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Hypertension is the presence of persistently elevated blood pressure. Approximately one third of adults (men and women) have hypertension with the condition being more prevalent as people get older.

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i.Primary hypertension: when blood pressure is elevated without evidence of another disease causing it. The set point for blood pressure control is elevated and therefore homeostatic mechanisms work to that set point. The exact causes of primary hypertension are therefore unclear but are thought to be multifactorial, including a potential genetic predisposition and complex interrelationship between the renal system, a hyperactive sympathetic nervous system and a hypersensitive RAAS. This form of hypertension is referred to as essential or idiopathic hypertension.

ii.Secondary hypertension: when another disorder causes blood pressure to rise; about 5% of people with hypertension have this form. This can be seen in renal disease, responses to medication, altered hormonal regulation and physiological factors such as coarctation of the aorta (congenital narrowing of the aorta).

iii.Malignant (hypertensive crisis): occurs rapidly to extreme levels (systolic >180 mmHg) in association with bilateral retinal haemorrhages and/or exudates (± papilloedema) that can lead to organ damage.

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Failure of the heart to effectively pump blood around the body, meaning its ability to respond to any increased demands for cardiac output is impaired.

Answer: Coronary artery disease and hypertension are leading causes of heart failure.

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·    Systolic and/or diastolic dysfunction that leads to a drop in cardiac output.

·    A result of myocardial oxygen demand surpassing supply and can occur as a result of impeded or occluded coronary circulation.

·    With supply lower than demand, hypoxia occurs resulting in cell injury or death leading to the myocardium that can no longer beat with the usual strength and efficiency.

·    In response, cardiac myocytes expand and stretch to compensate, becoming hypertrophied and less effective.

·    When these changes are progressive and large scale, the heart appears enlarged as a result of hypertrophy.

·    As the myocytes are less effective in this state, the ability of the heart to pump efficiently is impaired.

·    There can be impaired perfusion of the tissues in front of the pump (i.e. to the lungs or the rest of the body) and there may also be congestion behind the pump.

·    This congestion can occur in the pulmonary circulation or systemically (or both), depending on which side of the heart is affected. Cardiac output decreases and this can result in a backup of blood in the circulation behind the affected side of the heart.

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Oedema is the observable accumulation of excess interstitial fluid secondary to an imbalance between capillary filtration and lymph drainage.

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·    Venous hypertension: As explained in the section on heart failure, systemic and pulmonary oedema can occur as a result of an increase in hydrostatic pressure in the venous circulation in systemic and pulmonary circulation respectively. This impacts upon capillary filtration by preventing effective return of fluid back into capillaries.

·    Lymphatic insufficiency: If the lymphatic circulation is chronically overloaded by excess capillary filtrate, then lymphatic vessels will eventually fail. This will cause lymphoedema. Another cause is when lymph vessels are surgically removed (e.g. as part of surgery for breast cancer) and lymphatic drainage is no longer available or insufficient.

·    Malnutrition: Malnutrition can cause a reduction in the amount of plasma protein in the systemic circulation, most notably albumin. Plasma proteins provide osmotic pressure that holds fluid in the plasma and drawing it from the interstitial fluid. If this osmotic pressure in the circulation drops, then fluid is lost to the interstitial space and may not be picked up by the lymphatic system. This can lead to oedema formation.

·    Inflammatory response: An inflammatory response will cause localised oedema as a result of increased vascular permeability. This can be seen at a systemic level in sepsis and in thermal injuries (burns).

Answer: Arrhythmias are disorders of the cardiac conduction cycle causing an irregular heart beat.

Answer: They can be atrial in origin (or supraventricular) or ventricular in origin. Those that are atrial in origin occur in the atrial wall, sino-atrial node (SA node), atrioventricular node (AV node) or in the junctional tissues. Ventricular arrhythmias originate in the ventricular muscle or conduction system and are generally urgent and life-threatening.

Answer: Atrial fibrillation is uncoordinated atrial activation and irregular discharge that results in a deterioration in atrial function. It is thought to occur through one of three conductive processes:

·    Local ectopic rapidly discharging driver that gives rise to an irregular atrial response

·    Single localised re-entry circuit

·    Multiple functional re-entry circuits

Ion channel dysfunction, calcium regulation abnormalities, structural remodelling and autonomic dysregulation are the primary causes of these irregular processes.

Irregular depolarisation gives rise to fibrillation waves on ECG where a P wave (indicating atrial function) would have been expected.

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SADS refers to the sudden, untimely death of a young, apparently fit and healthy person. When that death is thought to be as a direct result of cardiac disease, it is referred to as a sudden cardiac death; in SADS the origins are thought to be arrhythmogenic in origin and often have no identifiable cause.. Coronary artery disease and acute myocardial infarction are common causes in older adults, whereas disorders with genetic origins are more prevalent in those aged 40 and under.

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i.Abnormalities of repolarisation and the QT interval: In these cases, there is prolonged repolarisation that extends the QT interval leading to syncope or cardiac arrest as a result of a polymorphic VT. A rare cause is short QT syndrome which can also lead to a polymorphic VT.

ii.Catecholaminergic polymorphic VT: Catecholaminergic polymorphic VT also is characterised with syncope or cardiac arrest and is related to emotional state/upset and physical exertion. This is as a result of calcium dysregulation is the presence of catecholamine release.

iii.Inherited cardiomyopathies: A genetically inherited condition, hypertrophic cardiomyopathy has been isolated as the most common genetic cardiac disorder that results in sudden death before 35 years of age. In cardiomyopathy, the ventricles stretch and become less effective. There can be development of scar tissue which can lead to VT, particularly polymorphic VT, and VF (see pathophysiological causes under VT and VF above).

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A group of cardiac disorders that affect the myocardium. They can be primary cardiomyopathies, whereby the origin is largely unknown, or secondary, where the condition occurs secondary to another disorder.

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Narrowing of the aorta that restricts the blood flow from the left ventricle. Over time, because the heart is pumping against resistance, it can lead to left ventricular pressure overload, left ventricular hypertrophy and eventually left ventricular failure (heart failure).

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AVSD is a spectrum of defects where there is incomplete development of the atrioventricular septum alongside atrioventricular (AV) valve abnormalities. AVSD is characterised by abnormal fusion of the superior and inferior endocardial cushions in the atrial and ventricular septum. Additionally, the AV node and bundle of His are displaced inferiorly. Theses structural abnormalities make it possible for blood to be shunted to and from both sides of the heart and for arrhythmias to occur.