the film, it was re-recorded by Okkervil River for the 2016 soundtrack.  The original version, performed by Australian singer Helen Reddy (who played Nora in the original film), was nominated for the Academy Award for Best Song in 1977.

text: Track listing[edit]

text: No.TitlePerformer(s)Length1."The Dragon Song"Bonnie “Prince” Billy2:282."Something Wild"Lindsey Stirling and Andrew McMahon in the Wilderness3:433."Nobody Knows"The Lumineers3:084."Something on Your Mind"St. Vincent2:595."So Long, Marianne"Leonard Cohen5:386."Gina Anne"Bosque Brown2:407."An Adventure" 3:048."Are You Gonna Eat Me?" 2:319."Brown Bunny" 1:0110."Reverie" 2:5211."Tree Fort" 1:0312."North Star" 1:2513."Bedtime Compass" 2:1514."Timber" 1:1915."Breathe" 2:2716."Gavin Knows What He's Doing" 3:4217."You Are Not Alone" 1:5818."Elliot Gets Lost" 4:2619."Takedown" 1:4420."It'll Be Just Like It Used to Be" 2:0321."Follow That Dragon" 3:0122."Elliot at the Bridge" 2:1923."Abyss" 1:3524."Go North" 1:4425."Saying Goodbye" 5:0326."The Bravest Boy I've Ever Met" 2:4627."The Dragon Song Revisited"Bonnie “Prince” Billy2:3428."Candle on the Water"Okkervil River4:01Total length:75:29

text: Reception[edit]

text: Box office[edit]

text: Pete's Dragon grossed $76.2 million in North America and $67.5 million in other territories, for a worldwide total of $143.7 million, against a budget of $65 million.[2]

text: In the United States and Canada, Pete's Dragon opened on August 12, 2016, across 3,702 theaters, of which 2,884 were in 3D, and 150 were premium large-format screens, as well as in 57 D-Box and 16 Dolby Cinema sites.[24] It was projected to gross $20–25 million in its opening weekend.[25] The film did not have Thursday night previews, and made $7 million on its first day, Friday.[26] In its opening weekend, it earned $21.5 million, finishing third at the box office, behind Suicide Squad and Sausage Party.[27] The opening was reminiscent of Disney's July release The BFG, which also carried strong reviews into the weekend only to deliver $18.7 million in its first three days,[28] and far from the $67–116 million debuts of other Disney live action-adaptations, such as Cinderella, Maleficent, Oz: The Great and Powerful, The Jungle Book and Alice in Wonderland. However, many box office critics did not worry about the opening figure, given the film's modest budget, and the fact that the film is not anywhere near as well known as those films' respective source material.[26][29] Disney’s distribution chief Dave Hollis was optimistic that film would become profitable by saying, "People who are coming out of the theater are just loving it and their advocacy is going to help us put together a nice, solid run."[30] Forbes noted that the film did not have any box office draws other than the stellar reviews and the notion of another Disney "live-action fairy tale."[26] Although the film witnessed a steep decline on its second Friday (-55%), it fell just by 47.2% on its second weekend, grossing $11.3 million.[31] On its third weekend, it fell just by 35%, grossing $7.3 million.[32] The following weekend, Pete's Dragon declined only 14.7%, grossing $6.5 million and moved up to fourth place.[33][34]

text: Outside North America, Pete's Dragon received a scattered release pattern.[35] The film was released day-and-date in conjucture with its U.S. premiere in 12 markets (roughly 30% of the overseas market), including the United Kingdom, Italy, and Russia.[24] It earned a total of $5.3 million, with Russia ($1.5 million), Italy ($1.4 million) and the U.K. ($1.1 million) representing its largest takings.[35] Moreover, it also opened in France ($1.8 million).[36] It had just a 1% drop in attendance in the U.K. in its second weekend.[36] It expanded to Germany the following weekend and continued its roll out in Australia, Mexico, Brazil and Korea throughout September, and finally Japan on December 23.[25][35]

text: Critical response[edit]

text: Review aggregator Rotten Tomatoes gives the film an approval rating of 88%, based on 216 reviews, with an average rating of 7.3/10. The website's critical consensus reads, "Pete's Dragon continues Disney's current live-action winning streak with an update that gives the original a visual overhaul without overwhelming its sweet, soulful charm."[37] On Metacritic, the film has a score of 71 out of 100, based on 42 critics, indicating "generally favorable reviews".[38] Audiences polled by CinemaScore gave the film an average grade of "A".[39]

text: The movie was given three-and-a-half out of four stars in The New York Post by Kyle Smith who called it, "A cinematic enchantment" as well as, "one of the year’s best movies."[40] Peter Travers of Rolling Stone gave the film 3 out of 4 stars and wrote, "Thanks to director David Lowery's humanizing magic, this tale of an orphan boy and a dragon is that rare family film you really can take to heart."[41] Nancy Churnin of The Dallas Morning News gave the film a "B+" and said that while the remake, "may owe more to E.T. the Extra-Terrestrial, along with a dash of The Jungle Book than it does to the original Pete's Dragon," she overall concluded that "this story of two vulnerable souls who help each other find their way works, too."[42] Barry Hertz of The Globe and Mail praised the film for its sincerity as well as its "honest effort to entertain and enthrall" audiences rather than simply being a cash grab.[43]

text: Glenn Kenny of The New York Times felt mixed about the film in his review saying, "It is slightly unfair to say that this reboot of Pete's Dragon is middling on a larger scale, but it's not entirely inaccurate either."[44] Michael O'Sullivan of The Washington Post gave the film two out of four stars and wrote, "While Pete's Dragon does a fine job of evoking the delight one might feel at flying over hill and dale on the back of a mythological creature, it is less successful in rendering real human emotion."[45]

text: Accolades[edit]

text:
Award

Date of Ceremony

Category

Recipient(s)

Result

Ref(s)

Golden Tomato Awards

January 12, 2017

Best Kids/Family Movie 2016

Pete's Dragon

4th Place

[46]

Heartland Film Festival

October 30, 2016

Truly Moving Picture Award

David Lowery, Walt Disney Pictures and Walt Disney Studios Motion Pictures

Won

[47]

Nickelodeon Kids' Choice Awards

March 11, 2017

Favorite Movie

Pete's Dragon

Nominated

[48]

Saturn Awards

June 28, 2017

Best Fantasy Film

Pete's Dragon

Nominated

[49]

text: Home media[edit]

text: Pete's Dragon was released on Blu-ray, DVD and digital download on November 29, 2016.[50] The film topped the home video sales charts for the week ending on December 4, 2016.[51]

text: The movie is available on Netflix "watch instantly" as of March 15, 2017.[52]


document_title: A Hologram for the King (film)

question_text: where was a hologram for the king filmed

text: A Hologram for the King (film)

text: Synopsis[edit]

text: The film tells the story of a washed-up, desperate American salesman who travels to Saudi Arabia to sell a holographic teleconferencing system to the Saudi government.[7][9] Set in 2010, before the Arab Spring, American consultant Alan Clay is depressed after losing his house and being divorced by his wife during the Great Recession; he arrives in Jeddah, Saudi Arabia to make a sale in an upcoming development called the King’s Metropolis of Economy and Trade (a fictionalized version of King Abdullah Economic City).[9]

text: Cast[edit]

text:
Tom Hanks as Alan Clay
Alexander Black as Yousef, Alan's driver
Sarita Choudhury as Zahra
Sidse Babett Knudsen as Hanne
Ben Whishaw as Dave
Tom Skerritt as Ron, Alan's father
Tracey Fairaway as Kit, Alan's daughter
David Menkin as Brad
Khalid Laith as Karim Al-Ahmed
Rolf Saxon as Joe Trivoli
Jay Abdo as Dr. Hadad
Dhaffer L'Abidine as Hassan

text: Production[edit]

text: Development[edit]

text: On June 12, 2013, Tom Tykwer was reported to be developing an adaptation of 2012 novel A Hologram for the King, written by Dave Eggers. Tykwer wrote and directed the film, which stars Tom Hanks as the lead. The film was made by Playtone, Primeridian Entertainment, and X-Filme Creative Pool.[6] On September 5, 2013, Lotus Entertainment began licensing international rights to the film.[10] On March 6, 2014 it was announced that Sarita Choudhury, Alexander Black, Tracey Fairaway, David Menkin, and Tom Skerritt had joined the cast of the film.[11]

text: Filming[edit]

text: Production was set to begin in first quarter of 2014.[10] Principal photography commenced on March 6, 2014 in Morocco.[12] Filming also took place in Hurghada in Egypt, as well as in Berlin and Düsseldorf in Germany. Shooting wrapped in June 2014.[13][14]

text: Reception[edit]

text: Critical response[edit]

text: Writing for the New York Times, Stephen Holden called the movie "a story of confusion, perplexity, frustration and panic," praising Tom Hanks's ability to turn it into "an agreeably uncomfortable comedy," meriting a "Critic's Pick" designation.[15] On Rotten Tomatoes, the film has a rating of 73% based on 139 reviews and an average rating of 6.2/10. The site's critical consensus reads, "A Hologram for the King amiably ambles through a narrative desert, saved by an oasis of a performance from the ever-dependable Tom Hanks."[16] On Metacritic, the film has a score of 59 out of 100 based on 30 critics, indicating "mixed or average reviews".[17]

text: Box office[edit]

text: The film grossed $1.1 million in its opening weekend, finishing 11th at the box office. With a total worldwide gross of $8,244,651 (U.S. domestic gross of $4,212,494), it is the lowest-grossing film to feature Tom Hanks in top billing since Every Time We Say Goodbye in 1986.[8]


document_title: Great Victoria Desert

question_text: what kind of animals live in the great victoria desert

text: Great Victoria Desert

text: Location and description[edit]

text: The Great Victoria is the largest desert in Australia[1] and consists of many small sandhills, grassland plains, areas with a closely packed surface of pebbles (called desert pavement or gibber plains) and salt lakes. It is over 700 kilometres (430 mi) wide (from west to east) and covers an area of 348,750 square kilometres (134,650 sq mi) from the Eastern Goldfields region of Western Australia to the Gawler Ranges in South Australia. The Western Australia Mallee shrub ecoregion lies to the west, the Little Sandy Desert to the northwest, the Gibson Desert and the Central Ranges xeric shrublands to the north, the Tirari and Sturt Stony deserts to the east, while the Nullarbor Plain to the south separates it from the Southern Ocean. Average annual rainfall is low and irregular, ranging from 200 to 250 mm (7.9 to 9.8 in) per year. Thunderstorms are relatively common in the Great Victoria Desert, with an average of 15–20 thunderstorms per annum. Summer daytime temperatures range from 32 to 40 °C (90 to 104 °F) while in winter, this falls to 18 to 23 °C (64 to 73 °F).

text: Habitation[edit]

text: The majority of people living in the region are Indigenous Australians from different groups including the Kogara, the Mirning and the Pitjantjatjara. It is the part of Australia with the most populous and most healthy indigenous population.[citation needed] Aboriginal populations have been increasing in this region. Young Indigenous adults from the Great Victoria Desert region work in the Wilurarra Creative programs to maintain and develop their culture.[2]

text: Despite its isolated location the Great Victoria is bisected by very rough tracks including the Connie Sue Highway and the Anne Beadell Highway.

text: Human activity has included some mining and nuclear weapons testing.[3]

text: History[edit]

text: In 1875, British explorer Ernest Giles became the first European to cross the desert. He named the desert after the then-reigning British monarch, Queen Victoria. In 1891, David Lindsey's expedition traveled across this area from north to south. Frank Hann was looking for gold in this area between 1903 and 1908. Len Beadell explored the area in the 1960s.

text: Environment[edit]

text: The Great Victoria desert is a World Wildlife Fund ecoregion [4] and an Interim Biogeographic Regionalisation for Australia (IBRA) region of the same name.[5]

text: As this area has had very limited use for agriculture, habitats remain largely undisturbed while parts of the desert are protected areas including Mamungari Conservation Park (formerly known as Unnamed Conservation Park) in South Australia, a large area of pristine arid zone wilderness which possesses cultural significance and is one of the fourteen World Biosphere Reserves[6] in Australia. Habitat is also preserved in the large Aboriginal local government area of Anangu Pitjantjatjara Yankunytjatjara in South Australia and in the Great Victoria Desert Nature Reserve of Western Australia.

text: The nuclear weapons trials carried out by the United Kingdom at Maralinga and Emu Field in the 1950s and early 1960s have left areas contaminated with plutonium-239 and other radioactive material.

text: Flora[edit]

text: Only the hardiest of plants can survive in much of this environment. Between the sand ridges there are areas of wooded steppe consisting of Eucalyptus gongylocarpa, Eucalyptus youngiana and mulga (Acacia aneura) shrubs scattered over areas of resilient spinifex grasses particularly Triodia basedowii.

text: Fauna[edit]

text: Wildlife adapted to these harsh conditions includes few large birds or mammals. However, the desert does sustain many types of lizard including the vulnerable great desert skink (Egernia kintorei) and a number of small marsupials including the endangered sandhill dunnart (Sminthopsis psammophila) and the crest-tailed mulgara (Dasycercus cristicauda). One way to survive here is to burrow into the sands, as a number of the desert's animals, including the southern marsupial mole (Notoryctes typhlops), and the water-holding frog do. Birds include the chestnut-breasted whiteface (Aphelocephala pectoralis) found on the eastern edge of the desert and the malleefowl of Mamungari Conservation Park. Predators of the desert include the dingo (as the desert is north of the Dingo Fence) and two large monitor lizards, the perentie (Varanus giganteus) and the sand goanna (Varanus gouldii).