Cardiovascular Flashcards

Question

Contractility

Answer 1

force of contraction and the change in fibre length - how hard the heart pumps. When muscle contracts myofibrils stay the same length but the sarcomere shortens - force of heart contraction that is independent of sarcomere length

Answer 2

myocardial ability to recover normal shape after systolic stress

Answer 3

the pressure required to fill the ventricle to the same | diastolic volume

Answer 4

how easily the heart chamber expands when filled with blood | volume

Answer 5

Force of contrition is proportional to the end diastolic length of cardiac muscle fibre - the more ventricle fills the harder it contracts

Answer 6

not at optimal length. Below optimal length means | the force of contraction is decreased - inefficient

Answer 7

= ↑ end diastolic volume = ↑ preload = ↑ sarcomere stretch = ↑ force of contraction thus = ↑ stroke volume and force of contractions

Answer 8

decreases venous return due to gravity thus, cardiac output decreases, which causes a drop in blood pressure, stimulating baroreceptors to increase blood pressure

Answer 9

- mitral and tricuspid valve closure

Answer 10

- aortic and pulmonary valve closure

Answer 11

- in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure

Answer 12

- ‘Gallop’, in late diastole, produced by blood being forced into a stiff hypertrophic ventricle - associated with left ventricular hypertrophy

Answer 13

Circumflex, Left anterior descending (LAD) and right coronary arteries

Answer 14

- Age - increases with age - Tobacco smoking - leads to endothelium erosion - High serum cholesterol - Obesity - since more pericardial fat and thus increase in inflammation - Diabetes - hyperglycaemia damages endothelium - Hypertension - Family history

Answer 15

- Found within peripheral and coronary arteries | - Focal distribution along the artery length

Answer 16

``` - A complex lesion consisting of: • Lipid • Necrotic core • Connective tissue • Fibrous “cap” - Eventually the plaque will either occlude the vessel lumen resulting in a restriction of blood flow (ANGINA), or it may rupture (thrombus formation and subsequent death) ```

Answer 17

- Initiated by an injury to the endothelial cells which leads to endothelial dysfunction - Once initiated, chemoattractants (chemicals that attract leukocytes) are released from endothelium to attract leukocytes which then accumulate and migrate into the vessel wall - Chemoattractants are released from site of injury and a concentration- gradient is produced - Inflammatory cytokines found in plaques: • IL-1 - KEY ONE • IL-6 • IFN - gamma - Fatty streaks: • Earliest lesion of atherosclerosis • Appear at a very early age (less than 10) • Consist of aggregations of lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall

Answer 18

- Intermediate lesions: • Composed of layers of: - Lipid laden macrophages (foam cells - macrophages that have taken up lots of lipids) - Vascular smooth muscle cells - T lymphocytes • There is adhesion and aggregation of platelets to the vessel wall (aspirin inhibits platelet aggregation) - Fibrous plaques/advanced lesions: • Impede blood flow • Prone to rupture • Covered by dense fibrous cap made of extracellular matrix proteins including collagen (strength) and elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris • May be calcified • Contains: - Smooth muscle cells - Macrophages and foam cells (lipid laden macrophages) - T lymphocytes - Red cells • Plaque is filled with fibrin

Answer 19

- Plaque rupture: • Plaque is constantly growing and receding • The fibrous cap needs to be resorbed and redeposited in order to be maintained • If balance shifts e.g. in favour of inflammatory conditions (increased enzyme activity) then the cap becomes weak and the plaque ruptures • Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessel within the plaque • Thrombus (clot) formation and subsequent vessel occlusion

Answer 20

is chest pain or discomfort as a result of reversible myocardial ischaemia This usually implies narrowing of one or more of the coronary arteries Tends to be exacerbated by exertion and relieved by rest

Answer 21

• Induced by effort and relieved by rest

Answer 22

• Angina of recent onset (less than 24hrs) or • Deterioration in previously stable angina, with symptoms frequently occurring at rest • Angina of increasing frequency or severity, occurs on minimal exertion or even at rest - form of acute coronary syndrome

Answer 23

• Caused by coronary artery spasm (rare)

Answer 24

- Myocardial ischaemia resulting in angina occurs when there is a mismatch between blood supply and metabolic demand - this can occur due to: • Atheroma/stenosis of coronary arteries thereby impairing blood flow - most common cause • Valvular disease • Aortic stenosis • Arrhythmia • Anaemia - thus less O2 can be transported - Ischaemic metabolites including adenosine, stimulate nerve endings and produce pain - More common in men

Answer 25

- Smoking - Sedentary lifestyle - Obesity - Hypertension - Diabetes mellitus - Family history - Genetics - Age - Hypercholesterolaemia

Answer 26

narrowing of coronary arteries that results | in ischaemia and thus pain i.e. angina

Answer 27

• Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier • Local cellular proliferation and incorporation of oxidise lipoproteins occurs • Mural thrombi on surface and subsequent healing and repeat of cycle

Answer 28

• As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed • This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix • May progress to unstable plaque

Answer 29

• The plaque continues to encroach upon the lumen and runs the risk of haemorrhage or exposure of tissue HLA-DR antigens which might stimulate T cell accumulation • This drives an inflammatory reaction against part of the plaque contents • Complications develop including ulceration, fissuring, calcification and aneurysm change

Answer 30

• Fatty streak: - These show macrophages filled with abundant lipid (foam cells) - Also smooth muscle cells with fat • Intimal cell mass: - These are collections of muscle cells and connective tissue without lipid - “cushions” • The atheromatous plaque: - Characterised by distorted endothelial surface containing lymphocytes, macrophages, smooth muscle cells and a variably complete endothelial surface - There is local necrotic and fatty matter with scattered lipid rich macrophages - Evidence of local haemorrhage may be seen with iron deposition and calcification - Complicated plaques are those which show calcification and mural thrombus - making them vulnerable to rupture • Complications of plaque rupture: - Acute occlusion due to thrombus - Chronic narrowing of vessel lumen with healing of the local thrombus - Aneurysm change - Embolism of thrombus +/- plaque lipid content

Answer 31

- Central chest tightness or heaviness - Provoked by exertion, especially after meal or in the cold windy weather or by anger or excitement - Relieved by rest or GTN spray - Pain may radiate to one or both arms, the neck, jaw or teeth - May be dyspnoea, nausea, sweatiness and faintness - Scoring: • 1. Have, central, tight, radiation to arms, jaw & neck • 2. Precipitated by exertion • 3. Relieved by rest or spray GTN • 3/3 = Typical angina • 2/3 = Atypical pain • 1/3 = Non-anginal pain

Answer 32

- Pericarditis/myocarditis - Pulmonary embolism - Chest infection - Dissection of the aorta - GORD

Answer 33

* Often normal * May show ST depression * Flat or inverted T waves * Look for signs of past MI

Answer 34

• Put ECG on patient, then make them run on treadmill uphill - trying to induce ischaemia • Monitor how long patient is able to exercise for • If you see ST segment depression then this is a sign of late-stage ischaemia • Many patients unsuitable e.g. can’t walk, very unfit, young females and bundle branch block

Answer 35

• CT the heart and if there is atherosclerosis in the arteries then the calcium will light up white - if there is significant calcium then this would indicate angina

Answer 36

• Radio-labelled tracer injected into patient • Its taken up by the coronary arteries where there is good blood supply - this will light up • Where there is little blood supply these areas will not light up • If there is no light after exercise then this is indicative of myocardial ischaemia

Answer 37

* Stop smoking * Encourage exercise * Weight loss

Answer 38

- Antiplatelet effect (inhibits platelet aggregation) in coronary arteries thereby avoiding platelet thrombosis - To reduce events - E.g. salicylate - COX inhibitor - reduces prostaglandin synthesis including thromboxane A2 resulting in reduced platelet aggregation - Side effects - gastric ulceration

Answer 39

- HMG-CoA reductase inhibitors - reduces cholesterol produced by liver - Reduce events and LDL-cholesterol - Anti-atherosclerotic

Answer 40

- Reduce force of contraction of heart - E.g. Bisoprolol and atenolol - Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway - B1 activation → Gs → cAMP to ATP → contraction - Reduces: • Heart rate (negatively chronotropic) • Left ventricle contractility (negatively inotropic) • Cardiac output - Side effects; tiredness, nightmares, bradycardia, erectile dysfunction and cold hands and feet - DO NOT GIVE in asthma, heart failure/heart block, hypotension and bradyarrhythmias

Answer 41

- Nitrate that is a venodilator - Dilates systemic veins thereby reducing venous return to right heart - Reduces preload - Thus reduces work of heart and O2 demand - Also dilates coronary arteries - Side effect: profuse headache immediately after use

Answer 42

- Primary arterodilators - Dilates systemic arteries resulting in BP drop - Thus reduces afterload on the heart - Thus less energy required to produce same cardiac output - Thus less work on heart and O2 demand - E.g. verapamil

Answer 43

• To restore patent coronary artery and increase flow reserve • Done when medication fails (most) or when high risk disease is identified • Percutaneuos Coronary Intervention (PCI): - Dilating coronary atheromatous obstructions by inflating balloon within it - Insert balloon and stent, inflate balloon and remove it, stent persists and keeps artery patent - Expanding plaque = make artery bigger - Pros; less invasive, convenient, short recovery & repeatable - Cons; risk of stent thrombosis, not good for complex disease • Coronary Artery Bypass Graft (CABG): - Left Internal Mammary Artery (LIMA) used to bypass proximal stenosis (narrowing) in Left Anterior Descending (LAD) coronary artery - Pros; good prognosis, deals with complex disease - Cons; invasive, risk of stroke or bleeding, one time treatment and need to stay in hospital - long recovery

Answer 44

* Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis * This causes full thickness damage of heart muscle * Can usually be diagnosed on ECG at presentation * Will produce a pathological Q wave some time after MI so also known as Q-wave infarction

Answer 45

• Angina of recent onset (less than 24hrs) or • Cardiac chest pain with crescendo pattern • Deterioration in previously stable angina, with symptoms frequently occurring at rest • Angina of increasing frequency or severity, occurs on minimal exertion or even at rest - form of acute coronary syndrome

Answer 46

• Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis • Is a retrospective diagnosis made after troponin results and sometimes other investigation results are available • This causes partial thickness damage of heart muscle • Also known as a Non-Q wave infarction will see ST depression and/ or T wave inversion

Answer 47

in a NSTEMI there is occluding thrombus which leads to myocardial necrosis and a rise in serum troponin or creatine kinase-MB (CK-MB)

Answer 48

occurs when cardiac myocytes die due to myocardial | ischaemia

Answer 49

- Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection

Answer 50

- MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension

Answer 51

- MI due to sudden cardiac death, related to PCI and related to CABG respectively

Answer 52

- Age - Male - Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55 - Smoking - Hypertension, diabetes mellitus, hyperlipidaemia - Obesity & sedentary lifestyle

Answer 53

- Rupture or erosion of the fibrous cap of a coronary artery plaque - Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation - The presence of a rich lipid pool within the plaque and a thin, fibrous cap is associated with an increased risk of rupture - Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow - Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/ fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia or Sudden CVS death - In unstable angina the plaque has a necrotic centre and ulcerated cap and the thrombus results in PARTIAL OCCLUSION - In myocardial infarction the plaque also has a necrotic centre but the thrombus results in TOTAL OCCLUSION

Answer 54

``` - Unstable angina: • Chest pain; new onset, at rest with crescendo pattern • Breathlessness • Pleuritic pain • Indigestion - New onset angina - Recent destabilisation of pre-existing angina with moderate or severe limitations of daily activities - Acute central chest pain, lasting more than 20 minutes, associated with: • Sweating • Nausea and vomiting • Dyspnoea • Fatigue • Shortness of breath • Palpitations - May present without chest pain (silent infarct) e.g. in elderly or diabetics - Distress and anxiety - Pallor - Increased pulse and reduced BP - Reduced 4th heart sound - May be signs of heart failure (increase in jugular venous pressure) - Tachy/bradycardia - Peripheral oedema ```

Answer 55

- Angina - Pericarditis - Myocarditis - Aortic dissection - Pulmonary embolism - Oesophageal reflux/spasm

Answer 56

• Can be normal • ST depression and T-wave inversion (this tends to occur hours/days after) (NSTEMI) are highly suggestive of an ACS, particularly if associated with anginal chest pain • Can get hyperacute (tall) T waves • With a STEMI, complete occlusion of a coronary vessel will result in a persistent ST-elevation, hyperacute (tall) T waves or new left bundle branch block pattern - may see pathological Q waves a few days after MI (sign of previous MI)

Answer 57

• Troponin (T & I): - T & I are the most sensitive and specific markers of myocardial necrosis - Serum levels increase within 3-12 hours from the onset of chest pain and peak at 24-48 hours - They then fall back to normal over 5-14 days - Can act as prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation • CK-MB: - CK-MB can be used as a marker for myocyte death - but has low accuracy since it can be present in the serum of normal individuals and in patients with significant skeletal muscle damage - However it can be used to determine re-infarction as levels drop back to normal after 36-72 hours • Myoglobin: - Becomes elevated very early in MI but the test has poor specificity since myoglobin is present in skeletal muscle

Answer 58

• Look for cardiomegaly, pulmonary oedema or a widened mediastinum (aortic rupture)

Answer 59

``` - Pain relief: • GTN spray • IV opioid - Anti-emetic - Oxygen: • Aim for 94-98% saturation • 88-92% for those with COPD ```

Answer 60

• Atheromatous plaque rupture results in platelets being exposed to ADP/ThromboxaneA2/ adrenaline/thrombin/collagen tissue factor • This results in platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other = aggregation) • Then thrombin (already present in surroundings) is able to enzymatically convert fibrinogen to fibrin (insoluble) resulting in the formation of a fibrin mesh over platelet plug and the formation of a thrombotic clot • Aspirin (oral): - COX1-inhibitor = blocks formation of thromboxane A2 thus prevents platelet aggregation • P2Y12 inhibitors (oral): - Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation - Can be used if allergic to aspirin - Can also be used alongside aspirin as a dual anti-platelet therapy - E.g. Clopidogrel, Prasugrel & Ticagrelor - Side effects: neutropenia (low neutrophils), thrombocytopenia (low platelets) and INCREASED RISK OF BLEEDING - AVOID if CABG planned • Glycoprotein IIb/IIIa antagonists (IV): - Only IV available - Used in combination with aspirin and oral P2Y12 inhibitors in patients with ACS undergoing Percutaneous Coronary Intervention (PCI) - INCREASES RISK OF MAJOR BLEEDING - E.g. Abciximab, Tirofiban and Eptifbatide

Answer 61

``` - Beta blockers (IV & oral): • E.g. Atenolol (IV then oral) or Metoprolol (IV then oral) • Side effects: Avoid with asthma, heart failure, hypotension and bradyarrhythmias - Statins (oral): • HMG-CoA reductase inhibitors • E.g. Simvastatin, Pravastatin and Atorvastin - ACE inhibitors (oral): • E.g. Ramipril and Lisonopril • Monitor renal function - Coronary revascularisation: • PCI • CABG - high risk mortality in high risk groups e.g. recent MI - Risk factor modification: • Stop smoking • Lose weight and exercise daily • Healthy diet • Treat hypertension & diabetes • Low fat diet with statins ```

Answer 62

• Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to COMPLETE occlusion of artery by thrombus

Answer 63

- ST elevation MI (STEMI): • Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis • This causes full thickness damage of heart muscle • Usually diagnosed on ECG at presentation • Tall T waves • ST elevation and subsequent pathological Q wave • May present as new left bundle branch block (LBBB) on ECG • COMPLETE - Non ST elevation MI (NSTEMI) or Non-Q infarction: • Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis • This causes partial thickness damage of heart muscle • A RETROSPECTIVE diagnosis made after troponin results and sometimes other investigation results are available • ST depression/T wave inversion • STEMI is the most common medical emergency

Answer 64

- Age - Male - History of premature coronary heart disease - Premature menopause - Diabetes mellitus - Smoking - Hypertension - Hyperlipidaemia - Obesity and sedentary lifestyle - Diabetes mellitus - Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55

Answer 65

- Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque - This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial necrosis within 15-30 minutes in a STEMI (since major artery occluded fully) - STEMI: • The sub-endocardial myocardium is initially affected but, continued ischaemia, the infarct zone extends through the sub-epicardial myocardium, producing a transmural Q wave MI • Early reperfusion may salvage regions of the myocardium - reducing future mortality and morbidity

Answer 66

- Any patient presenting with severe chest pain lasting more than 20 minutes may be suffering from an MI - Chest pain: • Severe central ongoing pain, lasting more than 20 minutes • Pain may radiate to the left arm, jaw or neck • Pain DOES NOT usually respond to sublingual GTN spray - opiate analgesia is required • Pain described as substernal pressure, squeezing, aching, burning or even sharp pain • Associated with; sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations - Breathlessness - Fatigue - Distress and anxiety - Pale, clammy and marked sweating - Significant hypotension (low BP) - Bradycardia or tachycardia

Answer 67

- Stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis and MSK chest pain

Answer 68

* Diagnosed on presentation * ST elevation * Tall T waves * L bundle branch block (LBBB) * T wave inversion and pathological Q waves follow

Answer 69

* Diagnosis is retrospective made after troponin results etc. * ST depression and T wave inversion

Answer 70

• Performed on admission to A & E • Continuous monitoring required due to high likelihood of significant cardiac arrhythmias

Answer 71

``` Anterior - ST elevation V1-3 Inferior - St elevation II, III, AVF Lateral - I, AVF V5-6 Posterior - ST depression V1-3 Dominant R wave ST elevation V5-6 Subendocardial - any ```

Answer 72

- After the first few minutes, the T waves become tall, pointed and upright, and there is ST segment elevation - After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop - After a few days, the ST segment returns to normal - After weeks or months, the T wave may return to upright but the Q WAVE REMAINS

Answer 73

- Troponin I or T increased - Myoglobin increased - Transthoracic echocardiography (TTE) may be helpful to confirm MI, as wall-motion abnormalities are detected early in STEMI

Answer 74

* Aspirin 300mg chewable * GTN (sublingual) * Morphine

Answer 75

* IV morphine * Oxygen if their sats are below 95% or are breathless * Beta-blocker - Atenolol * P2Y12 inhibitor - Clopidogrel

Answer 76

• PCI: - Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 MINUTES of first medical contact - If not possible then give patient fibrinolysis and then transfer to PCI centre after infusion • CABG

Answer 77

``` - Fibrinolysis - enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin - Risk factor modification: • Stop smoking • Lose weight and exercise daily • Healthy diet • Treat hypertension & diabetes • Low fat diet with statins - Secondary prevention: • Statins • Aspirin long term • Warfarin if large MI • o blockers • ACE inhibitors ```

Answer 78

• Sudden death - often within hours often due to ventricular fibrillation • Arrhythmias - in the first few days due to electrical instability following infarction, pump failure and excessive sympathetic stimulation • Persistent pain - 12 hours-few days after due to progressive myocardial necrosis • Heart failure: - When cardiac output is insufficient to meet the bodies metabolic demands - Due to ventricular dysfunction following muscle necrosis also resulting in arrhythmias • Mitral incompetence - can happen in the first few days or occur later. Due to myocardial scarring preventing valve closure • Pericarditis - due to transmural infarct resulting in inflammation of pericardium, more common in STEMI • Cardiac rupture: - Early rupture - the result of shearing between mobile and immobile myocardium - Late rupture - due to weakening of wall following muscle necrosis and acute inflammation • Ventricular aneurysm - due to stretching of newly formed collagenous scar tissue

Answer 79

• The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body • Is a syndrome and not a diagnosis on its own • Can result from any structural or functional cardiac disorder that impairs the hearts ability to function and meet the demands of supplying sufficient oxygen and nutrients to the metabolising body

Answer 80

- 65 and older - African descent - Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men - Obesity - People who have had an MI

Answer 81

- When the heart begins to fail, there are many systems involved that initiate physiological COMPENSATORY CHANGES that try to maintain cardiac output and peripheral perfusion in order to negate the effects of the heart failure - However as heart failure progresses, these mechanisms are overwhelmed and become pathophysiological also known as DECOMPENSATION

Answer 82

- Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole - This increased diastolic (or preload - the volume of blood in the ventricle before contraction) volume stretches the myocardial fibres and, as Starling’s law of the heart says, myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction - However, in heart failure, the failing myocardium actually doesn't contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease

Answer 83

- Outflow resistance (afterload) is the load or resistance against which the ventricle contracts - It is made up of: • Pulmonary and systemic resistance • Physical characteristics of the vessel walls • The volume of blood that is ejected - When there is an increase in afterload there is a increase in end-diastolic volume and a decrease in stroke volume and thus a DECREASE in cardiac output - This results in a increase of end-diastolic volume and dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload

Answer 84

- When baroreceptors (located in the arterial wall of the aorta, carotid and in the heart walls and major veins) detect a drop in arterial pressure or an increase in venous pressure (due to back flow of blood) they stimulate sympathetic activation - This increases the force of contraction (positively inotropic) of the heart (which increases stroke volume) as well as heart rate - both resulting in an increase in cardiac output - However in heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate resulting in their being less receptor to act on meaning the effect of sympathetic activation is diminished and cardiac output stops increasing in response to sympathetic activation

Answer 85

- Reduced cardiac output leads to diminished renal perfusion,thereby activating the renin-angiotensin system whereby; angiotensinogen is converted to angiotensin I under the action of renin, angiotensin I is then converted to angiotensin II under the act of angiotensin converting enzyme (ACE), angiotensin II then stimulates the release of aldosterone from the adrenal cortex above the kidneys - This results in increased Na+ reabsorption and thus water reabsorption as well as the release of ADH which stimulates water retention - This results in the increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus cardiac output - However, with increased force of contraction the cardiac myocytes require more energy and thus more blood however in heart failure (which is most commonly caused by ischaemic heart disease) there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output

Answer 86

* Inability of the ventricle to contract normally resulting in a decrease in cardiac output * Caused by ischaemic heart disease, myocardial infarction and cardiomyopathy (disease of heart muscle thus impairing function)

Answer 87

• Inability of the ventricles to relax and fill fully thereby decreasing stroke volume and decreasing cardiac output • Caused by hypertrophy (due to chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this) of ventricles resulting in there being less space for blood to fill in and thus decreased cardiac output • Also caused by aortic stenosis (the narrowing of the aortic valve) which also increases afterload and thus decreases cardiac output

Answer 88

• Often used exclusively to mean new onset or decompensation of chromic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension

Answer 89

* Develops slowly | * Venous congestion is common but arterial pressure is well maintained until very late

Answer 90

- Three cardinal symptoms are; shortness of breath, fatigue & ankle swelling but these are non-specific! - Dyspnoea especially when lying flat (orthopnoea) - Cold peripheries - Raised jugular venous pressure (JVP) - Murmurs and displaced apex beat - Cyanosis - Hypotension - Peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output - Tachycardia - Third & fourth heart sounds - Ascites - Bi-basal crackles - Use New York Heart Association (NYHA) classification for the assessment of the severity of symptoms: • Class I: No limitation (asymptomatic) - exercise = no fatigue, dyspnoea or palpitation • Class II: Slight limitation (mild HF (heart failure)) - comfortable at rest, normal activity = fatigue, dyspnoea and palpitations • Class III: Marked limitation (moderate HF) - comfortable at rest, gentle activity = fatigue, dyspnoea & palpitations • Class IV: Inability to carry out any physical activity without discomfort (severe HF) - symptoms occur at rest

Answer 91

- Blood tests: • Brain natriuretic peptide (BNP): - Secreted by ventricles in response to increase myocardial wall stress - Increased in patients with heart failure - Levels correlate with ventricular wall stress and the severity of heart failure • FBC, U&E’s and liver biochemistry - CXR: • Alveolar oedema • Cardiomegaly • Dilated upper lobe vessels of lungs • Effusions (pleural) - ECG: • Shows underlying causes; ischaemia, left ventricular hypertrophy in hypertension or arrhythmia • If ECG and BNP normal then heart failure is unlikely • If both abnormal then go to echocardiogram - Echocardiography: • Assess cardiac chamber dimension • Look for regional wall motion abnormalities, valvular disease and cardiomyopathies • Look for sign of MI

Answer 92

- Lifestyle changes: • Avoid large meals, lose weight, stop smoking, exercise, vaccination - Diuretics: • Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion • Generally provide symptomatic relief • Loop diuretic - furosemide • Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in the distal convoluted tubule) • Aldosterone antagonist (thereby inhibiting ADH release resulting in water loss) - spirolactone & epelerone - note with these beware of renal impairment and hyperkalaemia - ACE inhibitors: • Ramipril, enalipril, captopril • Side effects: cough (since inhibit ACE and thus the breakdown of substance P and bradykinin which results in cough), hypotension, hyperkalaemia and renal dysfunction • If cough is a problem then can give angiotensin receptor blockers (not as effective as ACE-inhibitors) e.g. canderstan or valsartan

Answer 93

``` - Beta-blockers: • Bisoprolol, nebivolol, carvedilol • Start at low dose and titrate upwards • DO NOT GIVE TO ASTHMATICS - Digoxin - Inotropes - Revascularisation: • When some viable myocardium remains • Illicit PCI stenting - Surgery to repair: • Mitral valve repair, aortic or mitral valve replacement - Heart transplant in young people - Cardiac resynchronisation - improve the coordination of the atria and ventricles ```

Answer 94

• Mitral valve is on the left side and is also known as the tricuspid valve, it separates the left atrium from the left ventricle

Answer 95

* Obstruction of left ventricle inflow that prevents proper filling during diastole * Mitral valve has 2 cusps

Answer 96

- Normal mitral valve area is 4-6cm2, symptoms begin at areas less than 2cm2 - Most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever due to infection with group A beta-haemolytic streptococcus e.g. Streptococcus Pyogenes - The condition is more common in men than women - Inflammation due to rheumatic fever leads to commissural fusion and a reduction in mitral valve orifice area, causing the characteristic doming pattern seen on echocardiography - Over many years, the condition progresses to valve thickening, cusp fusion, calcium deposition, a severely narrowed (stenotic) valve orifice and progressive immobility of the valve cusps - Prevalence and incidence is decreasing due to a reduction of rheumatic heart disease - Other causes include: • Infective endocarditis (3.3%) • Mitral annular calcification (2.7%) - rarely leads to mitral stenosis if extensive, particularly in elderly patients and those with end-stage renal disease

Answer 97

- History of rheumatic fever | - Untreated streptococcus infections

Answer 98

- Thickening and immobility of the valve leads to obstruction of blood flow from the left atrium to the left ventricle - In order for sufficient cardiac output to be maintained, the left atrial pressure increases and left atrial hypertrophy and dilatation occur - Consequently pulmonary venous, pulmonary arterial and right heart pressures also increase - The increase in pulmonary capillary pressure is followed by the development of pulmonary oedema - this is seen particularly when atrial fibrillation occurs, due to the elevation of left atrial pressure and dilatation, with tachycardia and loss of coordinated atrial contraction - This is partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction (reactive pulmonary hypertension) - Pulmonary hypertension leads to right ventricular hypertrophy, dilatation and failure with subsequent tricuspid regurgitation

Answer 99

- Usually there are no symptoms until the valve orifice is moderately stenosed i.e. area is less than 2cm2 - This usually doesn't occur until several decades after the first attack of rheumatic fever - Progressive dyspnoea - due to left atrial dilation resulting in pulmonary congestion (reduced emptying), which is worse with; exercise, fever, tachycardia and pregnancy - Haemoptysis - due to rupture of bronchial vessels due to the elevated pulmonary pressure - Right heart failure - due to the development of pulmonary hypertension with symptoms of weakness, fatigue and abdominal or lower limb swelling - Atrial fibrillation - due to left atrium dilation giving rise to palpitations - Systemic emboli - due to atrial fibrillation, most commonly in the cerebral vessels

Answer 100

- Prominent “a” wave in jugular venous pulsations - due to pulmonary hypertension and right ventricular hypertrophy - Mitral facies/malar flush - bilateral, cyanotic or dusky pink discolouration over the upper cheeks - pinkish-purple patches on the cheeks due to vasoconstriction in response to diminished cardiac output - Heart sounds: • Diastolic murmur (heard when blood flows over a valve): - Low-pitched diastolic rumble most prominent at the apex - Heard best with patient lying on the left side in held expiration • Loud opening S1 snap: heard at apex when leaflets are still mobile: - Due to the abrupt halt in leaflet motion in early diastole, after a rapid initial opening, due to fusion at the leaflet tips - As the valve cusps become more immobile, the loud first heart sound softens and the opening snap disappears • The more severe the stenosis, the longer the diastolic murmur and the closer the opening snap is to S2 (second heart sound)

Answer 101

``` - CXR: • Left atrial enlargement • Pulmonary oedema/congestion • Occasionally calcified mitral valve - ECG: • Atrial fibrillation • Left atrial enlargement - Echocardiogram: • GOLD STANDARD for diagnosis • Assess mitral valve mobility, gradient and mitral valve area ```

Answer 102

- Mitral stenosis is a mechanical problem and medical therapy does not prevent progression - Beta-blockers e.g. Atenolol and digoxin which control heart rate and thus prolong diastole for improved diastolic filling - Diuretics for fluid overload e.g. Furosemide - Percutaneous mitral balloon valvotomy: • Catheter is inserted into the right atrium vie the femoral vein under local anaesthesia • The interatrial septum is then punctured and the catheter advanced into the left atrium and across the mitral valve • The balloon is inflated and puts pressure on valve thereby separating the leaflets thereby increasing the size of the mitral valve opening thus enabling more blood to flow from left atrium into left ventricle - Mitral valve replacement

Answer 103

• Backflow of blood from the left ventricle to the left atrium during systole • Mild physiological mitral regurgitation (MR) is seen in 80% of normal individuals

Answer 104

- Occurs due to abnormalities of the valve leaflets, chordae tendinae, papillary muscles or left ventricle - Most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) - resulting in a floppy mitral valve that prolapses (mitral valve prolapse) - Other causes include: • Ischaemic mitral valve • Rheumatic heart disease • Infective endocarditis • Papillary muscle dysfunction/rupture • Dilated cardiomyopathy

Answer 105

- Associated with females - Lower BMI - Advanced age - Renal dysfunction - Prior MI

Answer 106

- Regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is longstanding, since the regurgitant flow is accommodated by the large left atrium - Pure volume overload due to leakage of blood into left atrium during systole - Compensatory mechanisms: Left arterial enlargement, left ventricle hypertrophy (since left ventricle must put in same effort to pump less blood(due to regurgitation) so needs to pump harder to maintain cardiac output and thus hypertrophy to increase stroke volume) and increases contractility: • Progressive left atrial dilatation and right ventricular dysfunction due to pulmonary hypertension • Progressive left ventricular volume overload leads to dilatation and progressive heart failure

Answer 107

- Auscultation: • Soft S1 and a pan systolic murmur at the apex radiating to the axilla • Prominent third extra heart sound (S3) in congestive heart failure/left atrium overload • In chronic mitral regurgitation, the intensity of the murmur does not correlate with the severity - Exertion dysponea i.e. exercise intolerant - Dysponea develop because of pulmonary venous hypertension that arises as a direct result of the mitral regurgitation and secondarily as a consequence of left ventricular failure - Fatigue and lethargy due to reduced cardiac output - Increased stroke volume is felt as a palpitation - Symptoms of right heart failure and eventually lead to congestive cardiac failure - Heart failure may coincide with increased haemodynamic burden e.g in pregnancy, infection or atrial fibrillation

Answer 108

- Compensatory phase: 10-15 years - Once patients ejection fraction becomes less than 60% and/or becomes symptomatic then mortality rises sharply - Severe mitral regurgitation has a 5%/year mortality rate

Answer 109

- ECG: • May show left atrial enlargement, atrial fibrillation and left ventricle hypertrophy in severe MR • But not diagnostic - CXR: • Left atrial enlargement and central pulmonary artery enlargement - Echocardiogram: • Estimation of left atrium and left ventricle size and function • Also gives valve structure assessment • Transoesophageal is very helpful

Answer 110

- Medications: • Vasodilators such as ACE-inhibitors e.g. Ramipril or Hydralazine (smooth muscle relaxer) • Heart rate control for atrial fibrillation with Beta blockers (Atenolol), Calcium channel blockers and digoxin • Anticoagulation in atrial fibrillation and flutter • Diuretics for fluid overload e.g. Furosemide - Serial echocardiography: • Mild: 2-3 years • Moderate: 1-2 years • Severe: 6-12 months ``` - Indications for surgery: • Any symptoms at rest or exercise then initiate repair if feasible • Asymptomatic: - If ejection fraction is less than 60% - If new onset atrial fibrillation ```

Answer 111

- Aortic valve is located on the left side of the heart and separates the left ventricle from the aorta - Aortic valve has 3 cusps - It is one of the two semilunar valves of the heart, the other being the pulmonary valve

Answer 112

• Narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue

Answer 113

- Normal aortic valve area is 3-4cm2 - Symptoms occur when valve area is 1/4th of normal - Primarily a disease of ageing - Congenital is the second most common cause - The most common type of valvular disease in the western world

Answer 114

• Supravalvular (above valve) e.g congenital fibrous diaphragm above the aortic valve • Subvalvular (below valve) e.g congenital condition in which a fibrous ridge or diaphragm is situated immediately below the aortic valve • Valvular - most common

Answer 115

3 main causes: • Calcific aortic valvular disease (CAVD) - essentially calcification of the aortic valve resulting in stenosis, most commonly seen in elderly • Calcification of a congenital bicuspid aortic valve (BAV) (valve has 2 leaflets instead of 3 due to genetic disease - this is the most common congenital heart disease) resulting in stenosis • Rheumatic heart disease - rare now due to eradication

Answer 116

- Congenital bicuspid aortic valve (BAV) predisposes to stenosis and regurgitation - bicuspid valves are more likely to develop stenosis - Congenital BAV is predominant in males

Answer 117

- Due to the narrowing there is obstructed left ventricular emptying and a pressure gradient develops between the left ventricle and the aorta resulting in an increased afterload - This results in increased left ventricular pressure and compensatory left ventricular hypertrophy - In turn, this results in relative ischaemia of the left ventricular myocardium (since hypertrophy results in increased blood demand), and consequent angina, arrhythmias and left ventricular failure - The obstruction to left ventricular emptying is relatively more severe on exercise - since exercise causes a many-fold increase in cardiac output, however due to the severe narrowing of the aortic valve, the cardiac output can hardly increase - thus, the blood pressure falls, coronary ischaemia worsens, the myocardium fails and cardiac arrhythmias develop - When this compensatory mechanism is exhausted left ventricular function decline rapidly

Answer 118

- Think aortic stenosis in ANY elderly person with chest pain, exertional dysponea or syncope (loss of consciousness due to lack of blood) - Classic triad: • Syncope - usually exertional • Angina (increases myocardial oxygen demand; with resulting demand/ supply mismatch) • Heart failure (usually after 60) • Dysponea on exertion due to heart failure - Sudden death - Slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus) - Heart sounds: • Soft or absent second heart sound • Prominent 4th (S4) heart sound due to left ventricular hypertrophy • Ejection systolic murmur-crescendo-decrescendo character • Loudness does NOT tell you anything about severity

Answer 119

- Aortic regurgitation | - Subacute bacterial endocarditis

Answer 120

- Echocardiogram: • Two measurement obtained are: - Left ventricular size & function; left ventricular hypertrophy, dilation and ejection fraction - Doppler derived gradient and valve area (AVA), allows for the assessment of the pressure gradient across the valve during systole - ECG: • Left ventricular hypertrophy • Left atrial delay • Left ventricular ‘strain’ pattern due to ‘pressure overload’ - depressed ST segments and T-wave inversion in leads orientated towards left ventricle i.e. I, AVL, V5 & 6 when disease is severe - CXR: • Left ventricular hypertrophy • Calcified aortic valve

Answer 121

- Rigorous dental hygiene/care due to the increased risk of infective endocarditis (IE) in anyone with valvular heart disease - consider IE prophylaxis in dental procedures - There is a limited role for medication due to the fact that aortic stenosis is a mechanical problem - Vasodilators are contraindicated in severe aortic stenosis due to the fact that they may trigger hypotension and thus syncope

Answer 122

- Surgical aortic valve replacement is the definitive treatment: • Indications: - Any SYMPTOMATIC patients with severe aortic stenosis (include symptoms with exercise) - Any patient with decreasing ejection fraction - Any patent undergoing CABG with moderate or severe aortic stenosis - An alternative for surgical replacement is percutaneous in what is known as Transcutaneous Aortic Valve Implantation (TAVI): • Minimally invasive • Pass catheter up the aorta then inflate balloon across the narrowed valve which will crack the calcification • Then pass another catheter which leaves a stent with a valve = new aortic valve

Answer 123

``` • Leakage of blood into the left ventricle from aorta during diastole due to ineffective coaptation (bringing together) of the aortic cusps, of which there are three ```

Answer 124

- Can be associated with aortic stenosis - Main causes: • Congenital bicuspid aortic valve (BAV) - chronic • Rheumatic fever - chronic • Infective endocarditis - acute

Answer 125

- SLE - Marfan’s and Ehlers-Danlos syndrome - connective tissue disorders - Aortic dilatation - Infective endocarditis or aortic dissection

Answer 126

- Aortic regurgitation is reflux of blood from the aorta through the aortic valve into the left ventricle during diastole - If net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase and, consequently, the left ventricular size must enlarge resulting in left ventricle dilation and hypertrophy - Progressive dilation leads to heart failure - Furthermore due to the fact that the remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole - regurgitation causes diastolic blood pressure to fall and thus coronary perfusion decreases - Also the large left ventricular size is mechanically less efficient, so that the demand for oxygen is greater and cardiac ischaemia develops

Answer 127

- In chronic regurgitation, patients remain asymptomatic for many years before symptoms develop - Exertional dysponea - Palpitations - Angina - Syncope - Wide pulse pressure - Apex beat is displaced laterally - Heart sounds: • Diastolic blowing murmur at the left sternal border • Systolic ejection murmur; due to increased flow across the aortic valve - Collapsing water hammer pulse (bounding and forceful rapidly increasing and subsequently collapsing) - Quincke’s sign - capillary pulsation in the nail beds - de Musset’s sign - head nodding with each heart beat - Pistol shot femoral - a sharp bang heard on auscultation - Asymptomatic until 4th or 5th decade

Answer 128

- Heart failure - Infective endocarditis - Mitral regurgitation

Answer 129

- Echocardiogram: • Evaluation of the aortic valve and aortic root • Measurement of left ventricle dimensions and function • Cornerstone for decision making and follow up evaluation - CXR: • Enlarged cardiac silhouette and aortic root enlargement • Left ventricular enlargement - ECG: • Signs of left ventricular hypertrophy due to ‘volume overload’ - tall R waves and deeply inverted T waves in the left-sided chest leads, and deep S waves in the right-sided leads

Answer 130

- In general consider infective endocarditis prophylaxis - Vasodilators such as ACE-inhibitors such as Ramipril will improve stroke volume and reduce regurgitation but only if patient is symptomatic or has hypertension - Serial echocardiograms to monitor progression - Surgery for valve replacement: • If symptoms are increasing, enlarging heart on CXR/ECHO, ECG deterioration (T wave inversion in lateral leads)

Answer 131

• An infection of the endocardium or vascular endothelium of the heart • Known as subacute bacterial endocarditis • Infection occurs on the following: - Valves with congenital or acquired defects (usually on the left side of the heart). Right sided endocarditis is more common in IV drug addicts - Normal valves with virulent organisms such as Streptococcus pneumoniae or Staphylococcus aureus - Prosthetic valves and pacemakers

Answer 132

- More common in developing countries - Disease of: • the elderly or those with prosthetic valves • the young IV drug user • the young with congenital heart disease - More common in males - Caused by: • Staphylococcus aureus (IVDU, diabetes and surgery) - most common cause • Pseudomonas aeruginosa • Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri & strep. oralis)

Answer 133

- IV drug use - Poor dental hygiene - Skin and soft tissue infection - Dental treatment - IV cannula - Cardiac surgery - Pacemaker

Answer 134

- Usually the consequence of two factors; the presence of organisms in the bloodstream and abnormal cardiac endothelium that facilitates their adherence and growth - Bacteraemia may arise for patient-specific reasons: • Poor dental hygiene - bacteria in tooth plaque can cause gum disease which results in bleeding and inflammation of gums meaning when brushing/in dental procedure this bacteria can enter the bloodstream and reach the heart • IV drug use • Soft tissue infections - It may also be associated with diagnostic or therapeutic procedures: • Dental treatment • Intravascular cannulae • Cardiac surgery • Permanent pacemakers

Answer 135

- Damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation - Aortic and mitral valves are most commonly involved - IV drug users are the exception since right-sided lesions are more common in them - Virulent organisms destroy the valve they are on resulting in regurgitation and worsening heart failure

Answer 136

- High clinical suspicion: • New valve lesion/regurgitant murmur • Embolic events of unknown origin • Sepsis of unknown origin • Haematuria, glomerulonephritis and suspected renal infarction • Fever plus: - Prosthetic material inside the heart - Risk factor for infective endocarditis e.g. IV drug user - Newly developed ventricular arrhythmias or conduction disturbances - Headache, fever, malaise, confusion, and night sweats - quite unspecific so often misdiagnosed and missed - Also finger clubbing

Answer 137

- If Staphylococcus aureus then will develop very quickly - high fever and feel ill rapidly, with the other virulent ones you don't feel as ill - Embolisation of vegetations e.g. stroke, pulmonary embolus, bone infections, kidney dysfunction and myocardial infarction - Valve dysfunction result in in arrhythmia and heart failure - Endocarditis should be excluded in ANY patient with a heart murmur and fever - Clinical manifestations: • Splinter haemorrhages on nail beds of fingers • Embolic skin lesions - black spots on skin (infarcts causes by bits of infective vegetation blocking small capillaries) • Osler nodes - tender nodules in the digits • Janeway lesions - haemorrhages and nodules in the fingers • Roth spots - retinal haemorrhages with white or clear centres seen on fundoscopy • Petechiae - small red/purple spots caused by bleeds in the skin

Answer 138

- Use Dukes criteria - Blood cultures: • 3 sets from different sites over 24 hours • Take BEFORE ANTIBIOTICS STARTED • Identifies in 75% of cases - Blood test: • CRP & ESR raised • Normochromic (normal concentration of haemoglobin), normocytic (normal sized red blood cells) anaemia • Neutrophilia - Urinalysis - look for haematuria

Answer 139

- CXR - cardiomegaly - ECG - long PR interval at regular intervals - Echocardiogram: • Two options: - Transthoracic echo (TTE) - safe, non invasive, no discomfort BUT often poor images so low sensitivity but can identify vegetations (if greater than 2mm) - however a negative TTE DOES NOT exclude the diagnosis of infective endocarditis - Transoesophageal echo (TOE) - much more sensitive but very uncomfortable, is useful for visualising mitral lesions and possible development of aortic root abscess - BETTER AT DIAGNOSING, ANSWER THIS IN EXAM!

Answer 140

- Antibiotic treatment (which one is decided on organism ascertained from cultures) for 4-6 weeks - If not staphylococcus then use penicillin ideally Benzylpenicillin & Gentamycin (doesn’t work on own since cannot get through bacterial cell wall) - If staphylococcus then use Vancomycin & Rifampicin (if MRSA) - Treat complications e.g. arrhythmia, heart failure, heart block, embolisation, stroke rehab and abscess drainage - Surgery - removing valve and replacing with prosthetic one: • Operate if the infection cannot be cured with antibiotics i.e. returns after treatment • Operate to remove infected devices • Operate to remove large vegetations before they embolise - In term of prevention recommend GOOD ORAL HEALTH and inform patients of symptoms that may indicate infective endocarditis

Answer 141

``` • Group of diseases of the myocardium that affect the mechanical or electrical function of the heart ```

Answer 142

- All carry an arrhythmic risk - Can occur at younger ages - Restrictive cardiomyopathy is rare in childhood and has a poor outcome once symptoms develop - In general they are inherited genetic conditions although there are some acquired ones - 4 types: • Hypertrophic • Dilated • Restricted • Arrythmogenic right ventricular

Answer 143

- Family history of cardiomyopathy - High blood pressure - Obesity - Diabetes - Previous MI

Answer 144

- Ventricular hypertrophy/thickening of the muscle

Answer 145

* Quite common, second most common cardiomyopathy (behind dilated) * 1/500 people have it * Autosomal dominant - familial * May present at any age * Most common cause of sudden cardiac death in the young * HCM refers to otherwise unexplained primary cardiac hypertrophy

Answer 146

• Caused by sarcomeric protein gene mutations e.g troponin T and B- myosin • All in the absence of hypertension and valvular disease • The hypertrophic, non-compliant ventricles impair diastolic filling resulting in reduced stroke volume and thus cardiac output • Another issue with thick powerful heart is that there is a disarray of cardiac myocytes so conduction is affected

Answer 147

* Hypertrophy of myocardium, particularly the intraventricular septum * Sudden death may be the first manifestation * Chest pain, Angina, dysponea, dizziness, palpitations, syncope * Left ventricular outflow obstruction may be a feature * Cardiac arrhythmia * Ejection systolic murmur * Jerky carotid pulse

Answer 148

• ECG: is abnormal and shows signs of left ventricular hypertrophy with progressive T wave inversion and deep Q waves • Echocardiogram: shows ventricular hypertrophy and a small left ventricle cavity • Genetic analysis can confirm diagnosis since most cases are autosomal dominant and familial

Answer 149

• Amiodarone - anti-arrythmatic medication, if at high risk of arrhythmia then can place an implantable cardiac defibrillator • Calcium channel blocker e.g. Verampil • Beta-blocker e.g. Atenolol

Answer 150

- Dilated left ventricle which contracts poorly/has thin muscle

Answer 151

• Most common cardiomyopathy • Autosomal dominant - familial • Can be caused by; ischaemia, alcohol, thyroid disorder or familial/ genetic

Answer 152

• Caused by cytoskeletal gene mutations • Left ventricle or right ventricle or all 4 chamber dilatation and thus dysfunction • Theory is that poorly generated contractile force leads to progressive dilatation of heart with some diffuse interstitial fibrosis

Answer 153

* Shortness of breath at first and fatigue * Dysponea * Heart failure since can’t contract * Arrhythmias * Thromboembolism * Sudden death * Increased jugular venous pressure

Answer 154

* CXR: cardiac enlargement * ECG: tachycardia, arrhythmia and non-specific T wave changes * Echo: shows dilated ventricles

Answer 155

• Heart failure and atrial fibrillation treated in conventional way

Answer 156

- Rare condition

Answer 157

• Causes are; amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

Answer 158

• There is normal or decreased volume of both ventricles with bi-atrial enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filing • Restrictive physiology • Poor dilation of the heart restricts its the ability of the heart to take on blood and pass it to the rest of the body • Rigid myocardium restricts diastolic ventricular filling

Answer 159

• Similar to constructive pericarditis • Dysponea, fatigue and embolic symptoms • Elevated jugular venous pressure with diastolic collapse and elevation of venous pressure with inspiration • Hepatic enlargement, ascites and dependent oedema • Third and fourth heart sounds

Answer 160

* CXR, ECHO & ECG are abnormal but non-specific | * Cardiac catheterisation helps to diagnose restrictive cardiomyopathy

Answer 161

* No specific treatment with poor prognosis * Patients die within a year * Can consider cardiac transplantation

Answer 162

• Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium • Cause is unknown • Familial form is usually autosomal dominant with incomplete penetrance but can be recessive

Answer 163

* Desmosome (normally hold cardiac cells together) gene mutation * Right ventricle replaced by fat and fibrous tissue * Muscle dies and replaced by fat as part of inflammatory process

Answer 164

* Cardiac cells are held less together thus conduction issues * ARRHYTHMIA is most common feature * Syncope * In late stages may be signs of right heart failure

Answer 165

• ECG usually normal but may show T wave inversion • ECHO may also be normal but in advanced disease may show right ventricular dilation • Genetic testing is the gold standard

Answer 166

• Beta-blockers e.g. Atenolol for patients with non-life-threatening arrhythmias • Amiodarone for symptomatic arrhythmias • Occasionally cardiac transplant indicated i.e. in cardiac failure or devastating arrhythmia

Answer 167

• 1% of all live births have some form of cardiac defect - common • Vary from minor to incompatible with life ex-utero • There is an overall male predominance • Although some individual lesions such as atrial septal defect and persistence ductus arteriosus occur more commonly in females • Usually due to misplaced structures or the arrest of the progression of normal structure development

Answer 168

- One child with defect increases the chance of the second child having another defect - Maternal prenatal rubella infection - persistent ductus arteriosus and pulmonary valvular and arterial stenosis - Maternal alcohol misuse - septal defects - Single genes associated e.g. Trisomy 21 (Down’s - septal, mitral and tricuspid valve defects) - Drugs e.g. Thalidomide, Amphetamines and Lithium - Diabetes of mother - Genetic abnormalities e.g. the familial form of arterial spatial defect and congenital heart block

Answer 169

- Congenital heart disease should be recognised as early as possible since the response is usually better the earlier treatment is initiated - Central cyanosis: • Occurs because of right-left shunting of blood or because of complete mixing of systemic and pulmonary blood flow resulting in poorly oxygenated blood entering the systemic circulation • Skin will go blueish • Seen in Tetralogy of Fallot and Tricuspid atresia - Clubbing of the fingers - associated with prolonged cyanosis

Answer 170

- Pulmonary hypertension: • Results from large left-to-right shunts • The persistently raised pulmonary flow leads to the development of increased pulmonary artery vascular resistance and consequent pulmonary hypertension • This resistance is due to the thickening of the vascular walls of the pulmonary arteries in response to the higher pressure • This resistance causes right ventricular pressure to increase and causes the REVERSAL OF SHUNT to right-to-left resulting in the patient going blue i.e. cyanosis • Known as Eisenmenger’s reaction and known as Eisenmenger’s complex specifically in relation to a ventricular-septal defect • The development of pulmonary hypertension significantly worsens the prognosis

Answer 171

- Growth retardation - common in children with cyanotic heart disease - Syncope: • Common when severe right or left ventricular outflow tract obstruction is present • Exertional syncope is associated with keeping central cyanosis and may occur in Fallot’s tetralogy - Adolescents and adults with congenital heart disease present with specific common problems related to the longstanding structural nature of these conditions: • Endocarditis - especially in small ventricular septal defects or bicuspid aortic valve • Calcification and stenosis of congenitally deformed valves e.g. bicuspid aortic valve • Atrial and ventricular arrhythmias • Sudden cardiac death • Right heart failure • End-stage heart failure

Answer 172

• Most common form of congenital heart disease, occurring in 1-2% of live births • More common in males than females • Normal aortic valve has 3 cusps (looks like Mercedes sign) • Bicuspid only has 2 cusps • These can work well at birth and go undetected but can be severely stenotic in infancy or childhood • Degenerate quicker than normal valves • Become regurgitant earlier than normal valves • Are associated with coarctation and dilation of the ascending aorta • May eventually develop aortic stenosis (requiring valve replacement) with to without aortic regurgitation thereby predisposing to infective endocarditis • Intense exercise may accelerate complications so do yearly echocardiograms on affected athletes

Answer 173

• Often first diagnosed in adulthood and represents one third of congenital heart disease • More common in women than men • Abnormal connection between the two atria • A probe can be passed through the layers of the foramen ovale (called the primum and secundum) so is sometimes known as “Probe patent foramen ovale” • Slightly higher pressure in the left atrium than the right atrium • Shunt is left-to-right • Thus NOT blue i.e. acyanotic • Increased flow into the right heart and lungs • If left untreated develop right heart overload and dilatation - the right ventricle is compliant and easily dilates to accommodate the increased pulmonary flow however this can result in: - Right ventricular hypertrophy - Pulmonary hypertension - Eisenmenger’s reaction - Increased risk of infective endocarditis

Answer 174

- Dysponea - Exercise intolerance - May develop atrial arrhythmias from right atrial dilatation - Pulmonary flow murmur - Fixed split second heart sound (delayed closure of the pulmonary valve because more blood has to get out) - CXR: • Large pulmonary arteries • Large heart - ECG: • Right bundle branch block (RBBB) due to right ventricle dilatation - Echocardiogram: • Hypertrophy and dilation of right side of heart and pulmonary arteries

Answer 175

- Surgical closure | - Percutaneous (key hole technique)

Answer 176

* Abnormal connection between the two ventricles * Many close spontaneously during childhood * Common - 20% of all congenital heart defects * Higher pressure in left ventricle than right ventricle * Thus left-to-right shunt * Thus does NOT go blue i.e. acyanotic * Increased blood flow through the lung

Answer 177

``` - Large defects: • The large volumes of blood flowing through the pulmonary vasculature lead to pulmonary hypertension and eventual Eisenmenger’s complex, when right ventricular pressure becomes higher than the left, as a result blood starts to shunt right-to-left resulting in cyanosis • Small breathless skinny baby • Increased respiratory rate • Tachycardia • CXR: - Big heart • Murmur varies in intensity - Small defects: • Large systolic murmur • Thrill (buzzing sensation) • Well grown • Normal heart rate • Normal heart size ```

Answer 178

- Medical initially since many will spontaneously close - Surgical closure - If small then no intervention is required - Prophylactic antibiotics - If moderately sized lesion; furosemide, ACE inhibitor e.g. ramipril and digoxin may suffice

Answer 179

• Associated with Downs syndrome • Basically a hole in the very centre of the heart • Involves; the ventricular septum, the atrial septum, the mitral and tricuspid valves • Can be complete or partial • Instead of two separate atrio-ventricular valves there is JUST ONE big malformed one which usually leaks

Answer 180

- Complete defect: • Breathlessness as neonate • Poor weight gain and feeding • Torrential pulmonary flow which can result in Eisenmenger’s resulting in cyanosis over time - Partial defect: • Can present in late adulthood • Presents similar to ventricular/atrial septal defect e.g. dysponea, tachycardia, excecrsicse intolerance etc.

Answer 181

- Pulmonary artery banding if large defect in infancy - band reduces blood flow to lungs thereby reducing pulmonary hypertension and Eisenmenger’s syndrome - Surgical repair is challenging - A partial defect may be left alone if there is no right heart dilatation

Answer 182

• Affects girls more than boys • Ductus arteriosus is a persistent communication between the proximal left pulmonary artery and the descending aorta • In foetal life pulmonary vascular resistance is high (since bronchioles are filled with fluid and vessels are vasoconstricted due to lack of O2) and the right heart pressure exceeds that of left - consequently flow is from right to left atrium through foramen ovale, and from pulmonary artery to aorta via ductus arteriosus • Normally, the ductus arteriosus closes within a few hours of birth in response to decreased pulmonary resistance; however in some cases e.g. in premature babies and in cases with maternal rubella, the ductus persists • If it remains open then there is an abnormal left-to- right shunt (from aorta to pulmonary artery) and eventually means that the lung circulation is overloaded with pulmonary hypertension (leading to Eisenmenger syndrome) and right side cardiac failure (due to right ventricular hypertrophy in response to increased afterload) subsequently • Also increases risk of infective endocarditis

Answer 183

- Continuous ‘machinery’ murmus - Bounding pulse - If large then large heart and breathlessness - Eisenmenger’s syndrome with differential cyanosis that is clubbed and blue toes BUT pink and not clubber fingers - Tachycardia - CXR: • With large shunt the aorta and pulmonary arterial system may be prominent - ECG: • May demonstrate left atrial abnormality and left ventricular hypertrophy - Echocardiogram: • May show dilated left atrium and left ventricle

Answer 184

- Can be closed surgically or percutaneously - Low risk of complications - Venous approach may require an AV loop - Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure

Answer 185

• More common in men than women • A narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus (distal to the origin of the left subclavian artery) • The net result is a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body, thus stronger perfusion to upper body compared to lower • Associated with Turner syndrome, berry aneurysms and patent ductus arteriosus • Resultant decreased renal perfusion leads to systemic hypertension that persists even after surgical correction

Answer 186

- Often asymptomatic for many years - Right arm hypertension - Bruits (buzzes) over the scapulae and back from collateral vessels - Murmur - Headaches and nose bleeds (due to hypertension) - Hypertension in the upper limbs - Discrepant blood pressure in the upper and lower body (will notice radial pulse BEFORE femoral pulse) - Long term problems: • Hypertension: - Early coronary artery disease - Early strokes - Sub-arachnoid haemorrhage - CXR: • Dilated aorta indented at the site of the coarctation - ECG: • Left ventricular hypertrophy - CT: • Can accurately demonstrate the coarctation and quantify flow

Answer 187

* Surgery * Balloon dilatation (preferred for re-coarctation) and stenting * Risk of aneurysm formation at the site of repair

Answer 188

``` • Most common form of cyanotic congenital heart disease • Consists of: - A large, maligned Ventricular Septal Defect (VSD) - An overriding aorta - Right ventricular outflow obstruction e.g. due to pulmonary stenosis - Right ventricular hypertrophy • The stenosis of the right ventricle outflow leads to the right ventricle being at a higher pressure than the left • Thus blue blood passes from the right ventricle to the left ventricle • The patients are BLUE i.e CYANOTIC ```

Answer 189

- Central cyanosis - Low birthweight and growth - Dysponea on exertion - Delayed puberty - Systolic ejection murmurs - CXR: • Boot shaped heart

Answer 190

- Full surgical treatment during first two years of life due to the progressive cardiac debility and cerebral thrombosis risk - Often get pulmonary valve regurgitation in adulthood and require redo surgery

Answer 191

``` • Narrowing of the outflow of the right ventricle • Can be; valvar, sub valvar or supra valvar • Severe: - Right ventricular failure as neonate - Collapse - Poor pulmonary blood flow - Right ventricular hypertrophy - Tricuspid regurgitation • Moderate/mild: - Well tolerated for many years - Right ventricular hypertrophy ```

Answer 192

- Balloon valvoplasty - place catheter with balloon through femoral vein then inflate balloon at stenosis to crush it but this can result in regurgitation - Open valvotomy - Shunt - to bypass the blockage

Answer 193

• Involves the aorta coming off the right ventricle and the pulmonary trunk coming off the left ventricle • Two closed circulations result • More common in men and associated with diabetes • Survival is only possible if there is communication between the two circuits and virtually all have some form of atrial septal defect with blood mixing • Treatment: - Atrial switch operation with good results

Answer 194

* Heart points to the right side of chest instead of to the left * Associated with severe cardiovascular abnormalities

Answer 195

• The pericardium acts as a protective covering for the heart • It consists of an outer fibrous pericardial sac and an inner serous pericardium • The inner serous pericardium is made up of: - Inner visceral epicardium - single cell layer that’s adherent to the epicardium (myocytes), that lines the heart and great vessels, and its reflection - Outer parietal pericardium - mainly collagen and elastin fibres, with no cells, that lines the fibrous sac - In between the layers is around 50ml of serous fluid that acts as a lubricant to allow the two surfaces to move over each other easily • Great vessels lie in the pericardium, if the proximal segment (ascending) of the aorta is ruptured then it will bleed in into the pericardial space and result in a cardiac tamponade

Answer 196

• Left atrium is mainly outside the pericardium • It promotes cardiac efficiency by limiting dilation, maintaining ventricular compliance and distributing hydrostatic forces • Aids atrial filling by creating a closed chamber, reduces external friction and acts as a barrier against infection and extension of malignancy • Anatomically fixes the heart to the sternum, diaphragm and costal cartilages • The pericardium is similar to an elastic band - initially stretchy but becomes stiff at higher tension, thus at low tension the pericardium has a small reserve volume • If this volume is exceeded the pressure is translated to the cardiac chambers and thus puts pressure on the heart • Small amount of volume added to this space has dramatic effects on filling e.g a cardiac tamponade • Pressure in the pericardium is very low • In a chronic pericardial effusion, the pericardium adapts slowly by laying down elastin & collagen and becomes more elastic so there is a much slower tamponade (thus there is no collapse of the right atrium) since the pressure equalises - but the entrance of fluid making up the effusion must be slow

Answer 197

• Acute inflammation of the pericardium; with or without effusion

Answer 198

- Majority are idiopathic and most commonly seen in the young, previously healthy patient - Occurs in men more than women - Occurs in adults more than children - Causes: • Infectious: - Viral (common): • Enteroviruses e.g. coxsackieviruses & echoviruses • Adenoviruses - Bacterial: • Mycobacterium tuberculosis (other bacteria are rare) - Fungal (very rare): • Histoplasma spp. - most likely to be seen in immunocompromised patient • Non-infectious: - Autoimmune (common): • Sjorgrens syndrome • Rheumatoid arthritis • SLE - Neoplastic; secondary metastatic tumours (common, above all is lung or breast cancer) - Dressler’s syndrome - post cardiac injury syndromes - Traumatic & iatrogenic: • Early onset (rare): - Direct injury - penetrating thoracic injury or oesophageal perforation - Indirect injury - non-penetrating thoracic injury or radiation • Delayed onset (common): - Pericardial injury syndromes (common) - Iatrogenic trauma e.g. coronary percutaneous intervention or pacemaker lead insertion

Answer 199

- Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes - A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop

Answer 200

- Chest pain: • Severe • Sharp & pleuritic (without constricting crushing character of ischaemic pain) • Rapid onset • Worse on inspiration or lying flat - relieved by sitting forward • Left anterior chest or epigastrium • Radiates to arm, more specifically the trapezius ridge (has co- innervation with the phrenic nerve) - whereas a STEMI would be arms, jaw & teeth - Dysponea - Cough - Hiccups - due to phrenic involvement - Pericardial friction rub present on auscultation - Fever and lymphocytosis (increase in lymphocytes) if due to virus or bacteria - Tachycardia

Answer 201

- Angina - MI - most important to rule out - Pleuritic pain - Pulmonary infarction - Pneumonia, GI reflux, peritonitis & aortic dissection

Answer 202

- ECG: • Is diagnostic • Widespread concave-upwards - SADDLE SHAPED ST ELEVATION (arrowed) • Diffuse ST segment elevation - present in all leads (must exclude STEMI which would have ST segment elevation but will be limited to the infarcted area e.g. anterior or inferior) • PR depression - CXR: • May demonstrate cardiomegaly in cases of effusion - if found then confirm with echocardiography • Often normal in idiopathic • Pneumonia is common with bacterial pericarditis - FBC: • Slight increase in white cell count • Anti Neutrophil Antibody in young females - SLE • Troponin - elevated suggests myopericarditis - ESR/CRP: • High ESR is indicative of autoimmune

Answer 203

- Restrict physical activity until resolution of symptoms and see improvement in ECG and CRP - NSAID e.g Ibuprofen for two weeks or Aspirin for two weeks - Colchicine for 3 weeks however is limited by nausea and diarrhoea but does reduce recurrence

Answer 204

- About 20% of cases of acute pericarditis go on to develop idiopathic relapsing pericarditis - This may occur within 6 weeks during weaning off NSAIDs or intermittently i.e. recurs more than 6 weeks after the initial presentation - The first line treatment is oral NSAIDs e.g. Ibuprofen - Colchicine has been proven to be more effective than Aspirin alone - In resistant cases, oral corticosteroids e.g. Prednisolone may be effective, and in some patients, pericardiectomy (removal of part/most of the pericardium) may be appropriate

Answer 205

• A pericardial effusion is a collection of fluid within the potential space of the serous pericardial sac • It commonly accompanies an episode of acute pericarditis • When a large volume collects in this space, ventricular filling is compromised, leading to the embarrassment of the circulation - this is a CARDIAC TAMPONADE

Answer 206

``` - Symptoms of a pericardial effusion commonly reflect the underlying pericarditis - Soft & distant heart sounds - Apex beat obscured - Raised jugular venous pressure - Dysponea ```

Answer 207

- High pulse but low blood pressure - High jugular venous pressure - Muffled 1st & 2nd heart sounds - Kussmaul’s sign - rise in jugular venous pressure and increased neck vein distension during inspiration - Pulsus paradoxus - an exaggeration in the normal variation in pulse pressure seen with inspiration, such that there is a drop in systolic blood pressure - Reduced cardiac output

Answer 208

``` - CXR: • Large globular heart - ECG: • Low-voltage QRS complexes • Sinus tachycardia - Echocardiogram: • Most useful for demonstrating effusion • Echo-free zone surrounding heart ```

Answer 209

``` - CXR: • Big globular heart - Beck’s triad: • Falling blood pressure • Rising jugular venous pressure • Muffled heart sounds - ECG: • Low voltage QRS - Echocardiogram: • IS DIAGNOSTIC • Echo-free zone around heart • Late diastolic collapse of RIGHT ATRIUM (remember most of L atrium is outside pericardium) • Early diastolic collapse of right ventricle ```

Answer 210

- Underlying cause should be sought and treated if possible - Most pericardial effusions resolve spontaneously - Pericardial effusions may re-accumulate most often due to malignancy - this may require a pericardial fenestration (a window in the pericardium is created to allow the slow release of fluid into the surrounding tissues)

Answer 211

- See expert help! - Require URGENT DRAINAGE via a PERICARDIOCENTESIS which will drain the fluid to relieve the pressure on the heart - Send fluid for culture, Ziehl-Nielsen stain and for cytology

Answer 212

- Certain causes of pericarditis such as tuberculosis, bacterial infection and rheumatic heart disease result in the pericardium becoming thick, fibrous and calcified - Cause is often unknown and can actually occur after any pericarditis

Answer 213

- In many cases, these pericardial changes do not cause any symptoms - If, however, the pericardium becomes so inelastic as to interfere with the diastolic filling of the heart, CONSTRICTIVE PERICARDITIS is said to have developed - As these changes are chronic, allowing the body time to compensate, this condition is not as immediately life-threatening as cardiac tamponade, in which the circulation is more acutely embarrassed - Constrictive pericarditis should be distinguished from RESTRICTIVE CARDIOMYOPATHY: • These conditions are very similar in their presentation, but the former is treatable! - In the later stages of constrictive pericarditis, the sub-endocardial layers of myocardium may undergo fibrosis, atrophy and calcification

Answer 214

- Kussmaul’s sign - rise in jugular venous pressure and increased neck vein distension during inspiration - Pulsus paradoxus - an exaggeration in the normal variation in pulse pressure seen with inspiration, such that there is a drop in systolic blood pressure - Diffuse heart sounds - Ascites - Oedema - Right heart failure signs - Atrial dilatation

Answer 215

- CXR: • Small heart with/without pericardial calcification - ECG: • Low-voltage QRS - Echocardiography: • Thickened, calcified pericardium • Small ventricular cavities with normal wall thickness

Answer 216

- Complete resection of the pericardium - risky with high complication rate

Answer 217

• Hypertension is a major cause of premature vascular disease, leading to cerebrovascular events, ischaemic heart disease and peripheral vascular disease • Mortality rises with increasing blood pressure

Answer 218

- Often symptomless so screening is vital - Major risk factor for CVD - Remain under diagnosed, under treated and poorly controlled in the UK - Prevalence is in those older than 35 - More common in men - Less than 140/90mmHg = Normotensive - Hypertension values: • Stage 1 hypertension: - More than or equal to 140/90mmHg clinic BP - Daytime average Ambulatory blood pressure monitoring (ABPM - 24hr BP monitor) or Home blood pressure monitoring (HBPM); greater than or equal to 135/85mmHg • Stage 2 hypertension: - More than or equal to 160/100mmHg clinic BP - Daytime average ABPM or HBPM greater than or equal to 150/95mmHg • Severe hypertension: - Clinic systolic BP greater than or equal to 180mmHg and/or diastolic BP greater than or equal to 110mmHg - Start immediate anti-hypertensive drug treatment!

Answer 219

- The commonest cause of cardiac failure and a major risk factor for atherosclerosis and cerebral haemorrhage - Hypertension can be classified according to whether the cause is unknown ‘essential (primary or idiopathic) hypertension’ or is known ‘secondary hypertension’ - Most cases are classified as essential - Essential hypertension: • Primary cause unknown • Accounts for the majority of cases • Multifactorial involving: - Genetic susceptibility - Excessive sympathetic nervous system activity - Abnormalities of Na+/K+ membrane transport - High salt intake - Abnormalities in renin-angiotensin-aldosterone system • Drug therapy: - Prescription drugs associated with hypertension include: • Corticosteroids e.g. Prednisolone • Cyclosporin • Erythropoietin • Some types of the contraceptive pill - Alcohol, amphetamines, ecstasy and cocaine are also causes of hypertension

Answer 220

- Secondary hypertension: • Commonly caused by renal disease or pregnancy • Other potential underlying conditions include; endocrine causes, coarctation of the aorta and drug therapy • Renal disease & hypertension: - Kidney disease can be both the cause and result of hypertension - CHRONIC KIDNEY DISEASE is the MOST COMMON CAUSE of secondary hypertension - Diabetes is the most common cause of chronic kidney disease - The vascular changes induced by hypertension (the acceleration of atherosclerosis and endothelial cell dysfunction resulting in the promotion of pheochromocytoma vasoconstriction) may cause or exacerbate renal disease - Chronic glomerulonephritis is another potential cause although less common now • Coarctation of the aorta: - Systemic hypertension is once of the commonest features in coarctation - Raised blood pressure will be detected in either arm, but NOT in the legs - The femoral pulse is often delayed relative to the radial - Undetected or untreated patients die from cardiac failure, hypertensive cerebral haemorrhage or dissecting aneurysm

Answer 221

• Endocrine causes: - Cushing’s syndrome: • Hypersecretion of corticosteroids (which enhance adrenalines resulting in a vasoconstrictive effect) is associated with systemic hypertension - Conn’s syndrome: • Adrenal tumour that secretes ALDOSTERONE (resulting in Na+ retention and thus water retention thereby increasing blood volume and pressure) can cause hypertension - Phaemochromocytoma: • Adrenal tumour that secretes CATECHOLAMINES (resulting in the stimulation of alpha-adrenergic receptors resulting in vasoconstriction, increased cardiac contractility as well as the stimulation of beta-adrenergic receptors resulting in an increase in heart rate and contractility) can cause hypertension - Note these tumours are rare

Answer 222

- Age - risk increases as you age - Race - hypertension is more common in blacks - Family history - hypertension runs in families - Overweight and obese - Little exercise - Smoking - Too much salt in diet - Alcohol - Diabetes - Stress

Answer 223

- Vascular changes: • Hypertension accelerates atherosclerosis • Also causes the thickening of the media of muscular arteries • It is the smaller arteries and arterioles that are especially affected in hypertension • The resulting endothelial cell dysfunction is associated with impaired nitric oxide-mediated vasodilatation and enhanced secretion of vasoconstrictors including endothelins and prostaglandins - Heart: • Hypertension is a major risk factor for ischaemic heart disease - Nervous system: • Intracerebral haemorrhage is a frequent cause of death in hypertension - Kidneys: • Hypertension can be the cause or result of renal disease • Kidney size is often reduced and small vessels show intimal thickening and medial hypertrophy and the numbers of sclerotic glomeruli are increased

Answer 224

- Malignant hypertension: • Characteristic features are a markedly raised diastolic blood pressure, usually over 120mmHg and progressive renal disease • Quite rare • Renal vascular changes are prominent and there is usually evidence of acute haemorrhage and papilloedema (optic disc swelling caused by increase intercranial pressure) • Can occur in previously fit individuals, often black males in their 30s-40s • Consequences: - Cardiac failure with left ventricular hypertrophy and dilatation - Blurred vision due to papilloedema and retinal haemorrhages - Haematuria and renal failure due to fibrinoid necrosis of glomeruli - Severe headache and cerebral haemorrhage

Answer 225

- Usually asymptomatic (except malignant hypertension) | - Found on screening

Answer 226

- Look for end-organ damage e.g. left ventricular hypertrophy, retinopathy and proteinuria - indicates severity and duration of hypertension and associated with a poorer prognosis - Urinalysis: • For protein, albumin:creatine ratio and haematuria - Blood tests: • Serum creatinine • eGFR • Glucose (to assess diabetes risk) - Fundoscopy/Opthalmoscopy: • Looking for retinal haemorrhage or papilloedema - ECG: • To detect left ventricular hypertrophy - Echocardiography: • To further detect left ventricular hypertrophy - 24 hour ambulatory blood pressure monitoring

Answer 227

- Treatment GOAL is 140/90mmHg - Change diet: • High consumption of vegetable and fruits and low-fat diet - Regular physical exercise - Reduce alcohol intake - Reduce salt intake - Lose weight - Stop smoking - ACD pathway: • A - ACE-inhibitor e.g. Ramipril or Enalapril, or Angiotensin receptor blocker (ARB) (use if ACEi is contraindicated e.g. due to cough) e.g. Candesartan or Losartan • C - Calcium channel blocker (CCB) e.g. Nifedipine or Amlodipine • D - Diuretics e.g. Bendroflumethiazide (thiazide, distal tube - less potent) or Furosemide (loop diuretic, loop of henle - more potent) • NOTE: Beta-blocker e.g. Bisoprolol or Metoprolol (B1 selective) are NOT the FIRST LINE TREATMENT FOR HYPERTENSION but consider in young people especially if they are intolerant of ACEi/ARB • Less than 55 yrs old: - Ramipril/Candesartan - + Nifedipine - + Bendroflumethiazide - + Furosemide • Older than 55 yrs/black/African-Caribbean origin: - Ramipril/Candesartan + Nifedipine - + Bendroflumethiazide - + Furosemide • If higher dose not tolerated then consider beta-blocker

Answer 228

• An abnormality of the cardiac rhythm is called a cardiac arrhythmia • Arrhythmias may cause: - Sudden death - Syncope - Heart failure - Chest pain - Dizziness - Palpitations - No symptoms at all • There are two main types of arrhythmia: - Bradycardia: • Heart rate is slow (less than 60bpm during the day and less than 50bpm at night) • Usually asymptomatic unless the rate is very slow • Normal in athletes owing to increased vagal tone and thus parasympathetic activity - Tachycardia: • Heart rate is fast (more than 100bpm) • More symptomatic when the arrhythmia is fast and sustained • Subdivided into: - Supraventricular tachycardias - arise from the atrium or the AV junction - Ventricular tachycardias - arise from the ventricles

Answer 229

- SAN → Action potential → Muscle cells of atria → Depolarisation of the AVN → Slow → Interventricular septum → Bundle of His → Right and left bundle branches → Free walls of both ventricles → Purkinje cells → Ventricular myocardial cells - Sinoatrial node (SAN) is found at the junction between the superior vena cava (SVC) and right atrium - The action potential travels through gap junctions to get to the muscle cells - The AVN is found in the lower interatrial septum - The slow spread of the action potential between the AVN and ventricles is to allow for the complete contraction of the atria before the ventricles are excited

Answer 230

- The normal cardiac pacemaker is the sinoatrial node and it depolarises spontaneously - The rate of SAN discharge is modulated by the autonomic nervous system - Normally, the parasympathetic system predominates, resulting in slowing of the spontaneous discharge rate - A reduction of PARASYMPATHETIC TONE or an increase in SYMPATHETIC STIMULATION leads to TACHYCARDIA - Conversely, increased PARASYMPATHETIC TONE or decreased SYMPATHETIC STIMULATION produces BRADYCARDIA - The sinus rate in women is slightly faster than in men - Normal sinus rhythm is characterised by P waves that are upright in leads I & II of the ECG, but inverted in the cavity leads AVR & V1

Answer 231

- Fluctuations of autonomic tone result in changes of the sinus discharge rate - During inspiration: • Parasympathetic tone falls and the heart rate quickens - During expiration: • Parasympathetic tone increases and so heart rate falls - This variation is normal especially in children and young adults

Answer 232

• A chaotic irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate

Answer 233

- Most common sustained cardiac arrhythmia - Males more than females - Around 5-15% of patients over age of 75 - Can either be paroxysmal (self terminating) or persistent (continues without intervention) - Clinical classification: • Acute: onset within the previous 48 hours • Paroxysmal: stops spontaneously within 7 days • Recurrent: two or more episodes • Persistent: continuos for more than 7 days and not self terminating • Permanent

Answer 234

• Idiopathic (5-10%) • Any condition that results in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium may cause atrial fibrillation • Hypertension (most common in developed world) • Heart failure (most common in developed world) • Coronary artery disease • Valvular heart disease; especially mitral stenosis • Cardiac surgery (1/3rd of patients after surgery) • Cardiomyopathy (rare cause) • Rheumatic heart disease • Acute excess alcohol intoxication

Answer 235

- Older than 60 - Diabetes - High blood pressure - Coronary artery disease - Prior MI - Structural heart disease (valve problems or congenital defects)

Answer 236

- Atrial fibrillation (AF) is maintained by continuous, rapid (300-600/min) activation of the atria by multiple meandering re-entry wavelets - These are often driven by rapidly depolarising automatic foci, located predominantly within the pulmonary veins - The atria respond electrically at this rate but there is NO COORDINATED MECHANICAL ACTION and only a proportion of the impulses are conducted to the ventricles i.e. there is no unified atrial contraction instead there is atrial spasm - The ventricular response depends on the rate and regularity of atrial activity, particularly at the entry to the AV node, and the balance between sympathetic and parasympathetic tone - Cardiac output DROPS by 10-20% as the ventricles are not primed reliably by the atria - NOTE: people with atrial fibrillation are at a higher risk of thromboembolic events e.g. stroke due to the fact that when the atria are spasming and some parts are not contracting it causes the blood to POOL in these parts and thus remain still and when blood remains still and DOESN’T MOVE and thus begins to CLOT forming a THROMBUS that could easily turn into an EMBOLI and result in a stroker - thus why people with atrial fibrillation are given some sort of blood thinner e.g. Warfarin

Answer 237

- Symptoms are highly variable - May be asymptomatic - Palpitations - Dyspnoea and or chest pains following the onset of atrial fibrillation - Fatigue - NO P WAVES on ECG - Rapid & irregular QRS rhythm - Apical pulse rate is greater than the radial rate - 1st heart sound is of variable intensity

Answer 238

- Atrial flutter | - Supraventricular tachyarrhythmias

Answer 239

- ECG: • ABSENT P WAVES • IRREGULAR & RAPID QRS COMPLEX

Answer 240

- Acute management: • When AF is due to an acute precipitating event, such as alcohol toxicity, chest infection or hyperthyroidism - the provoking cause should be treated • Cardioversion: - Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator - NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion - If this fails then achieved medically by IV infusion or anti-arrhythmic drug such as flecainide or amiodarone • Ventricular rate control: - Achieved by drugs that block AV node: • Calcium channel blocker e.g. Verapamil • Beta-blocker e.g. Bisoprolol • Digoxin • Anti-arrhythmic e.g. Amiodarone

Answer 241

- Long term & stable patient management: • Two strategies; which to choose should be decided based on individual patient needs • Rate control: - AV nodal slowing agents plus oral anticoagulation - Beta-blocker e.g. Bisoprolol - Calcium channel blocker e.g. Verapamil or Diltiazem - If above fails then try Digoxin and then consider Amiodarone • Rhythm control: - Advocated for younger, symptomatic and physically active patients - Cardioversion to sinus rhythm and use Beta-blockers e.g. Bisoprolol to suppress arrhythmia - Can use pharmacological cardioversion e.g. Flecainide if no structural heart defect or use IV Amiodarone instead if there is structural heart disease - Appropriate anti-coagulation e.g. Warfarin due to thromboembolism risk with cardioversion

Answer 242

- Use the CHA2DS2-VASc score to calculate stroke risk and thus need for anticoagulation: • Congestive heart failure (1 point) • Hypertension (1 point) • A2ge greater or equal to 75 (2 points) • Diabetes mellitus (1 point) • S2troke/TIA/thromboembolism (2 points) • Vascular disease (aorta, coronary or peripheral arteries) (1 point) • Age 65-74 (1 point) • Scex Category: female (1 point) • If score is 1 then it merits consideration of anticoagulation and or aspirin • If score is 2 and above then oral anticoagulation is required

Answer 243

• Atrial flutter is usually an ORGANISED atrial rhythm with an atrial rate typically between 250-350bpm

Answer 244

``` - Often associated with atrial fibrillation and frequently require a similar initial therapeutic approach - Either paroxysmal or persistent - Much less common than atrial flutter - More common in men - Prevalence increases with age - Causes: • Idiopathic (30%) • Coronary heart disease • Obesity • Hypertension • Heart failure • COPD • Pericarditis • Acute excess alcohol intoxication ```

Answer 245

- Atrial fibrillation

Answer 246

- Palpitations - Breathlessness - Chest pain - Dizziness - Syncope - Fatigue

Answer 247

- Atrial fibrillation | - Supraventricular tachyarrthymias

Answer 248

``` - ECG: • Definitive diagnosis • Regular sawtooth-like atrial flutter waves (F waves) between QRS complexes due to continuous atrial depolarisation • Note if F waves are not visible then they may be able to be unmasked by by slowing atrioventricular conduction by carotid sinus massage or IV adenosine (AV nodal blocker) ```

Answer 249

- Electrical cardioversion but anticoagulate before e.g low molecular weight heparin e.g. Enoxaparin or Dalteparin if acute i.e. atrial flutter started less than 48 hours ago - Catheter ablation - creating a conduction block to try an restore rhythm and block offending re-entrant wave - IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g. Bisoprolol to suppress further arrhythmias

Answer 250

• Can occur at any level in the conducting system • Block in either the AV node or the His bundle results in AV BLOCK • Whereas block lower in the conduction system produces BUNDLE BRANCH BLOCK

Answer 251

• First-degree AV block: - This is simple prolongation of the PR interval to greater than 0.22 seconds - Every atrial depolarisation is followed by conduction to the ventricles but with delay - Causes: • Hypokalaemia • Myocarditis • Inferior MI • Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - ASYMPTOMATIC so no treatment!

Answer 252

• Second-degree AV block: - Occurs when some P waves conduct and other do not - Acute MI may produce second degree heart block - Mobitz I block: • Also known as the Wenckebach block phenomenon • A progressive PR interval prolongation until beat is ‘dropped’ and P wave fails to conduct i.e. excitation completely fails to pass through the AVN/bundle of His • The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave • Causes: - Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - Inferior MI • Results in light headiness, dizziness and syncope • Does not require a pacemaker unless its poorly tolerated - Mobitz II block: • PR interval is constant and QRS interval is dropped • Failure of conduction through the His-Purkinje system • Causes: - Anterior MI - Mitral valve surgery - SLE and Lyme disease - Rheumatic fever • Results in shortness of breath, postural hypotension and chest pain • High risk of developing sudden complete AV block and a pacemaker should be inserted

Answer 253

• Third degree - COMPLETE AV BLOCK: - Complete heart block occurs when all atrial activity fails to conduct to the ventricles - Ventricular contractions are sustained by spontaneous escape rhythm which originates below the block - P waves are COMPLETELY INDEPENDENT of QRS complex - Causes: • Structural heart disease e.g. transposition of great vessels • Ischaemic heart disease e.g. acute MI • Hypertension • Endocarditis or Lyme disease - Narrow-complex escape rhythm: • QRS complex less than 0.12 seconds • Implies block originates in the His bundle and thus the region of block lies more proximally in the AV node • Recent-onset, narrow-complex AV block that has transient causes may responses to IV atropine • Chronic narrow-complex AV block requires permanent pacemaker if it is symptomatic - Broad-complex escape rhythm - B = BELOW His: • QRS complex is greater than 0.12 seconds • Implies block originates BELOW the bundle of His and thus the region of block lies more distally in the His-Purkinje system • Dizziness and blackouts often occur • Permanent pacemaker implantation is recommended

Answer 254

- Depends on aetiology - One option is permanent pacemaker - IV atropine

Answer 255

• Usually asymptomatic • The His bundle gives rise to the right and left bundle branches • The left branch subdivides into the anterior and posterior divisions of the left bundle • Bundle branch conduction delay results in the slight widening of the QRS complex (up to 0.11 seconds) - this is incomplete bundle branch block • Complete block of a bundle branch: - This is associated with a wider QRS complex (larger than 0.12 seconds) - The shape of the QRS depends on whether the right or the left bundle is blocked

Answer 256

- Right bundle branch block (RBBB): • Causes; Pulmonary embolism, Ischaemic heart disease & Atrial/ Ventricular septal defect • Right bundle no longer conducts, meaning that the two ventricles do not get impulses at the same time, and instead spread from left to right • Produces the late activation of the right ventricle • Seen as deep S wave in leads I & V6 and as a tall late R wave in lead V1 • On ECG:- Looks like maRRow - maRRow - Right bundle branch block - MarroW: • M - QRS looks like an M in lead V1 • W - QRS looks like W in V5 & V6 • Causes wide physiological splitting of the SECOND HEART SOUND

Answer 257

- Left bundle branch block (LBBB): • Causes; Ischaemic heart disease and aortic valve disease • Produces the late activation of the left ventricle • Seen as deep S wave in lead V1 and a tall late R wave in leads I & V6 • Since the left bundle branch conduction is normally responsible for the initial ventricular activation, left bundle branch block also produce abnormal Q waves • On ECG: - Looks like wiLLiam - wiLLiam - Left bundle branch block - WilliaM: • W - QRS looks like a W in leads V1 & V2 • M - QRS looks like an M in leads V4-V6 • Causes reverse splitting of the SECOND HEART SOUND

Answer 258

``` • Defined as heart rate greater than 100bpm • Causes: - Anaemia - Anxiety - Exercise - Pain - Heart failure - Pulmonary embolism • Treated by treating causes • If necessary then beta-blockers can be used e.g. Bisoprolol ```

Answer 259

• Arise from the atria or atrioventricular junction • NOTE: TACHYARRHYTHMIA & TACHYCARDIA can be used INTERCHANGEABLY • ATRIOVENTRICULAR JUNCTIONAL TACHYCARDIAS: - AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (AVRT) are usually referred to as paroxysmal supraventricular tachycardias (SVTs) - They are often seen in young patients with no or little structural heart disease - First presentation is commonly between ages 12-30 - In these tachycardias the AV node is an essential component

Answer 260

- More common in women than men - Strikes suddenly without obvious provocation but there are some risk factors - An attack may stop spontaneously or may continue indefinitely until medical intervention

Answer 261

- Exertion - Emotional stress - Coffee - Tea - Alcohol

Answer 262

- There are two pathways within the AV node in AVNRT: • One has a short effective refractory period (the window of time where cells cannot be excited again after they have already been excited) and SLOW conduction • One has a longer effective refractory period and FAST conduction - In sinus rhythm, the atrial impulse that depolarises the ventricles usually conducts through the fast pathway - If the atrial impulse occurs early e.g. atrial premature beat when the fast pathway is still refractory then the slow pathway takes over in propagating the atrial impulses to the ventricles - By the time the impulse has been propagated to the ventricles the FAST PATHWAY has finished its refractory period and is once again able to transmit impulses - Thus the same impulse that was carried by the SLOW PATHWAY can be transmitted to the ventricles but ALSO travel back UP the FAST PATHWAY which by that time would be out of its refractory period - Then by that time the SLOW PATHWAY would have recovered from its refractory period (since its very short) so the signal will be able to go back down the SLOW PATHWAY again - This sets up a RE-ENTRANT LOOP at the AV NODE hence why its AVNRT and the loop sends signals through the AV node at a MUCH FASTER RATE than a normal pacemaker would so you see TACHYARRHYTHMIA! with a heart rate of 100-250 bpm - It then travels back through the fast pathway, which has already recovered its excitability, thereby initiating the slow-fast AVNRT in which the atria contract SLOWLY in one cycle and then FAST in the next

Answer 263

- Rapid regular palpitations with abrupt onset and sudden termination - Chest pain and breathlessness - Neck pulsations - prominent jugular venous pulsations due to atrial contractions against closed AV valves - Polyuria (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)

Answer 264

- ECG: • Sometimes the QRS complexes will show typical bundle branch block • P waves are either not visible or are seen immediately before (normal) or after the QRS complex due to simultaneous atrial and ventricular activation

Answer 265

- Large circuit involving the AV node, the His bundle, the ventricle and an abnormal connection of myocardial fibres from the ventricle back to the atrium - This ‘abnormal connection’ is called the accessory pathway or bypass tract and results from an incomplete separation of the atria and the ventricles during fetal development - Thus there are two circuits; the normal AV circuit and this accessory circuit which both transmit impulses from the atria to the ventricles - Note: with the accessory circuit impulse can travel from atria to ventricle (anterograde) or from ventricle back to atria (retrograde)

Answer 266

- Atrial activation occurs after ventricular activation - Patients are prone to atrial fibrillations and sometime ventricular fibrillation - Good example of AVRT is in WOLFF-PARKINSON-WHITE (WPW) SYNDROME - a aberrant pathway syndrome: • Where there is normal AV conduction but also an accessory pathway • So when the SAN depolarises the impulse can travel to the AVN via the atria as well as to the accessory pathway • If the accessory pathway conducts from the atrium to the ventricle during sinus rhythm, the electrical impulse can conduct QUICKLY over this abnormal connection to depolarise part of the ventricles ABNORMALLY this is known as pre- excitation

Answer 267

• Pre-excitation is reflected on an ECG like this: - Short PR interval - Wide QRS complex that begins as a slurred part known as a delta wave • This pre-excitation is not the thing that results in the AVRT and will not result in a tachyarrhythmia • However, if you had a premature beat coming from the SAN; the signal will travel to the AVN and it the accessory pathway is in a refractory period i.e. it CANNOT TRANSMIT THE SIGNAL • Then the impulse will travel down via the AVN, down the interventricular septum through the bundle of His through the left and right bundle branches and into the free walls of both ventricles via the Purkinje cells until it meets the ACCESSORY PATHWAY • At this point the accessory pathway will be out of its refractory period and will thus be able to conduct the impulse BACK into the atria • Once back in the atria the impulse can then travel back to the AVN thereby setting up a RE-ENTRY CIRCUIT and the signal will just go around and around resulting in the TACHYARRHYTHMIA!

Answer 268

- Palpitations - Severe dizziness - Dysponea - Syncope

Answer 269

- ECG: • Short PR interval • Wide QRS complex that begins as a slurred part known as a DELTA WAVE • Both hallmarks of Wolff-Parkinson-White (WPW) syndrome

Answer 270

- Patients presenting with haemodynamic instability (hypotension & pulmonary oedema) require emergency cardioversion - If stable then vagal manoeuvres: • Breath-holding • Carotid massage • Valsalva manoeuvre - abrupt voluntary increase in intra-abdominal and intrathoracic pressure by straining - several seconds after the release of the strain, the resulting intense vagal effect may terminate the AVNRT or AVRT - If manoeuvres unsuccessful then IV adenosine - causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT - Surgery: • Catheter ablation of the accessory pathway in AVRT • Modification of the slow pathway in AVNRT

Answer 271

Umbrella term encompassing: - Ventricular ectopics - Ventricular tachycardia - Sustained ventricular tachycardia - Ventricular fibrillation - Some of these condition are cardiac channelopathies - these are congenital disorders that are caused by mutations that affect the function of cardiac ion channels and hence the electrical activity of the heart, these include: • Long QT syndrome

Answer 272

• Premature ventricular contraction

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- These are the most common POST-MI arrhythmia | - Can also occur in healthy patients

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- Patient complains of extra beats, missed beats or heavy beats - If the ectopics are frequent then left ventricular dysfunction may develop - These premature beats have a broad (greater than 0.12 seconds) and bizarre QRS complex because they arise from an abnormal (ectopic) site in the ventricular myocardium - Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory (i.e. cannot accept new impulses) to the next sinus impulse - resulting in missed beat - Can provoke VENTRICULAR FIBRILLATION - potentially fatal

Answer 275

- May be uncomfortable especially when frequent - Pulse is irregular owing to the premature beats - Usually are asymptomatic - Can feel faint or dizzy

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- ECG: | • Widened QRS complex - greater than 0.12 seconds

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- Reassure patient | - Give beta-blockers e.g. Bisoprolol if symptomatic

Answer 278

• Pulse of more than 100bpm with at leat 3 irregular heart beats in a row • Commonly found in patients with structurally normal hearts (known as idiopathic ventricular tachycardia), in these cases it is usually a benign condition with an excellent long-term prognosis • Occasionally it is pathological and known as Gallavardin’s tachycardia and if untreated may lead to cardiomyopathy • Essentially there is rapid ventricular beating so much so that they is inadequate blood filling of ventricles since they are filled in between beats and thus id beating faster there is less time to fill and thus less blood fills • Results in decreased cardiac output and thus a decrease in the amount of oxygenated blood that is circulated around the body

Answer 279

- Breathlessness (lack of lung perfusion) - Chest pain (lack of heart perfusion) - Palpitations - Light headed or dizzy (lack of brain perfusion)

Answer 280

Treatment of symptoms is usually with beta-blockers e.g. Bisoprolol

Answer 281

• Ventricular tachycardia for longer than 30 seconds

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- Dizziness (pre-syncope) - Syncope - Hypotension - Cardiac arrest - Pulse rate between 120-220 bpm

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- Rapid ventricular rhythm | - Broad & abnormal QRS complex (greater than 0.14 seconds)

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- Haemodynamically unstable (e.g. hypotensive or pulmonary oedema): • Emergency electrical cardioversion - Stable: • IV beta-blocker e.g. Esmolol • IV Amiodarone - Prevented by the use of beta-blockers and implantable cardiac defibrillator

Answer 285

• Involves very rapid and irregular ventricular activation with NO MECHANICAL EFFECT i.e NO CARDIAC OUTPUT • Patient is pulseless and becomes unconscious and respiration ceases (CARDIAC ARREST) • ECG shows shapeless, rapid oscillations and there is no hint of organised complexes • Usually caused by a ventricular ectopic beat • Only effective treatment is ELECTRICAL DEFIBRILLATION • Survivors are at increased risk of sudden death so long term, implantable cardioverter-defibrillators are the first-line therapy

Answer 286

• Describes an ECG where the ventricular repolarisation - QT interval is greatly prolonged

Answer 287

- Congenital: • Jervell-Lange-Nielsen syndrome (autosomal recessive) - mutation in cardiac potassium and sodium-channel genes • Romano-Ward syndrome (autosomal dominant) - Acquired: • Hypokalaemia • Hypocalcaemia • Drugs; Amiodarone and Tricyclic antidepressants e.g. Amitriptyline • Bradycardia • Acute MI • Diabetes

Answer 288

- Syncope - Palpitations - Due to polymorphic ventricular tachycardia that usually terminate spontaneously but may degenerate to ventricular fibrillation

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- Syncope - Palpitations - Due to polymorphic ventricular tachycardia that usually terminate spontaneously but may degenerate to ventricular fibrillation

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• ECG shows prolonged QT interval

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- Treat underlying cause - If acquired long QT then give IV isoprenaline (contraindicated for congenital long QT)

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• Classified as true and false • An aneurysm is defined if there is a permanent dilatation of the artery to TWICE the normal diameter • Normal diameter of aorta is around 2cm - this increases with age

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- Abnormal dilatations that involve all layers of the arterial wall - Arteries most frequently involved are: • Abdominal aorta (most common) • Iliac, popliteal and femoral arteries • Thoracic aorta

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- Also known as pseudoaneurysm - Involves the collection of blood in the OUTER LAYER ONLY (ADVENTITIA) which communicates with the lumen e.g after trauma from a femoral artery puncture

Answer 295

Aortic aneurysms are classified as ABDOMINAL or THORACIC

Answer 296

- Most commonly occur BELOW the renal arteries (infra-renal) - Incidence increases with age - AAA’s are present in 5% of the population above 60 - More common in men than women - Abdominal aneurysm is classified as an aortic diameter EXCEEDING 3cm - Causes & Risk factors: • Most have no specific identifiable causes • Severe atherosclerotic damage • Family history • Tobacco smoking • Male • Increasing age • Hypertension • COPD • Trauma • Hyperlipidaemia

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- Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss - The dilatation affects ALL THREE LAYERS of the vascular tunic - If it doesn't then it is a pseudoaneurysm

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• Often asymptomatic and only picked up via a routing abdominal examination or plain X-ray • Pain in abdomen, back, loin or groin • Pulsatile abdominal swelling (less pronounced)

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• Rupture is more likely if there is; increased BP, female, smoker, strong family history • Intermittent or continuous abdominal pain (radiates to the back, iliac fossa’s or groin) • Pulsatile abdominal swelling (more pronounced) • Collapse • Hypotension • Tachycardia • Profound anaemia • Sudden death

Answer 300

- GI bleed - Ischaemic bowel - MSK pain - Perforated GI ulcer - Pyelonephritis - Appendicitis

Answer 301

- Abdominal ultrasound - can assess aorta to degree of 3mm | - CT and or MRI angiography scans

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- Small aneurysms below 5.5cm are generally just monitored - Treat underlying causes - Modify risk factors e.g. smoking and diet - Smoking cessation - Vigorous BP control - Lowering of lipid in blood - Surgery: • Patients tend to do better if aneurysm is symptomatic, larger than 5.5cm and expanding yearly • Open surgical repair • Endovascular repair - stent inserted via femoral or iliac arteries

Answer 303

- Normal size of the mid-descending thoracic aorta is 26-28mm - The ascending, arch or descending thoracic aorta may become aneurysmal - Ascending thoraco-abdominal aneurysms occur most commonly in patients with Marfan syndrome or hypertension - Descending or arch TAAs occur secondary to atherosclerosis and are now rarely due to syphilis - Causes: • STRONG GENETIC LINK - in some families it appears to be an autosomal dominant trait • Certain connective tissue disorders: - Marfan’s syndrome - Ehlers-danlos syndrome - Loeys-dietz syndrome • Mycotic aneurysm is endocarditis • Aortic dissection in some cases • Weight lifting, cocaine and amphetamine use - perhaps due to the large rise in BP when undertaking these activities

Answer 304

- Hypertension - Increasing age - Smoking - Bicuspid or unicuspid aortic valves - Atherosclerosis - COPD - Renal failure - Previous aortic aneurysm repair

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- Involves inflammation, proteolysis and reduced survival of the smooth muscle cells in the aortic wall - Once the aorta reaches a crucial diameter (around 6cm in the ascending and 7cm in the descending) it loses all distensibility so that a rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture

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- Most TAA’s are asymptomatic - May be diagnosed incidentally e.g. on routing CXR or cardiological investigation or if complicated by dissection, rupture or other complications - Pain in chest, neck, upper back, mid-back or epigastrium - Aortic regurgitation - Fever if there is infective cause - Symptoms due to compression of local structures - Acute pain - Collapse, shock and sudden death - Cardiac tamponade - Haemoptysis

Answer 307

- Thoracic back pain - Arterial ischaemia - Collapse - MI

Answer 308

- CT or MRI used for assessment of TAA - Aortography may be helpful for assessing the position of the key branches in relation to the aneurysm - Transoesophageal echocardiography can be useful for identifying aortic dissection - Ultrasound

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- Immediate urgent surgery is required for ruptured TAA - Symptomatic TAA’s merit surgery regardless of size - Regular monitoring by CT or MRI every 6 months - Rigorous BP control using beta-blockers e.g. Bisoprolol - Smoking cessation - Treat underlying cause

Answer 310

- Aortic dissection begins with a tear in the intima (inner wall) - Blood then penetrates the diseased medial layer and flows between the layers of the aorta, forcing the layers apart resulting in dissection - A medical emergency that can lead to death - The most common emergency affecting the aorta - Affects men more than females - Most common between the ages of 50-70 and is rare below 40 - Very rare in children - Can be classified according to the timing of diagnosis from the origin of symptoms: • Acute - less than 2 weeks • Subacute - 2-8 weeks • Chronic - more than 8 weeks

Answer 311

- Inherited - Degenerative - Atherosclerotic - Inflammatory - Trauma e.g. shearing stresses in a road traffic accident (RTA)

Answer 312

- Aortic dissection begins with a tear in the intimal lining of the aorta - The tear allows a column of blood under pressure to enter the aortic wall, forming a haemotoma which separates the intima from the adventitia and creates a false lumen - The false lumen extends for a variable distance in either direction; anterograde (towards bifurcations) and retrograde (towards the aortic root) - The most common sites for the intimal tears are: • Within 2-3cm of the aortic valve • Distal to the left subclavian artery in the descending aorta

Answer 313

- Sudden onset of severe and central chest pain that radiates to the back and down the arms - mimics a MI - Pain is often describes as tearing in nature and may be migratory - Hypertension - Pain is maximal from the time of onset, unlike in MI where the pain gains in intensity - Patients may be shocked and may have neurological symptoms secondary to loss of blood supply to the spinal cord - May develop aortic regurgitation, coronary ischaemia and cardiac tamponade - Distal extension may produce acute kidney failure, acute lower limb ischaemia or visceral ischaemia - Peripheral pulses may be absent

Answer 314

- Acute coronary syndrome, MI, Aortic regurgitation without dissection, MSK pain, pericarditis, cholecystitis, atherosclerotic embolism

Answer 315

- CXR: • Widened mediastinum - Urgent CT scan, Transoesophageal echocardiography or MRI will CONFIRM DIAGNSOS

Answer 316

- At least 50% are hypertensive and may require urgent antihypertensive medication to reduce blood pressure to less than 120mmHg - give IV beta-blockers e.g. IV metoprolol or vasodilators e.g. IV GTN - Adequate analgesia e.g. morphine - Surgery to replace aortic arch - Endovascular intervention with stents - Patients require long term follow-up with CT or MRI

Answer 317

``` - Essentially its the partial blockage of leg or peripheral vessels by an atherosclerotic plaque and or resulting thrombus resulting in insufficient perfusion of the lower limb resulting in LOWER LIMB ISCHAEMIA - Commonly caused by atherosclerosis and usually affects the aorta-iliac and infra-inguinal arteries - More common in men than women ```

Answer 318

- Smoking - Diabetes - Hypercholesterolaemia - Hypertension - Physical inactivity - Obesity

Answer 319

- ALWAYS due to ATHEROSCLEROSIS of the arteries distal to the aortic arch - Atherosclerosis can result in many complications: - Symptoms of Ischaemia: • Normal oxygen pressures in different activities:

Cardiovascular Flashcards

(347 cards)