learning outcomes

Question 1

Explain the generation of heart sounds (phonocardiogram).b

Answer 1

the phonocardiogram is a recording of the sounds and murmurs made by the heart using a phonocardiograph. It works by plotting vibrations made by the closure of the atrioventricular valves and the closure of the semilunar valves. It’s more accurate than a stethoscope for tracking heart functions.

Question 2

Illustrate the sequence of changes in pressure and volume in the chambers of the heart throughout the cardiac cycle.

Answer 2

initially we have the late diastole, in which both sets of chambers are relaxed and fill passively. The next phase is the atrial systole in which the atria contracts and forces a small amount of blood into the already filled ventricle valve through the Atrioventricular valves, but there isn’t sufficient pressure for opening the semilunar valves. The ventricles then contracts, forcing open the semilunar valves and the blood is ejected in ventricular systole, and atria at this point is in diastole. There is the then the isovolumic ventricular relaxation as the ventricles relax, and the pressure falls closing the semilunar valves. Then we go back to the late diastole phase.
closure of the tricuspid and bicuspid valve is S1 which makes the first heart sound, the closure of the semilunar valves is S2 making the two heart sounds.

Question 3

Explain the significance of Starling forces and the lymphatic system in relation to oedema.

Answer 3

starlings forces varies in capillary bed, due to the osmotic pressure forcing fluid into the capillaries, as fluid if forced out of the capillaries through hydrostatic pressure. Overall 20 litres is lost through this and 17 litres is regained this way, the remaining 3 litres is absorbed by the lymphatic system. An oedema is formed through the accumulation of excess fluid, this may be due to lymphatic obstruction through surgery or filariasis, raised central venous pressure from ventricular failure, hypoproteinaemia from nephrosis, liver failure and nutrition or increased capillary permeability from inflammation or rheumatism

Question 4

Identify the processes involved in transport between capillaries and tissues.

Answer 4

the gross structure of the capillaries is designed for exchange, with lots of thin walled capillaries with such a small diameter resulted in a large surface area to volume ratio. They had either leaky endothelial junctions, or fenestrated pores to allow for exchange or discontinuous with massive channels. The process itself is either through the self-regulating diffusion, or by carrier mediated transport such as the glucose transporter.

Question 5

Describe the mechanism that prevents blood clotting in vessels.

Answer 5

clotting involves the formation of a platelet clot and fibrin clot. The fibrin is formed from fibrinogen being activated by thrombin to fibrin which then binds around the platelet plug adhering to the basement membrane. The anti-clotting mechanisms involve stopping blood contacting collagen, the production of prostacyclin and NO which inhibits platelet aggregation, the production of tissue factor pathway inhibitor which prevents thrombin production, the expression of thrombomodulin or heparin which binds to thrombin and inactivates it and the secretion of plasminogen activator which helps form plasmin which breaks down clots

Question 6

Describe the dominant factors controlling blood flow in cardiac vascular beds

Answer 6

the dominant factors in controlling blood flow are the basic haemodynamics such as Darcy’s law that flow is equal to the change in pressure over resistance, extrinsic effects of neural and hormonal influences, local intrinsic effect.
special areas include coronary circulation as aortic pressure increases, blood flow decreases s it is interrupted by systole, it demonstrate excellent active hyperaemia and many beta 2 receptors.

Question 7

Justify the importance of Poiseuille’s Law in relation to the control of resistance and blood flow

Answer 7

with darcy’s law and Poiseuille’s law which stated that varying radius controls resistance, therefore the varying radius of arterioles, or the total peripheral resistance and also effects change in pressure or the mean arterial pressure because the change in pressure is equal to flow multiplied by resistance.

Question 8

Define active hyperaemia,

Answer 8

active hyperaemia in which increasing metabolic activity increased concentration of metabolites such as carbon dioxide, hydrogen and potassium, which triggers the release of EDRF causing arteriolar dilation, the subsequent increase in blood flow is t wash out the metabolites to match blood flow to metabolic needs.

Question 9

identify the various neural factors affecting arteriolar tone.

Answer 9

neural control of the smooth muscle of arterioles include sympathetic nerves which release norepinephrine binding to alpha1 receptors causing constriction reducing flow and increasing total peripheral resistance.

Question 10

Indicate the factors affecting pressure and flow in veins.

Answer 10

pressure is low and the vessels are distensible and collapsible so they are effected by external factors. Such as gravity which causes venous distension in the legs, decreasing the end diastolic volume, reducing cardiac output and mean arteriolar pressure and causes venous collapse in the neck.
skeletal muscle pump also effects the blood flow, as movement forces blood through the veins. As well as respiratory pump, in that breathing generates a negative upper body pressure and a positive body pressure below it essentially forces the blood up to the heart.
there is venomotor tone, the contraction of smooth muscle around venules and veins, and systemic filling pressure created by ventricles and transmitted through the vascular tree to the veins.

Question 11

Define systolic pressure, diastolic pressure and pulse pressure.

Answer 11

systolic pressure is the peak pressure of the arteries, the pulse pressure is the difference between the between the systolic and diastolic pressure, and the diastolic pressure is the lowest artery pressure.

Question 12

Explain the origin of the Korotkoff sounds and their use.

Answer 12

Korotkoff sounds originate from the use of a sphygmomanometer and a stethoscope of the brachial artery, as blood is pumped passed through from the high decreasing pressure of the sphygmomanometer noise is generated. If the pressure of the sphygmomanometer is above or below systolic pressure there is silence, as it is just under systolic, there is a tapping sound and as it decrease is progresses to a thumping, then muffled.

Question 13

Illustrate the changes in the aortic pressure wave as it passes through the vascular tree

Answer 13

the aortic pressure increases up to systole, the aortic valve closes and then gradually decreases to diastole and repeats. The elastic arteries act as a pressure reservoir dampening decreasing variations. The pressure wave can be altered by stroke volume, velocity of ejection, elasticity and peripheral resistance.

as the pressure flows from the left ventricle to the right atrium the pressure gradually decreases.

Question 14

Illustrate the changes in blood velocity and total cross-sectional area of the vessels through the vascuar tree.

Answer 14

small drop through the arteries in pressure from 95-90mmHg which is a low resistance conduit, then a large drop through arterioles from 90-40 mmHg as it is the resistance vessels. Pressure is already low when the blood gets to the capillaries for exchange, it then leaves a small pressure difference from 20 – 5 mm Hg for the veins as systemic filling pressure. Pulmonary pressure is then a fifth of that of systemic. As a rule as the cross sectional area decreases, the velocity of the blood flow increases.

Question 15

Describe the effect of the Valsalva manoeuvre on the cardiovascular system.

Answer 15

the Valsalva manoeuvre refers to an increase in thoracic pressure within the chest cavity due to air being forced against a closed glottis. This increase in pressure results in a drop in the mean arterial pressure, as a result the rate of signals being fired by the aortic baroreceptors decrease. In response the medulla will stimulate a sympathetic signal to increase heart rate and stroke volume, and increasing the total peripheral resistance.

Question 16

Describe the components and function of the aterial baroreceptor reflex.

Answer 16

the arterial baroreceptor reflex originates from baroreceptors in the aortic arch and the carotid artery sinus’s. if they detect an increase In pressure, they send signals through the vagus nerve and the glossopharyngeal nerves respectively to the cardiovascular centres in the medulla. In response a response parasympathetic in nature is sent through the vagus nerve, it reduces the heart rate and the total peripheral resistance. As a result the cardiac output and blood pressure decrease. If it drops too low, a sympathetic response is sent, stimulating the adrenal gland and the sinoatrial and atrioventricular node to increase the heart rate, the stroke volume, causing increased vasoconstriction increasing the total peripheral resistance and increasing the cardiac output thus the blood pressure.

Question 17

Describe the effect of changes in posture on the cardiovascular system in relations to baroreceptors

Answer 17

as someone stands up, the blood begins to pool in capacitance veins in the legs. As a result the mean arterial pressure will decreases, reducing the signals being fired by the baroreceptors inducing a sympathetic response by the medulla increasing the heart rate, stroke volume and total peripheral resistance increasing blood pressure. Also as a reflex the vagal tone will decrease, contributing to the increase in heart rate and cardiac output.

Question 18

what is the relationship between mean arterial pressure, cardiac output and total peripheral resistance?

Answer 18

mean arterial pressure is equal to cardiac output multiplied by the total peripheral resistance.

Question 19

Identify the reflex pathways involving antidiuretic hormome,

Answer 19

the hypothalamus when stimulated by its osmoreceptors detecting changes in the interstitial fluid, angiotensin 2 or by decreased blood volume detected by baroreceptors in the aortic arch and carotid sinus stimulates the pituitary gland to release ADH which increases permeability of the collecting duct and causing vasoconstriction.

Question 20

Identify the reflex pathways atrial natriuretic peptide and brain natriuretic peptide in the control of plasma volume.

Answer 20

atrial natriuretic peptide is released by myocardial cells in the due to the increased pressure in the atrium. In response to increased mean arterial pressure it inhibits renin, decreases the permeability of the collecting duct resulting increased secretion of sodium and stimulates the medulla centres to reduce mean arterial pressure.

Question 21

Identify the reflex pathways involving renin-angiotensin-aldosterone

Answer 21

the release of renin by the juxtaglomerular cells of the kidney occurs in response to a reduced concentration of Chloride and sodium ions, sympathetic nerves or constriction of afferent arterioles in response to the drop-in mean arterial pressure. The renin will convert angiotensin into angiotensin 1 which is then converted into angiotensin 2 which acts as a vasoconstrictor, stimulating the hypothalamus to produce ADH and stimulates the adrenal cortex to produce aldosterone which increases the permeability of the collecting duct to increase the blood volume and reduces diuresis.

Question 22

identify the various hormonal factors affecting arteriolar tone.

Answer 22

hormonal factors such as epinephrine are released by the adrenal medulla which bind to alpha 1 receptors causing arteriolar constriction, having the same effect as norepinephrine but in some tissue is activates beta 2 receptors such in skeletal muscles increasing flow reducing the total peripheral resistance(TPR). Angiotensin 2 also has a similar effect as epinephrine in response to low blood volume increasing TPR, vasopressin an antidiuretic hormone which like angiotensin is released in response to low blood volume and as a result has a similar effect Atrial natriuretic peptide and brain natriuretic peptide are released in response to high blood volume, having an opposite effect causing dilation and reducing TPR.

Question 23

Describe the dominant factors controlling blood flow in cerebral vascular beds

Answer 23

the dominant factors in controlling blood flow are the basic haemodynamics such as Darcy’s law that flow is equal to the change in pressure over resistance,

Cerebral circulation is also must be kept stable at all times, shows excellent autoregulation.
As well as the blood brain barrier.

Question 24

Describe the dominant factors controlling blood flow in pulmonary vascular beds

Answer 24

pulmonary circulation as oxygen decreases there is arteriolar constriction which is the opposite of most tissues because it redirects flow to ventilated areas.

Question 25

Describe the dominant factors controlling blood flow in renal vascular beds

Answer 25

Renal circulation’s main function is filtration which requires pressure, so it must demonstrate excellent pressure autoregulation otherwise changes in mean arteriolar pressure would have massive effects.

Question 26

Define autoregulation

Answer 26

pressure autoregulation occurs when mean arteriolar pressure drops, decreasing flow so metabolites accumulate triggering the release of EDRF which causes dilation and flow is restored to maintain supply despite MAP changes.

Question 27

Define reactive hyperaemia.

Answer 27

Reactive hyperaemia is when the blockage of the blood supply causes a increase in blood flow, this response is essentially and extreme version of pressure autoregulation.

Question 28

Recognise the role of the kidneys in regulating plasma volume and therefore blood pressure.

Answer 28

The role of the kidneys is for secretion and absorption of plasma fluids, by regulating how much fluid is reabsorbed from the secreted fluid is decided by the osmolarity generated by pumping sodium out. By increasing permeability of the collecting duct, it can increase blood pressure of vice versa.

Question 29

Identify the receptors involved in sensing plasma volume.

Answer 29

Osmoreceptors in the hypothalamus for the interstitial fluid baroreceptors in the aortic arch and the carotid sinus’s juxtaglomerular cells in the kidney myocardial cells in the atrium

Question 30

Explain the effects of the sympathetic and parasympathetic systems on heart rate.

Answer 30

sympathetic system releases noradrenaline from nerves and the release of adrenaline from the adrenal medulla, increasing heart rate by acting on beta one receptors on the sinoatrial node. This is called tachycardia. parasympathetic system the vagus nerve release acetylcholine acting on muscarinic receptors on the sinoatrial node to hyperpolarise cells and reduce heart rate which is called bradycardia.

Question 31

Explain the effects of the sympathetic and parasympathetic systems on stroke volume.

Answer 31

the sympathetic system nerves release noradrenaline and stimulate the adrenal cortex to secrete adrenaline both operating on beta one receptors increasing contractility making it an inotrope, or a agent which alters contraction by giving a stronger but shorter contraction. the parasympathetic system has very little effect since the vagus doesn’t innervate the ventricular muscle.

Question 32

Explain the effects of preload and afterload on stroke volume.

Answer 32

an important component of preload is that the energy of contraction is as a result of the initial length of muscle. Preload thus is affected by the end diastolic volume, increasing it increases stroke volume and vice versa. Therefore, it is restricted to the influence of the capacitance vessels such as veins. afterload is the load against what the muscle has to contract, this is determined by the cardiac output and the total peripheral resistance. Therefore, afterload is restricted to the arterioles. Increasing total peripheral resistance decreases stroke volume.

Question 33

Recognise the effectiveness of treatment for hypertension in the young population.

Answer 33

hypertension treatment varies for young people with their main source of treatment consisting of ACE inhibitors or angiotensin receptor antagonists if not suitable then beta blocker, if this is ineffective they are then moved up to diuretics, then calcium channel blockers, normally though a younger person with high blood pressure will be referred to a specialist for treatment and screened for underlying causes

Question 34

Recognise the effectiveness of treatment for hypertension in the elderly population.

Answer 34

For elderly people they are normally put onto calcium channel antagonists, then thiazide-type diuretic, if this is ineffective a combination of ACE inhibitors if viable, and anti-diuretics will be considered as well, then beta blockers. As well as less commonly used drugs in small doses. Co-morbidities have to be taken into account, and their target goal is higher than young people being <145/85.

Question 35

define hypertension

Answer 35

the official definition is that saying when the benefits of treatment outweigh the risks in terms of morbidity and mortality. hypertension is defined as an elevated normal blood pressure on a daily basis. There are several stages, with the first being stage one with 140/90mm Hg clinically or 135/85 daily, stage two 160/100 mm Hg clinically and 150/95 mmHg daily and stage three being anything above 180/110 mm Hg.

Question 36

Know the aetiology of hypertension.

Answer 36

hypertension is one of the most leading causes of death in the world, It can be primary in nature as a result of lifestyle and idiopathic causes or it can be secondary due to renal or endocrine disease. Many factors are involved such sodium intake, environmental such as stress, genetic, lifestyle, smoking, alcohol intake, age or even birth weight etc.

Question 37

Be able to discuss the outcome of untreated hypertension.

Answer 37

The outcome of untreated hypertension is severe muscle damage that increase exponentially the longer it is untreated and can likely lead to death either as the primary or secondary cause. Organs commonly effected are the kidneys through renal failure or renal arteriolar stenosis, retinopathy, left ventricular hypertrophy, cardiac heart disease, congestive heart failure, peripheral vascular disease, stroke, proteinuria, haemorrhage, MI and impaired cognitive abilities.

Question 38

Define ischaemia, hypoxia and infarction.

Answer 38

ischaemia refers to the lack of oxygen to a tissue to meet its demands. Hypoxia is either low oxygen level or low partial pressure of oxygen. It can be anaemic, with abnormal blood, stagnant hypoxia due to occlusion or shock and cytotoxic with abnormal transport of oxygen at tissues.

Question 39

Explain the relationship between atheroma and ischaemia.

Answer 39

an atheroma, a localised accumulation of lipids encapsulated in fibrous tissue within the intima of arteries can reduce the flow of blood to an area altering the vessel structure resulting in ischaemia due to the fact oxygen is no longer reaching the tissues. It if it established this results in stable angina however any complications result in instability, ulceration, ischaemia, infarction and if it occurs in the aorta an aneurysm.

Question 40

Describe the consequences of ischaemia

Answer 40

the consequences include infarction of the brain or heart, a transient Ischaemic attack (stroke like symptoms) cardiac failure, abdominal aneurysm, or peripheral vascular disease. This is because of the reduced oxygen to meet energy demands, often resulting in dysfunction, pain and cellular damage.

Question 41

Recognise the supply and demand issues affecting the heart and coronary blood flow and the relevance of these issues to ischaemic heart disease

Answer 41

factors effect oxygen supply includes the percentage of air being inspired, the pulmonary function, the constituent and flow of blood, vessel structure and oxygen transport at tissues. Tissue’s requiring the oxygen have varying demands depending of their activity. specifically, for the heart cardiac failure or atheroma disrupting the flow, or anything altering the pulmonary function such as an oedema or myocardial infarcture can reduce supply or anaemia. This is the issue because the heart has a high intrinsic demand due to its constant exertion.

Question 42

Understand the difference between subendocardial and transmural infarction of the myocardium and the clinical significance of the two types of infarct.

Answer 42

death of the myocardial tissue that extends from the endocardium to the epicardium as a result of myocardial infarction and it referred to as transmural, also known as a STEMI. A subendocardial infarction involves the innermost layer of the myocardium but doesn’t extend to the epicardium and is also referred to as a non-Stemi. With a STEMI complications such as a papillary muscle rupture are more likely.

Question 43

Learn about the patho-physiology of mitral stenosis

Answer 43

when the valve becomes less than 2 cm2. The Left atrial pressure increases as well as pulmonary venous, and capillary increases. Pulmonary vascular resistance increases as well as pulmonary arterial pressure resulting in pulmonary hypertension. Right heart dilation occurs with tricuspid regurgitation and pulmonary regurgitation.

Question 44

Learn about the patho-physiology of mitral regurgitation

Answer 44

effective regurgitation orifice not fixed, annular enlargement of contractility, afterload and preload. Left ventricular compensation. Acute has reduced end systolic pressure and volume as well as a drop-in tension. Chronically end diastolic volume increases and left ventricular hypertrophy develops. There is a reduction in left ventricle compliance due to thickening of the myocardium In response to increased pulmonary vascular resistance and remodelling, or it can be increased compliance due to enlargement but with atrial fibrillations.

Question 45

Learn about the patho-physiology of aortic stenosis

Answer 45

if rheumatic there is adhesion/fusion of commissures and stiffening of cusp margins. However if degenerative lots of inflammation, thickening and calcification. As a result there is increased LV systolic pressure which results in hypertrophy increasing the left atrial pressure and left ventricular end diastolic pressure. This leads to increased myocardial oxygen consumption and eventually ischaemia leading to left ventricular failure.

Question 46

Learn about the patho-physiology of aortic regurgitation

Answer 46

increased Left ventricular end diastolic volume systolic pressure, leading to hypertrophy and dilation. This results in increased oxygen consumption then ischaemia and heart failure.

Question 47

Recognise the symptoms of mitral stenosis valve disease and natural progression of the disease

Answer 47

mitral stenosis; dyspnoea, haemoptysis, pulmonary oedema, systemic embolization, Left atrium enlargement, Chest pain, hoarseness due to compression of the Left recurrent laryngeal nerve and infective endocarditis

Question 48

Recognise the symptoms of aortic stenosis valve disease and natural progression of the disease

Answer 48

aortic stenosis: asymptomatic but chest pain, syncope, breathlessness, heart failure.

Question 49

Recognise the symptoms of mitral regurgitation valve disease and natural progression of the disease

Answer 49

mitral regurgitation: acute includes breathlessness, cardiogenic shock and pulmonary oedema. Chronically it can induce fatigue, exhaustion and right heart failure as well as dyspnoea or palpitations.

Question 50

Recognise the symptoms of aortic regurgitation valve disease and natural progression of the disease

Answer 50

aortic regurgitation; chronic exertional breathlessness, acute is poorly tolerated.

Question 51

Learn about the diagnostic investigations for mitral stenosis

Answer 51

: LA CXR enlargement, echocardiography (thickening and scarring, fusion of commissures)

Question 52

Learn about the diagnostic investigations mitral regurgitation

Answer 52

ECG LA enlargement, Right ventricular hypertrophy. CXR shows cardiomegaly, Left atrium enlargement and calcification of mitral annulus.

Question 53

Learn about the diagnostic investigations aortic stenosis

Answer 53

calcification of atrioventricular valves. Echocardiography demonstrates Lv hypertrophy, pressure gradient and AV cusp mobility.

Question 54

Learn about the diagnostic investigations aortic regurgitation

Answer 54

ST wave changes on ECG, cardiomegaly in CXR. Echocardiography demonstrates thickening of cusps and vegetations, dilation, hypertrophy of LV and regurgitant flow.

Question 55

treatment for aortic stenosis

Answer 55

aortic valve replacement or repair.

Question 56

treatment for aortic regurgitation

Answer 56

vasodilator therapy to delay surgery. Aortic valve replacement or repair.

Question 57

treatment for mitral stenosis

Answer 57

diuretics, NA restriction, sinus rhythm restoration or ventricular rate control. Anticoagulation. Interventional treatment includes a valvotomy or a mitral valve replacement

Question 58

treatment for mitral regurgitation

Answer 58

acute MR requires preload/afterload reduction through sodium nitroprusside and dobutamine. Intervention requires mitral valve repair or replacement.

Question 59

Describe the pathophysiology of stable angina

Answer 59

stable angina is the result of possible arteritis, artery spasm, anaemia, thyrotoxicosis, or structural changes in the heart such as left ventricular hypertrophy due to hypertension resulting in an increased oxygen and metabolite demand in which the supply cannot meet. More commonly it is the result of atheroma, a lipid encased in a fibrous shell that occludes a blood vessel, reducing blood flow in the coronary arteries to the heart. The lack of oxygen supply becomes increasing symptomatic upon aggravation through stress or exercise resulting in chest pain due to the section of the heart suffering from ischaemia not necrosis.

Question 60

Discuss the epidemiology and risk factors of stable angina.

Answer 60

risk factors of stable angina include lifestyles, smoking status, whether they have hypertension or hyperlipidaemia, diabetes mellitus, family history, gender, creed, genetics and diet. However, as atherosclerosis is an accumulative disease that progresses over a long time they tend to be older patients.

Question 61

Know its clinical presentation of stable angina.

Answer 61

chest pain that is aggravated upon exercise, cold weather, large meals and emotional stress. It’s best highlighted by the patient highlighting the chest area and describing the pain as a band of pressure around the chest causing pain with radiation to neck and/or jaw. Often look for tar staining, obesity, xanthalasma or corneal arcus as a sign of hyperlipidaemia. Other signs include mitral regurgitation or aortic stenosis, tachycardia, high blood pressure, abdominal aortic aneurysm, arterial bruits, absent peripheral pulses and retinopathy.

Question 62

Discuss relevant investigations of stable angina

Answer 62

investigations of stable angina include a CXR to rule out differentials and to observe for a pulmonary oedema. A full blood count, with lipid profile and fasting glucose is essential with liver and thyroid tests. An ECG to check for pathological Q waves, or ST segment depressions. A CT angiogram may be taken or an exercise tolerance test, if not effective or due to the nature of the patient being young or working high risk jobs or the readings from the ETT test highlighted warning signs, an invasive angiogram may be performed, a radionuclide myocardium perfusion test may be taken or a cardiac catheterisation may be inserted through the femoral or radial artery. Any signs of heart failure such as basal crackles, peripheral oedema or elevated JVP may be a sign too.

Question 63

discuss the importance of treatment and diagnosis of stable angina

Answer 63

if the root cause of stable Angina is atheroma, if it becomes complicated and ruptures, the following thrombosis will occlude the whole artery leading to infarcture and necrosis of the heart tissue. It’s important to recognise Angina to start treatment, reducing risk factors, medications such as Aspirin to reduce platelet aggregation, ACE inhibitors to reduce the risk of atheroma rupture and statins to reduce cholesterol. It’s also important to reduce the symptoms through beta blockers to reduce arrhythmia, calcium channel blockers both central (resting heart rate 60bpm) and peripheral (vasodilation), IK inhibitors to reduce SA node firing rate, nitrates to induce vasodilation, K+ channel blockers due induce vasodilation. if intervention is required operations such as percutaneous coronary intervention is possible which carries little risk but hasn’t been proven to be an important prognosis improvement for stable angina. It involves squashing atheromatous plaque into walls with a balloon and a stent. Alternatively a coronary bypass graft using a reversed long saphenous vein to graft. This treatment carries risk especially with myocardial infarcture and co-morbidities however it has been shown to reduce symptoms in by up to 80% for five years.

Question 64

List the factors causing embolism.

Answer 64

Fat embolism can be caused after fractures. Amniotic fluid, foreign bodies or bone marrow, Gas from decompression (N2) or air embolus from surgery. Septic material from endocarditis, tumour or trophoblast in pregnant women can all be types of embolus. Thrombus from myocardial infarctures, eft atrial dilation, aortic aneurysms, plaques or valvular vegetations.

Question 65

Describe the process of thrombosis.

Answer 65

anything that can damage the blood vessel wall or alter it’s flow can result in turbulent blood flow. There is the loss of intimal cells and denuded plaque resulting in the exposure of collagen which allows platelets to adhere. Once the platelet plug is formed a fibrin meshwork forms and can trap red blood cells. This cycle continues as the blood flow is further disturbed.

Question 66

Explain the significance of Virchow's triad.

Answer 66

changes in the blood vessel wall changes in blood constituents changes in pattern of flow this is important as they are all factors that can result in thrombosis.

Question 67

Explain the relationship between atheroma and thrombosis.

Answer 67

the formation of an atheroma, a lipid encapsulated in a fibrous shell can result in disrupting the laminar flow making it turbulent. The disruption in flow is sufficient to damage the intima, and degrade the endothelial cells to reveal collagen resulting in the formation of a thrombosis. Especially if the atheroma becomes complicated and ruptures.

Question 68

List the factors causing thrombosis

Answer 68

atheromatous, hypercholesterolaemia, hyper viscosity, traumatic hypercoagulability, aortic aneurysm, stasis of blood. risk factors for the thromboembolism include cardiac failure, trauma, burns, nephrotic syndrome, malignancy, contraception, age, immobilisation or obesity, spasms, external compression, vasculitis or vascular steal.

Question 69

Describe the pathophysiology of myocardial infarction

Answer 69

myocardial infarctions occur when the coronary arteries become occluded due to an embolism, or atheromatous plaque has developed and ruptured leading to thrombosis. As a result, necrosis is occurring as the oxygen and metabolic supply to the myocardial cells has been cut off, and the cells begin to break down. As essential structures fail ventricular fibrillations may occur, free wall ruptures, septal wall ruptures, papillary muscle rupture, ventricular tachycardia or left ventricular thrombus.

Question 70

Know the epidemiology of myocardial infarction

Answer 70

most commonly it occurs with people who have new exertional angina (52%), already had an acute MI (225) then unstable angina (13%) and then sudden cardiac death (13%). Often it happens in older population with a variety of contributing factors such as lifestyle, genetics, smoking, hypercholesterolaemia, hypertension.

Question 71

Describe the characteristic ECG changes and other diagnostic aids.

Answer 71

on an serial ECG it can be identified by either a elevated ST wave (transmural) if caused by complete coronary occlusion after 3 days a Q wave will still be present, or a non-elevated ST wave (subendocardial) in which the T wave can become inversed due to partial coronary occlusion and after 3 days there will be no Q wave. Other diagnostic aids include ECHO if suspected complications to check mitral leaflet, left ventricle and right ventricle. A heart catheterization in both the left and right ventricles to monitor pressure changes especially in a complication is suspected. It can quantify the shunt, measure pressure and establish coronary anatomy. One other helpful diagnostic tool is monitoring the myocardial troponin levels in blood serum.

Question 72

Recognise the common complications of myocardial infarction.

Answer 72

sudden cardiac death can occur with irregular ineffectual ventricular fibrillating activity requiring defibrillation to restore cardiac output and avoid asystole. Mechanical complications include free wall ruptures which are the most common from the left anterior descending coronary artery leading to hemopericardium unless if can be drained by a pigtail catheter, papillary muscle rupture which presents with sudden severe breathlessness, autonomic activation and chest pain with signs of shock, tachycardia, harsh systolic murmur, right parasternal heave, palpable thrill and elevated JVP, and rupture of the interventricular septum which is more likely with an anterior MI meaning an echocardiography is recommended to differentiate. arrhythmic complications include ventricular tachycardia characterised by a complex regular rapid premature beat. more long term is a left ventricular thrombus resulting in dysfunction. Requires anticoagulation with warfarin and regular ECHO assessments with it often being found apically.

Question 73

Describe the potential adverse drug reactions which a patient may suffer following drug treatment of ischaemic heart disease

Answer 73

Risk of GI bleeding with clopidogrel. 14% level of population resistance to Clopidogrel due to low CYP2C19 levels. With heparin the main risks are major and minor bleeding, with thrombocytopenia (abnormally low platelets) being common with tirofiban platelets. With beta blockers the risk of fatality is increased if they are at risk of cardiogenic shock (>70 years, coronary vasospasms, cocaine, >110bpm, <120 mmHg). .

Question 74

Describe the mechanism of action of thrombolytic therapy.

Answer 74

they are serine proteases that convert plasminogen to the natural fibrinolytic agent plasmin. Plasmin then lyses clots by breaking down fibrinogen and fibrin within the clot. It can either be specific to fibrin such as alteplase, reteplase, tenecteplase converting plasminogen to plasmin in absence of fibrin or they can be non-fibrin specific streptokinase catalyse and work on systemic fibrinolysis.

Question 75

Discuss the strengths and weaknesses of thrombolytic therapy.

Answer 75

they cannot be used with prior history of intercranial haemorrhage, trauma, malignancy, stroke or vascular lesion. Neither can they be used if suspected aortic dissection or bleeding. However they do have a 23% reduction in mortality and even more effective when used with aspirin.

Question 76

State the benefits of aspirin therapy in patients with ischaemic heart disease and weaknesses.

Answer 76

aspirin is a potent inhibitor of platelet thromboxane A2 production which normally stimulates platelet aggregation and vasoconstriction. Regular use in acute MY reduces mortality by 23% and with thrombolytic agents by 42%. With unstable angina reduces the risk of MI and death by 50%. However it increases the risk of bleeding.

Question 77

Discuss the strengths and weaknesses of beta adrenoceptor antagonists

Answer 77

reduce mortality of acute MI by 10-15%. It reduces oxygen consumption of the heart by lowering its rate, blood pressure and contractility. However it cannot be used if there is the risk of cardiogenic shock as it increases fatality (cocaine use, vasospasms, HR >110, bp <120 mm Hg >70).

Question 78

Discuss the strengths and weaknesses of heparin and ADP blockers such as clopidrogel

Answer 78

works on the GPllb/llla complex on platelets which allows for fibrinogen to activate them. ADP blockers stimulate a conformational change preventing binding to fibrinogen. Major adverse effect is bleeding and thrombocytopenia.

Question 79

Outline the investigation of stroke.

Answer 79

blood tests, ECG, CT scan, MRI scan, carotid doppler, echocardiogram.

Question 80

Be aware of the risk factors for stroke

Answer 80

modifiable; hypertension, atrial fibrillations, non modifiable; race, Age, family history.

Question 81

Describe the acute treatments for stroke

Answer 81

FAST symptoms recognised and patient rushed to stroke unit. Urgent CT scan, if cerebral oedema than an emergency hemicraniectomy will be necessary. However, treat with iv alteplase if ischaemia from thromboembolism. Clot retrieval may be necessary.

Question 82

Understand the primary and secondary prevention of stroke

Answer 82

clopidogrel or aspirin plus dipyridamole, statin and blood pressure drugs. A carotid endarterectomy may be necessary as it will reduce risk.

Question 83

Describe the surgical techniques available for the treatment of ischaemic heart disease.

Answer 83

A CABG, a coronary artery bypass graft through the use of either the reversed saphenous vein, internal mammary arteries or radial arteries.

Question 84

Explain the potential complications of surgery.

Answer 84

sternotomy related problems of surgery include wire infection, pain, sternal dehiscence or malunion. Post operatively there is the risk of cardiac tamponade, death, stroke. Cardiopulmonary bypass machine only effective for 12 hours, with the potential of coagulopathy. risk of air embolism during valve replacement.

Question 85

Describe briefly the surgical procedures for the complications of ischaemic heart disease.

Answer 85

the treatment for Tamponade really requires re-opening the chest to allow for draining of excess fluid.

Question 86

Know the indications for valve replacement.

Answer 86

senile tricuspid Aortic stenosis, bicuspid aortic stenosis or degenerative mitral regurgitation.

Question 87

List the types of prosthetic valves in common use

Answer 87

biological valve (needs replaced every 15 years), mechanical valve (warfarin required for life, last >40 years). For degenerative MR, repair is a better option than replacement.

Question 88

Discuss the early and late results of surgical treatment.

Answer 88

for CABG long term 50% have no further cardiac problems ten years later, the other 50% have minor problems controlled with medication and 5% require a repeat surgery.

Question 89

Describe the medical treatment of infective endocarditis

Answer 89

infection by strep viridans, or staph aureus, with only about a 50% chance of cure with antibiotics alone. Indications for surgery being severe regurgitation, vegetations, pyrexia and renal failure.

Question 90

Recognise how disturbances in these forces can cause oedema

Answer 90

accumulation of fluid in extravascular components such as extracellular fluid or cavities. left ventricular failure which will increase pressure and retrograde flow back into the veins which increases volume and filtration thus resulting in a pulmonary oedema. A peripheral oedema can be caused by right heart failure, blood is retained in systemic veins increasing pressure and filtration. It’s all about hydrostatic pressure. lymphatic blockage will also alter flow. abnormal renal function results in sodium and water retention. As the plasma volume increases, pressure increases and results in an oedema. low protein oedema, oncotic pressure decreases as an results in increased filtration this can be caused by nephrotic syndrome, hepatic cirrhosis or malnutrition. permeability oedema; endothelial lining damage results in pores results in large molecules as well as water filtering out.

Question 91

Explain congestive heart failure.

Answer 91

heart unable to clear blood from ventricles, ineffective. As a result cardiac output decreases, as well as renal glomerular filtration rate (GFR) so sodium and water retention increases which results in fluid overload. Blood is them dammed in veins resulting in oedema, and liver congestion.

Question 92

List the causes of vascular congestion.

Answer 92

congestion refers to the excess of blood in vessels of a particular organ or tissue, not due to inflammation but rather a passive process deep vein thrombosis can cause an oedema by causing the reduction in flow, reducing the pressure gradient then with oxygen there is ischaemia and infarction. hepatic cirrhosis, fibrosis can result in altered blood flow with the potential of blockage resulting in increased pressure and congestion as the blood flows through collateral circulation.

Question 93

Define the terms exudate and transudate.

Answer 93

transudate – alterations in haemodynamic forces resulting in fluid overload, lack of proteins but lots of fluid and electrolytes and low specific gravity. exudate is inflammatory due to tumour, allergy or infection. Lots of proteins are present and has a high specific gravity

Question 94

Describe the Starling forces affecting fluid movement across the capillaries.

Answer 94

constant movement of fluid, driver by the hydrostatic pressure from the heart and balanced by the osmotic pressure and endothelial permeability.

Question 95

Discuss the treatment options in heart failure and evidence for their use.

Answer 95

diuretics are used such as bumetanide, and furosemide for symptomatic relief, Ace inhibitors such as Ramipril, enalapril or candesartan/valsartan. Then there are betablockers carvedilol/bisoprolol. Aldosterone receptor blockers spironolactone/eplerenone and ARNI’s entresto.

Question 96

Discuss the aetiology of heart failure.

Answer 96

obesity, diabetes, hypertension can be factors in causing heart disease but often left ventricular dysfunction, valvular heart disease, pericardial effusion, cardiac arrhythmias, myocardial ischaemia, restrictive cardiomyopathy, right ventricular failure. Left ventricular systolic dysfunction has a number of causes such as dilation, texins, viral, infection, hypertrophy, sarcoidosis, hypertension, muscular dystrophy

Question 97

Discuss the epidemiology of heart failure.

Answer 97

increasing prevalence, effecting 1-2% of the population and accounting for 1 million inpatient bed days.

Question 98

Know the prognosis of heart failure

Answer 98

not a final diagnosis as it depends on the underlying cause. However often a poor prognosis of 30-40% mortality in 1 year. Also depends on the New York Association for heart failure 1 being no limitation, 2 being mild with comfortability on mild exertion, 3 being moderate with only being comfortable at rest, and then 4 with symptoms at rest.

Question 99

Describe the clinical presentation of heart failure.

Answer 99

dyspnoea, fatigue, fluid retention with neurohormonal activation. Signs of aortic stenosis, left ventricular septal defect, or ischemic heart disease. symptoms; breathlessness, fatigue, oedema, reduced exercise capacity signs; tachycardia, raised JVP, chest crepitation, 3rd heart sound, displaced or abnormal apex beat. Responsiveness to therapy important too.

Question 100

Know the relevant investigations of heart failure.

Answer 100

ECHO( allows you to identify and quantify by measuring ejection fraction), radionucleotide, left ventriculogram, cardiac MRI. Potentially for screening a 12 lead ECG, and a BNP test through the blood which would exclude heart failure if low. If the cause is suspected to be LVSD then renal function, family history, ECG, ECHO, coronary angiogram, CT, MRI and examined by a cardiologist.

Question 101

be able to discuss the management of a family with a genetic diagnosis

Answer 101

firstly family testing is important to assess relative risk, and prevent morbidity and mortality. Then family planning and the patients concerns and expectations must be respected and understood.

Question 102

Understand the genetics and molecular pathology of congenital heart disease

Answer 102

down syndrome; atrioventricular septal defects (trisomy 21) turner syndrome; coarctation of aorta (45,x) noonan syndrome; pulmonary stenosis (PTPN11 on chromosome 12, autosomal dominant) costello syndrome (cardiomyopathy) 22q11 (catch 22 – cardiac malformation) Williams syndrome (aortic stenosis, hypercalcemia, deletion of elastin on chromosome 7, deletion of contiguous genes and LIM kinase) marfan's aortic root dilatation, connective tissue disease (autosomal dominant, multisystem on fibrillin 1 gene, chromosome 12q21, TGFbetaR 2, chromosome 3p22.)

Question 103

Understand the importance of single gene, chromosomal and microdeletion syndromes.

Answer 103

chromosomal causes of heart disease include trisomies and monosomies microdeletions such as 22Q11 deletion or William’s syndrome single gene deletion; marfans

Question 104

Recognise the relevance of a genetic diagnosis to treatment

Answer 104

it’s important for developing the prognosis, annual reviews, managing lifestyle factors such as it may prevent diving or certain medications and it is important for treatment in terms of beta blockers, or nicorandil or even if surgery is essential and when.

Question 105

Describe the management of deep vein thrombosis and pulmonary thromboembolism.

Answer 105

anticoagulation parenteral; unfractionated or low molecular weight heparin, or enteral; warfarin and direct oral coagulants. Thrombolysis for massive PE’s include alteplase.

Question 106

Describe the presentation of deep vein thrombosis and pulmonary thromboembolism

Answer 106

signs of stasis; immobility, long haul travel signs of vessel damage; endothelial dysfunction such as hypertension, smoking or cholesterol, or endothelial damage; catheters, trauma, surgery. hypercoagulability; acquired through pregnancy, sepsis or cancer or inherited. Deep vein thrombosis can present itself as limb swelling, discomfort, calf tenderness, warmth, eryhthema, prominent collateral veins, pitting oedema. Signs of embolism include; surgery, trauma, prior VTE, cardiovascular disease, contraceptive, hypertension, COPD, hormone therapy, obesity, thrombotic disorders, neurological disability. of pulmonary embolism it can present as pleuritic chest pain, breathlessness, blood in sputum, tachycardia, and pleural rub. A massive PE can result in severe dyspnoea, collapse, cyanosis, tachycardia, low blood pressure and raised JVP.

Question 107

Describe the investigation of deep vein thrombosis and pulmonary thromboembolism

Answer 107

clinical assessment of probability score (Wells), blood test D-dimer(highly sensitive but not specific) , and imaging using ultrasound. For pulmonary similar tests but instead of ultrasound a V/Q scan and a Ct pulmonary angiogram.

Question 108

Discuss the strengths and weaknesses of carotid endarterectomy.

Answer 108

an incision is made to open the carotid, then the plaque Is removed and then repaired. General risks include wound infection, bleeding, scarring, nerve damage and poor reactions to the anaesthetic. There is also the risk of perioperative stroke with the plaque rupturing, hypoperfusion and virchow’s triad. Benefit is that it can prevent a stroke.

Question 109

Describe the clinical presentation of arterial occlusive disease.

Answer 109

often may have a history of drug abuse, haematological disorder, trauma, MI, endocarditis, atherosclerosis, AF. Perhaps a smoker, diabetic, male, hypertension, hyperlipidaemia, obese and older. Signs of contralateral paralysis, visuospatial neglect, dysphasia.

Question 110

Describe the clinical presentation of anuerysmal disease.

Answer 110

male, older, smoking, hypertension, family history. Can be due to a degenerative disease, connective tissue disease or infection. Often asymptomatic, hence why there is a screening process using ultrasound on over 65’s. Once it is impending there is back pain and tenderness, upon rupture there is a painful pulsatile mass, haemodynamic instability and hypoperfusion. It can also present with distal embolization, aortacaval/aortoenteric fistula, ureteric occlusion or duodenal obstruction.

Question 111

Discuss the possible treatment options of dilated cardiomyopathy

Answer 111

dilated – correct anaemia, remove exacerbating factors, or endocrine disturbance, reduce fluid and salt intake, manage weight, ACEI, AT2 blocker, diuretics, beta blockers, spironolactone, anticoagulants, cardiac transplant, or ICD implant.

Question 112

Discuss the possible treatment options of restrictive cardiomyopathy

Answer 112

restrictive – limited diuretic use, beta blockers, anticoagulants, ICD, cardiac transplant, treat amyloid of Fabrys.

Question 113

Discuss the possible treatment options for hypertophic cardiomyopathy

Answer 113

hypertrophic – general measures avoid heavy exercise, dehydration, genetic testing, drugs to enhance relaxation such as beta blockers, verapamil and disopyrimide to treat symptoms. Anticoagulants for atrial fibrillations, or surgery, or septal ablation if obstructive. May need an ICD.

Question 114

Discuss the possible treatment options for myocarditis

Answer 114

myocarditis – treat heart failure and arrhythmias, immunotherapy, or stop toxic exposure.

Question 115

Discuss and differentiate dilated cardiomyopathy.

Answer 115

ventricular function impairment, result of pathological insult such as infections, toxins, injury, inflammatory, or genetic.

Question 116

Discuss and differentiate restrictive cardiomyopathy.

Answer 116

familial forms, amyloid, sarcoidosis, storage disease, endomyocardial. Often filling and relaxation of myocytes effected, essentially reduced compliance.

Question 117

Discuss and differentiate hypertrophic cardiomyopathy.

Answer 117

impaired relaxation, with some functional abnormality. It can be generalised or segmental, can lead to mitral valve defects and coronary artery defects leading to ischaemia, fibrosis and arrhythmias.

Question 118

Discuss and differentiate myocarditis

Answer 118

myocarditis – inflammation of myocardium, associated with pericarditis. Impairs function, conduction resulting in arrhythmia. Infiltration of pro-inflammatory cells into myocardium, often causing heart failure or block.

Question 119

Describe the genetics of hypertrophic cardiomyopathy

Answer 119

high prevelance, it’s a sarcomere gene defect. Autosomal dominant but with incomplete penetrance.

Question 120

Describe the clinical presentation of the dilated cardiomypoathy

Answer 120

dilated - It’s progressive with a slow onset, breathlessness even when lying down, fatigue, oedema, weight gain and cough. Narrow pulse pressure, elevated JVP, displaced apex, S3 and S4 noises, pleural effusion, sacral oedema, acites and hepatomegaly.

Question 121

Describe the clinical presentation of the hypertrophic cardiomyopathy

Answer 121

fatigue, dyspnoea, angina, presyncope, syncope, arrhythmias, notched pulse pattern, double impulse, thrills, murmurs, JVP can be raised.

Question 122

Describe the clinical presentation of the

Answer 122

heart failure, shortness of breath, Acute, fever.

Question 123

Identify the possible surgical interventions for the treatment of chronic arterial occlusive disease.

Answer 123

should be treated similar to those with established coronary heart disease. Antiplatelet, statins, BP control, smoking cessation, exercise and diabetes control. In sever or critical looking at angioplasty, surgical bypass or endovascular reconstruction. If necessary amputation.

Question 124

identify the possible surgical interventions for the treatment of acute arterial occlusive disease.

Answer 124

Acute episodes should be treated with analgesia, and anticoagulants. If it’s only an embolus, embolectomy, of thrombosis in situ then bypass, or thrombolysis/thromboectomy. If not then amputation.

Question 125

identify the possible surgical interventions for the treatment of diabetic foot wound

Answer 125

diabetic foot wound should be prevented, cleaning of wounds and regular investigations. Attempts bay be made of bypass to revasculate but very limited successes with stents or angioplasty most likely option is to amputate.

Question 126

Describe the clinical presentation ofchronic arterial occlusive disease

Answer 126

``` signs of; ulceration, pallor, hair loss, capillary refill time, temperature, pulses and sensation, doppler, ankle brachial pressure index, leg elevation for buerger’s test. fontaine classification; stage 1 – asymptomatic stage 2 – mild claudication pain A->200m B - <200m stage 3 – pain at rest in feet stage 4 – necrosis or gangrene ```

Question 127

Describe the clinical presentation ofchronic arterial occlusive disease

Answer 127

history of chronic, risk factors for thromboembolism, cardiac history, onset and functional status. Pain, Pallor, perishingly cold, paraesthesia, paralysis, pulseless.

Question 128

Clinical presentations for infective endocarditis

Answer 128

older patients with valve disease, intra cardiac devices or immunocompromised. Often with mitral valve prolapse or congenital heart diseases. Often fever, chills, night sweats, fatigue, anorexia, weight loss, weakness, arthralgia, headache, SOB. Signs; cardiac murmur, janeway lesions, osler nodes, roth spots, meningeal signs, splinter haemorrhages, cutaneous infracts, vasculitis or vascular phenomena such as aneurysms, haemorrhages etc.

Question 129

microbiology of infective endocarditis

Answer 129

caused by streptococci viridans, staph, enterococci, haemophilus parainfluenzae, fungi, Brucella, kingella etc.

Question 130

investigations for infective endocarditis

Answer 130

– 3x blood culture 30 mins apart, inflammation markers, urinalysis, ECg, CXR, SPECT/CT, MRI, ECHO. Looking for vegetation, abscess, dehiscence of new valve

Question 131

antibiotic prophylaxis for infective endocar

Answer 131

Current trends regarding antibiotics prophylaxis – if at risk of IE then prophylaxis should be used but only limited to those with high risk even for dental procedures. Good oral hygiene and regular dental

Question 132

1st degree heart block –

Answer 132

delayed conduction through the Atria-ventricular node. As a result there is a prolonged PR interval. This is because the P wave, atrial depolarisation will occur as normal, just however there is a delay before the signal is relayed to the ventricles to from the QRS complex. Normal PR interval is 0.12-0.2 seconds, greater than 5 small boxes is a 1st degree heart block. There is still a 1:1 ratio between the P waves and QRS complexes.

Question 133

2nd degree heart block –

Answer 133

atrial impulse is delayed through the atria-ventricular node. Patients may be asymptomatic or experience syncope, light-headedness, chest pain, hypotension, bradycardia.

Question 134

2nd degree Mobitz 2 –

Answer 134

normal PR interval followed by a blocked sinus P wave. PR interval in the first beat after the block is similar to the interval before the block, a pause encompassing the blocked P wave is equal to twice the sinus cycle length. Damage is in the His Purkinje system and due to structural damage. Failure of conduction by the P wave. Fixed PR interval, wide QRS complex.

Question 135

2nd degree AV block (2:1) –

Answer 135

there are two P waves for every QRS. Cannot tell whether the block is above or below the AV node.

Question 136

3rd degree heart block –

Answer 136

complete dissociation of P and QRS waves due to absence of conduction through the atrioventricular node and can occur anywhere along the AV node to the Purkinje fibres. Also known as an escape rhythm. Severe bradycardia and syncope will be likely experienced.

Question 137

atrial fibrillation –

Answer 137

irregular rhythm due to disorganized signals to the atria causing them to rapidly contract. increased risk of stroke due to pooling of blood. This is due to signals travelling abnormally from a different site other than the Sino-Atrial node.

Question 138

atrial flutter –

Answer 138

rapid regular beating due to an anomaly in conduction of depolarisation. Produces a regular tachycardia

Question 139

supraventricular tachycardia –

Answer 139

high rate of contractions in the atrium of the heart at a rate of 150-250bpm. T waves of previous complex cover the P wave of the next.

Question 140

wolff Parkinson-white syndrome –

Answer 140

congenital extra pathways of electrical conduction in the heart resulting in supraventricular tachycardia. Also referred t as a pre-excitation syndrome. Presence of a delta wave at the start of the QRS complex.

Question 141

sinus arrest –

Answer 141

when the R-R interval becomes greater than 2 small boxes. Essentially a long pause following a normal complex with an escape beat following with a drop in blood pressure.

Question 142

Ectopic beat –

Answer 142

conduction outside the heart causing an impulse formation.

Question 143

Atrial ectopic (Premature Atrial Complex) -

Answer 143

arise from pacemaking tissue within atria, normally an abnormal P wave followed by a normal QRS wave.

Question 144

Ventricular Ectopic (Premature Ventricular Contraction) –

Answer 144

occur prior to before the normal wave of depolarisation. Produces QRS complexes with prolonged duration and abnormal morphology. Can occur as single, or multiple events.

Question 145

presentation of atrial fibrillation –

Answer 145

asymptomatic, cardiogenic shock, palpitations, dyspnoea, fatigue, dizziness, syncope,, presyncope, angina, heart failure, haemodynamic dysfunction, tachycardia cardiomyopathy, thromboembolisms. Presence of heart disease, drug use, alcohol, infections, surgery.

Question 146

treatment for Atrial fibrillation –

Answer 146

anticoagulation with heparin, cardioversion DC or pharmacological amiodarone.

Question 147

tilt testing –

Answer 147

response of blood pressure and heart rate to the force of gravity, bradycardia can cause fainting so it’s designed to rigger symptoms whist under observation.

Question 148

MAZE procedure -

Answer 148

surgical ablation using small incisions to generate scare tissue to prevent abnormal electrical signals to prevent arrhythmia.

Question 149

ARIBAR

Answer 149

``` Any electrical activity? QRS Rate? Irregular or regular rhythm Broad or narrow QRS? Atrial activity? Relationship between atria and ventricles ```