Cardiology Flashcards

Question

Short PR interval indicates what syndrome? What allows early activation of the ventricle? Long PR interval?

Answer 1

WPW syndrome, Accessory pathway | First degree heart block

Answer 2

I,III, aVL- smaller than V5 | 30mm

Answer 3

Flat By 1mm or more Point between QRS and ST segment

Answer 4

Asymmetrical- first half having gradual slope than second At least 1/8 but less than 2/3 of amplitude of R Symmetrical, tall, peaked, biphasic or inverted

Answer 5

In lead aVL Heart rate 0.35-0.45 seconds Adjacent R waves

Answer 6

Small, round, symmetrical and positive in lead II, direction same as T wave, more prominent at slow heart rates Rule of 300/1500 10 second rule

Answer 7

Number of big boxes between 2 QRS complexes and divide this into 300 for regular rhythms Number of beats on ECG x6 for irregular rhythms

Answer 8

Overall direction of heart's electrical activity Ventricular enlargement, conduction blocks LAD RAD

Answer 9

Quadrant and equiphasic approach | Predominantly positive, predominantly negative, equiphasic

Answer 10

QRS complex in leads I and aVF Determine if predominantly positive or negative Combination should place axis into one of 4 quadrants

Answer 11

Most equiphasic QRS complex Identified lead lies 90 degrees away from lead QRS in this second lead is positive or negative

Answer 12

Tachy= above 100, Brady= below 60 Anterior (V3-V4) and lateral (V5-V6) leads Inferior II, III, aVF leads

Answer 13

60-65%, 300-400g Angiotensin 2, ET-1 and insulin-like growth factor 1, TGF-Beta, activate mitogen-activated protein kinase Pulmonary congestion and overload of right side Venous congestion and hypertension Stiffer heart Vacuolated cardiac myocytes following injury (usually hypoxic) may enhance myocyte survival but poor contraction

Answer 14

Single chamber until 5th week of gestation, divided by intra-ventricular and intra-atrial septa from endocardial cushions Faulty embryonic development VSD, ASD, PDA, Fallots Single genes= trisomy 21= Downs, Turners, Di-George, infections- rubella, drugs, diabetes

Answer 15

VSD, ASD, PDA, trunks arteriosus Tetralogy of Fallot, tricuspid atresia Complete transposition of great vessels, coarctation, pulmonary stenosis, aortic stenosis, coronary artery origin from pulmonary artery, Ebstein malformation, endocardial fibroelastosis

Answer 16

Right side--> left side shunting associated with right cardiac failure and right site cardiac hypertrophy Cardiac arrhythmia, pulmonary hypertension, right ventricular hypertrophy and cardiac failure, risk of infective endocarditis

Answer 17

Left to right shunting, meaning lung circulation is overloaded with pulmonary hypertension and right side cardiac failure Risk of infective endocarditis Surgically, by catheters or by prostaglandin inhibitors (indomethacin)

Answer 18

Pulmonary stenosis, ventricular septal defect, dextraposition/ over-riding septal defect, right ventricle hypertrophy Boot-shape Right ventricle shunted into left heart---> cyanosis from birth Surgical correction during first 2 years of life, progressive cardiac debility and risk of cerebral thrombosis

Answer 19

The aorta coming off the right ventricle and pulmonary trunk off the left ventricle Male bias, particular associated with diabetes, only if there is communication between the circuits and virtually all have an atrial septal defect allowing blood mixing Arterial switch with less than 10% overall mortality

Answer 20

Narrowing of the aorta at, or just distal to the insertion of the ductus arteriosus (distal to the origin of the left subclavian artery) Narrowing just after arch, excessive blood flow through carotid and subclavian vessels into systemic vascular shunts Decreased renal perfusion after surgical correction even Turner's syndrome and berry aneurysms of the brain

Answer 21

Congenital aortic stenosis and coarctation Profound dense collagen and elastic tissues deposited don endocardial aspect of left ventricle--> stiffening of heart A familial pattern, both= rare

Answer 22

Stable angina, acute coronary syndromes, myocardial infarction Cardiac arrest/ sudden death, chest pain, shortness of breath

Answer 23

Systemic hypertension, cigarette smoking, diabetes mellitus, elevated cholesterol Atherosclerosis, thrombosis/ thromboembolism, artery spasm, collateral blood vessels, BP/HR/CO abnormalities, arteritis

Answer 24

Arrhythmias- supra ventricular and ventricular, left ventricular failure- cardiogenic shock, extension of infarction, rupture of myocardium, cerebral infarction, carotid atheroma, aortic aneurysm, PVD, gangrene

Answer 25

Mismatch of supply of oxygen- due to anaemia, hyperaemia, polycythaemia and demand of myocardium- due to HTN, tachycarrhythmia, valvular heart disease, hyperthyroidism, hypertrophic cardiomyopathy Cold weather, heavy meals and emotional stress= exacerbating factors

Answer 26

Stable- induced by effort and relieved by rest Unstable (crescendo)- of recent onset or deterioration in previously stable angina with symptoms frequently occurring at rest, increasing frequency/ severity, on minimal exertion/ at rest, form of acute coronary syndrome Prinzmetal's angina- caused by coronary artery spasm (rare)

Answer 27

Central chest tightness or heaviness, provoked by exertion, provoked by exertion, especially after meal or in cold windy weather or by anger/ excitement Relieved by rest/ GTN spray, pain may radiate to one/ both arms, neck, jaw or teeth May be dyspnoea, nausea, sweatiness and faintness

Answer 28

1. Have central, tight, radiation to arms, jaw and neck 2. Precipitated by exertion 3. Relieved by rest or spray GTN 3/3= typical angina, 2/3= atypical, 1/3= non-anginal pain

Answer 29

Pouiseuille: as radius falls, pressure increases and so volume decreases- after radius falls below 75% it becomes noticeable- pt will not experience any symptoms until artery falls below 75%

Answer 30

Onset, position, quality- nature/ character, relationship, radiation, relieving factors, severity, timing, treatment Pericarditis, pulmonary embolism, chest infection, aorta dissection, gastro-oesophageal, musculoskeletal, psychological

Answer 31

May be normal/ show ST depression, flat/ inverted T waves, look for signs of past MI ECG on patient, then make them run on treadmill uphill, monitor length of exercise, ST segment depression= sign of late-stage ischaemia, may patients= unsuitable CT scan calciums scoring- CT heart, atherosclerosis- calcium= white SPECT/ myoview- radio-labelled tracer injected into patient, taken up by coronary arteries where there is good blood supply- this will light up, no light after exercise= myocardial ischaemia

Answer 32

Stop smoking, encourage exercise, weight loss, treat underlying conditions Aspirin- anti platelet effect, COX inhibitor Statins- HMG-CoA reductase inhibitors Beta blockers- reduce heart contraction, B1 activation--> Gs--> cAMP to ATP--> contraction GTN spray Ca2+ channel blocker Revascularisation- increase flow reserve: PCI and CABG

Answer 33

Dilating coronary atheromatous obstructions by inflating balloon within it, insert balloon and remove it, stent persists and keeps artery patent, expanding plaque= make artery bigger Pros= less invasive, convenient, short recovery and repeatable Cons= risk of stent thrombosis, not good for complex disease

Answer 34

Left internal mammary artery (LIMA) used to bypass proximal stenosis (narrowing) in LAD coronary artery Pros: good prognosis, deals with complex disease Cons: invasive, risk of stroke/ bleeding, one time treatment, need to stay in hospital- long recovery

Answer 35

HR (negatively chronotropic,) left ventricle contractility (negatively inotropic,) cardiac output Tiredness, nightmares, bradycardia, erectile dysfunction and cold hands and feet Asthma, heart failure/ heart block, hypotension and bradyarrhythmias

Answer 36

Venodilator- nitrate Dilates systemic veins thereby reducing venous return to right heart Reduces preload, work of heart and O2 demand, also dilates coronary arteries Profuse headache immediatly after use

Answer 37

Primary arterodilators Dilates systemic arteries resulting in BP drop, reduces afterload on heart, less energy to produce same CO Less work on heart and O2 demand e.g. verapamil

Answer 38

STEMI, NSTEMI (acute myocardial infarction) and unstable angina Complete occlusion of a major coronary artery, causes full thickness damage of heart muscle Diagnosed on ECG at presentation--> Q wave some time after MI so also known as Q-wave infarction

Answer 39

Angina of recent onset (less than 24 hours,) or cardiac chest pain with crescendo pattern, deterioration in previously stable angina, with symptoms frequently occurring at rest Angina of increasing frequency or severity, on minimal exertion or even at rest When developing a complete occlusion of a minor or partial occlusion of a major coronary artery previously affected by atherosclerosis Causes partial thickness damage of heart muscle Diagnosis after troponin results and sometimes other investigation results available Also known as non-Q wave infarction--> myocardial necrosis and rise in serum troponin/ creatine kinase-MB (CK-MB)

Answer 40

Type 1= spontaneous MI with ischaemia due to primary coronary event e.g. plaque erosion/ rupture, fissuring or dissection Type II= MI secondary to ischaemia due to increased O2 demand/ decreased supply such as in coronary spasm, coronary embolism, anaemia, arrythmias, hypertension or hypotension Type 3,4,5: MI due to sudden cardiac death, related to PCI and related to CABG respectively

Answer 41

Age, male, family history of IHD, smoking, hypertension, diabetes mellitus, hyperlipidaemia, obesity and sedentary lifestyle Rupture/ erosion of fibrous cap of coronary artery plaque--> platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation Platelets release serotonin and thromboxane A2--> myocardial ischaemia

Answer 42

Necrotic centre and ulcerated cap--> partial occlusion | Necrotic centre--> total occlusion

Answer 43

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 e.g. in elderly/ diabetics Distress and anxiety, pallor, increased pulse and reduced BP, reduced 4th heart sound, may be signs of heart failure, tachy/ bradycardia, peripheral oedema

Answer 44

Angina, pericarditis, myocarditis, aortic dissection, pulmonary embolism, oesophageal reflux/ spasm Can be normal, ST depression and T-wave inversion, hyperacute T waves STEMI--> persistent ST-elevation, hyperacute T waves or new LBBB pattern, may see pathological Q waves few days after MI

Answer 45

Most sensitive and specific markers of myocardial necrosis Serum levels increase within 3-12 hours from onset of chest pain and peak at 24-48 hours, fall back to normal over 5-14 days Prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation

Answer 46

Myocyte death- low accuracy= present in serum of normal individuals and in patients with significant skeletal muscle damage Re-infarction as levels drop back to normal after 36-72 hours Very early in MI, test= poor specificity since myoglobin present in skeletal muscle Cardiomegaly, pulmonary oedema or widened mediastinum (aortic rupture)

Answer 47

Aspirin(oral) P2Y12 inhibitors (oral)- inhibit ADP-dependent activation of IIb/IIIa glycoproteins, preventing amplification response of platelet aggregation, alongside aspirin in dual anti-platelet Glycoprotein IIb/ IIIa antagonists- only IV Beta blockers(IV and oral) Statins (oral)- HMG- CoA reductase inhibitors ACE inhibitors

Answer 48

PCI and CABG Risk factor modification- stop smoking, lose weight and exercise daily, healthy diet, treat hypertension and diabetes, low fat diet with statins

Answer 49

Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombus STEMI- complete occlusion of major coronary artery, full thickness damage, diagnosed on ECG at presentation, tall T waves, ST elevation, pathological Q wave NSTEMI- complete occlusion of minor/ partial occlusion of major coronary artery, partial thickness damage, retrospective diagnosis after troponin results, ST depression/ T wave inversion STEMI Age, male, history of prem coronary heart disease, premature menopause, diabetes mellitus, smoking, hypertension, hyperlipidaemia, obesity and sedentary lifestyle, family history of IHD

Answer 50

Rupture/ erosion of vulnerable fibrous cap of coronary artery atheromatous plaque--> platelet aggregation, adhesion, local thrombosis, vasoconstriction and distal thrombus embolisation--> prolonged complete arterial occlusion--> myocardial necrossi within 15-30 minutes in STEMI STEMI= sub-endocardial myocardium initially affected but continuted ischaemia, infarct zone extends through sub-epicardial myocardium--> transmural Q wave MI, early reperfusion may salvage regions

Answer 51

Severe chest pain for more than 20 minutes Pain radiate to left arm, jaw, neck Does not usually response to sublingual GTN spray- opiate analgesia required Pain described as substernal pressure, squeezing, aching, burning or sharp pain, with sweating, nausea, vomiting, dyspnoea, fatigue and/ or palpitations Breathlessness, fatigue, distress and anxiety, pale, clammy and marked sweating, significant hypotension, bradycardia or tachycardia

Answer 52

Stable angina, unstable angina, NSTMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis, MSK chest pain On presentation, ST elevation, tall T waves, LBBB, T wave inversion and pathological Q waves NSTEMI= retrospective diagnosis, ST depression and T wave inversion

Answer 53

``` ST elevation V1-V3 ST elevation II, III, AVF I, AVL, V5-V6 ST depression V1-V3, dominant R wave, ST elevation V5-V6 Any ```

Answer 54

Aspirin 300mg chewable, GTN (sublingual,) morphine IV morphine, oxygen if their sats are below 95%/ breathless, beta-blocker- atenolol, P2Y12 inhibitor- clopidogrel PCI: presented to all patients who present with acute STEMI who can be transferred--> primary PCI centre within 120mins of first medical contact, not possible- give fibrinolysis and transfer to PCI centre after infusion CABG- fibrinolysis enhance breakdown of occlusive thromboses by activating plasminogen--> plasmin

Answer 55

Stop smoking, lose weight and exercise daily, healthy diet, treat hypertension and diabetes, low fat diet with statins Statins, aspirin long term, warfarin if large MI, B blockers and ACE inhibitors

Answer 56

Sudden death- often due to VF, arrhythmias- in first few days, persistent pain- 12 hours to few days after due to necrosis Heart failure- ventricular dysfunction and necrosis Mitral incompetence- first few days or later Pericarditis- transmural infarct--> inflammation of pericardium, more common in STEMI Cardiac rupture- early= from shearing between mobile and immobile myocardium Late= due to weakening of wall following muscle necrosis and acute inflammation Ventricular aneurysm- due to stretching of newly formed collagenous scar tissue

Answer 57

Friedman and Rosenman- competitive, hostile, impatient Questionnaires- MMPI, Jenkins Activity survey and Bortner Rating Scale, self-report= poorer predictors, structured clinical interview

Answer 58

Antecedents e.g. social deprivation | MMPI, Beck depression inventory (BDI,) general health questionnaire, Spielbergers' State anxiety inventory

Answer 59

Psychosocial job characteristics Psychological demands, control and social support Quantity and quality found to be related- helps coping with life events, motivation to engage in healthy behaviours

Answer 60

Observe/ explore behaviour patterns Identify signs of depression/ anxiety, ask questions from assessment tools, ask patients about their job/occupation, available support and liaise with relevant services

Answer 61

Classification based on physical characteristics into which humankind was divided- separate biological races no longer accepted as scientifically valid/ ethically useable, ethnic group= preferable Group of people whose members identify with each other through common heritage- common language, culture of ideology which stresses common ancestry, superseded biological idea of 'race'

Answer 62

Income, class- ownership of assets, status- hierarchy/ prestige Indicates inability to cope with hostile environment, not lucky enough to have coping mechanisms needed for everyday living Inability of individual group/ community to participate effectively in economic, political and cultural life: alienation and distance from mainstream society e.g. travellers, asylum seekers, refugees, from BME groups

Answer 63

Genetic/ biological factors, individual behaviour/ cultural factors, material/ structural factors, migration and racism, inequalities in access to healthcare, artefact 50% more likely to die from stroke, but lower mortality from CHD 87%

Answer 64

x7 Poorest and most marginalised groups including migrant communities- latent can be missed and extrapulmonary TB misunderstood, unstable living conditions can interfere with treatment and recovery Lower in BME, lower in S Asia, Caribbean and Africa than Ireland and Scotland- smoking?

Answer 65

Arterial- high pressure: platelet rich, can lead to stroke/ MI, venous= low pressure, fibrin rich, cause PE/ DVT

Answer 66

Coronary--> MI, cerebral--> CVA/ stroke, peripheral--> peripheral vascular disease (claudication, rest pain, gangrene) Smoking, hypertension, diabetes, hyperlipidaemia, obesity/ sedentary lifestyle, stress/ type A personality

Answer 67

If MI--> history, ECG, cardiac enzymes, if CVA--> history and examination, CT scan/ MRI, peripheral vascular disease--> history and examination, ultrasound, angiogram

Answer 68

Aspirin, thrombolytic therapy- streptokinase tissue plasminogen activator, degrades fibrin Aspirin, clopidogrel, fibrinolytics IV (streptokinase, alteplase) Treat risk factors- during window of opportunity

Answer 69

Pulmonary embolism and DVT Surgery, immobilisation, oestrogens, malignancy, long haul flights, inherited thrombophilia, acquired- anti-phospholipid syndrome, Lupus anticoagulant, hyperhomocysteinaemia

Answer 70

Mechanical- hydration, early mobilisation, compression stockings, chemical- LMWH, lower dose, thromboprophylaxis: low risk= <40 yrs, high risk= hip, knee, pelvis surgery, malignancy, increased risk factors, prolonged immobility

Answer 71

1) D-dimer- negative= normal, positive= also in pregnancy, infection, malignancy and post-op 2) Compression ultrasound of proximal veins- can't squash= DVT in femoral and popliteal veins

Answer 72

a) Anticoagulants- SC/IV e.g. heparin, Fondaparinux, enoxaparin, Dalteparin, LMWH for min 5 days b) Warfarin- oral= prevent recurrence, short term, lifelong for mechanical valve replacement Compression stockings, treat underlying cause Spontaneous= more likely to recur than provoked

Answer 73

Typically around calf and ankle, unilateral, difficulty walking, warmth, non-specific, diagnosis= unreliable, pain, swelling, signs= tenderness, swelling, warmth, discolouration

Answer 74

Clot starts in leg--> IVC into right side of heart--> pulmonary heart, big= blocks both, obstructs--> pulmonary hypertension, tachycardia, cyanosis, R heart strain, close to death Breathlessness, pleuritic chest pain(could be infection, MSK, pneumothorax,) signs/ symptoms of DVT, no other likely diagnosis (could be asthma, COPD, pneumonia, MI, HF) Tachycardia, tachypnoea, pleural rub

Answer 75

CXR usually normal in PE, look for pneumonia, ECG- sinus tachy, exclude cardiac cause, mainly to exclude alternative causes D-dimer- excludes diagnosis, ventilation/ perfusion scan- mismatch defects, better for pregnant- less radiation, CTPA spiral CT with contrast- visualise major segmental thrombi

Answer 76

As for DVT- ensure normal Hb, platelets, renal function, baseline clotting, LMW heparin adjusted for 5 days, oral warfarin INR for 6 months Treat cause if possible, IVC filter if cannot anticoagulate using unaffected groin

Answer 77

2 layers- visceral single cell layer adherent to epicardium, fibrous parietal layer 2mm thick, collagen and elastin fibres, 50ml serous fluid Great vessels Left atrium= mainly outside pericardium, parietal layer= fibrous attachments to fix heart to thorax

Answer 78

Restrains filling volume of heart, stiff at higher tension, small reserve volume, if volume exceeded- pressure translated to cardiac chambers, small amount added to space has dramatic effect on filling but so does removal of small amount= tamponade physiology

Answer 79

Inflammation of pericardium Viral-flu, Epstein-Barr, varicella, HIV, bacterial- pneumonia- rheumatic fever, TB, staphs, streps, MAI in HIV Fungi, autoimmune- Sjogrens syndrome, scleroderma, systemic vasculitides, neoplastic- secondary metastatic tumours, metabolic- uraemia, myxodema

Answer 80

Central chest pain worse on inspiration or lying flat plus/ minus relief by sitting forward, friction rub may be heart, evidence of cardiac tamponade/ pericardial effusion, fever

Answer 81

ECG classically concave- saddle-shaped, ST segment elevation Blood test- FBC, ESR, U and E, cardiac enzymes- troponin may be raised, viral serology, blood cultures CXR- cardiomegaly ECHO- if suspected pericardial effusion

Answer 82

Analgesia- ibuprofen, treat the cause, consider colchicine before steroids/ immunosuppressants if relapse or continuing symptoms occur

Answer 83

Pneumonia, pulmonary embolus, chosochondritis, gastro- oesophageal reflux, myocardial ischaemia/ infarction, aortic dissection, pneumothorax, pancreatitis, peritonitis, herpes zoster Mainly of right heart failure w/JVP, Kussmaul's sign, soft diffuse apex beat, quiet heart sounds, S3, diastolic pericardial knock, hepatosplenomegaly, ascites and oedema

Answer 84

CXR- small heart and/ not with pericardial calcification-if not, CT/MRI helps distinguish from other cardiomyopathies, ECHO--> cardiac catheterisation Management: surgical excision

Answer 85

Accumulation of fluid in pericardial sac Any cause of pericarditis Dyspnoea, raised JVP, bronchial breathing at left base, signs of cardiac tymponade

Answer 86

CXR- enlarged, globular heart ECG- low-voltage QRS complex and alternating QRS morphologies, ECHO- echo-free zone surrounding heart Treat cause, pericardiocentesis may be diagnostic (suspected bacterial pericarditis) or therapeutic (cardiac tamponade) Send fluid for culture, ZN stain/ TB culture and cytology

Answer 87

Accumulation of pericardial fluid- raises intrapericardial pressure, hence poor ventricular filling and fall in CO Any pericarditis, aortic dissection, haemodialysis, warfarin, trans-septal puncture at cardiac catheterisation, post cardiac biopsy Pulse, BP, pulsus paradoxus, JVP, Kussmaul's sign, muffled S1 and S2

Answer 88

Beck's triad- falling BP, rising JVP, muffled heart sounds CXR- big globular heart ECG- low voltage QRS and or electrical alternans ECHO= diagnostic Seek expert help, effusion needs urgent drainage, send fluid for culture, ZN stain/ TB culture and cytology

Answer 89

Primary heart muscle disease of the myocardium--> affect the mechanical or electrical function of the heart Echo and cardiac MR Hypertrophic, dilated, primary restrictive, arrythmogenic right ventricular

Answer 90

Thickening of ventricular muscle wall Cause= autosomal dominant- familial Very common- most common cause of suddent cardiac death in young

Answer 91

Sarcomeric protein gene mutations (troponin T and B-myosin)- affects mechanical and electrical function SV reduced, fibrotic tissues throughout--> arrhythmias, rhythm and conduction= affected as fibrosis= electrical insulator Angina, dyspnea, palpitations, dizzy spells or syncope Sudden death, atrial/ ventricular arrhythmias, thromboembolism, infective endocarditis, heart failure B-myosin mutation= hypertrophy and dysrhythmia, troponin T mutation= risk of sudden death

Answer 92

ECG- abnormal, pattern of LVH, cardiac imaging--> ventricular hypertrophy on ECHO and MR Genetic analysis can confirm as most cases= autosomal dominant and familial Amiodarone IV If high risk- implantable cardiac defibrillator

Answer 93

Dilated LV which contracts poorly/ thin muscle- affects young people Autosomal dominant- familial Cytoskeletal gene mutations--> LV/RV or all 4 chambers dilatation and dysfunction, poorly generated contractile force--> progressive dilation of heart w/ some diffuse interstitial fibrosis

Answer 94

SOB at first, less often embolism/ arrhythmia, presents w/HF symptoms as can't contract CXR= cardiac enlargement, ECG= abnormal changes- T wave flattening, cardiac imaging- dilated ventricles Tx: HF and AF treated in conventional way

Answer 95

Desmosome gene mutations--> RV replaced by fat and fibrous tissue--> muscle dies and replaced by fatty material as result of inflammation Arrhythmias= main, ventricular tachycardia- Naxos disease associated (thickening of palms/ soles and woolly hair)

Answer 96

Ion channel protein gene mutations, but normal heart structure Recurrent syncope Long QT syndrome- can die from sounds shocking them/ being given QT prolonging drugs, short QT syndrome, Brugada, catecholaminergic polymorphic ventricular tachycardia

Answer 97

Inherited abnormality of cholesterol metabolsim--> serious premature coronary and other vascular disease, increases risk of MI, early death Dominantly- 50% chance, only look at relatives in first degree, heterogeneity--> variance, age-related penetrance

Answer 98

The inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirement of metabolising tissue of the body Any structural/ functional cardiac disorder, impairing ability of the heart to function and meet its demands of supplying sufficient oxygen/ nutrients to metabolising body

Answer 99

IHD(commonest in developed world), hypertension (Africa,) metabloid syndrome, alcohol excess, cardiomyopathy, any factor increasing myocardial work

Answer 100

SOBOE, SOB at rest, fatigue and oedema, specific= orthopnoea(SOB when lying flat,) paroxysmal nocturnal dyspnoea Peripheral oedema, pulmonary crackles and tachycardia, raised JVP, cardiomegaly, murmurs, raised NP, displaced apex beat exhaustion, cold peripheries, cyanosis, hypotension, narrow pulse pressure, abnormal pulse, RV heave, wheeze

Answer 101

Left ventricular systolic dysfunction- from IHD/MI, cardiomyopathy, valvular HD and HT Right ventricular systolic dysfunction- from LVF, pulmonary stenosis, lung disease, secondary to LVSD, w/primary and secondary pulmonary HTN, right ventricular infarction and adult congenital disease Diastolic heart failure- constrictive pericardititis, cardiac tamponade, restrictive CM, HTN Low-output heart failure- C) falls, pump failure, systolic and/ not with diastolic HF, decreased HR High-output heart failure- rare, CO= normal/ increased in face of needs, CO= fails to meet these needs, initially RVF, later= LVF evident

Answer 102

``` When heart begins to fail, may systems initiate physiological compensatory changes that try to maintain CO and peripheral perfusion in order to negate effects- become overwhelmed=decompensation Venous return- increased diastolic volume stretches fibres, can contract as much in response to increased preload, CO may decrease Outflow resistance (afterload)- pulmonary with systemic resistance, physical characteristics of vessel walls, volume of blood ejected Increased afterload= increased end-diastolic volume and dilatation of ventricle= more resistance, further exacerbates afterload issue ```

Answer 103

There is chronic activation--> receptors being acted on by sympathetic system to down regulate resulting in there being less receptor to act on--> effect of symp activation is diminished, CO stops increasing

Answer 104

Diminished renal perfusion, increased BP, venous pressure, pre-load, stretching and contraction of heart, SV and CO Increased contraction requires more energy and blood- with HF this is not met, myocytes die--> decrease in force of contraction, SV and CO

Answer 105

Inability of ventricle to contract normally--> decrease in CO IHD, MI and cardiomyopathy Inability of ventricles to relax, decreasing SV and CO Hypertrophy- increased BP and afterload leads to myocytes growing bigger to compensate, less space for blood AS also- increases afterload etc.

Answer 106

New onset/ decompensation of chronic HF characterised by pulmonary and/ or peripheral oedema with or without signs of peripheral hypotension Develops slowly, venous congestion common but arterial pressure is well maintained until very late

Answer 107

HD present but no undue dyspnea from normal activity--> no limitation (asymptomatic) Comfortable at rest but dyspnea when active--> slight limitation (mild HF) Less than ordinary activity causes dyspnea--> marked limitation (moderate HF) Dyspnea at rest--> inability to carry out any physical activity w/o discomfort (severe HF)

Answer 108

Brain natriuretic peptide (BNP): secreted by ventricles in response to increase myocardial wall stress, levels correlate with wall stress and severity, FBC, U and Es and liver biochem CXR: alveolar oedema, cardiomegaly, dilated upper lobe vessels of lungs, effusions (pleural) ECG= underlying causes; ischaemia, LVH in HTN/ arrythmia, if ECG and BNP abnormal--> ECHO ECHO= assess chamber dimension, look for regional wall motion abnormalities, valvular disease and cardiomyopathies, sign of MI

Answer 109

Avoid large meals, lose weight, stop smoking, exercise, vaccination Diuretics, ACE inhibitors, Beta-blockers, digoxin, inotropes, revascularisation, surgery to repair, heart transplant in young people, cardiac resynchronisation

Answer 110

Reduce preload--> decreased systemic and pulmonary congestion Symptomatic relief Loop= furosemide, Thiazide= bendroflumethiazide, aldosterone antagonist- spirolactone and epelerone Renal impairment and hyperkalaemia

Answer 111

Ramipril, enalipril, captopril Cough= substance P and bradykinin breakdown, hypotension, hyperkalaemia and renal dysfunction Give ARB instead if cough e.g. canderstan or valsartan

Answer 112

Bisoprolol, nebivolol, carvedilol- start at low dose and titrate upwards, do not give to asthmatics When some viable myocardium remains, illicit PCI stenting

Answer 113

Major cause of premature vascular disease--> cerebrovascular events, IHD and peripheral vascular disease Often symptomless- screening= vital, major risk factor for CVD, remain under diagnosed, under treated and poorly controlled in UK, prevalence in over 35, more common in men Less than 140/90mmHg

Answer 114

More than/ equal to 140/90mmHg clinic BP, 135/85mmHg More than/ equal to 160/100 Hg clinic BP, 150/95mmHg Greater than/ equal to 180mmHg and/ or diastolic BP greater than/ equal to 110mmHg Start immediate anti-hypertensive drug treatment

Answer 115

Cardiac failure and atherosclerosis and cerebral haemorrhage Unknown ' essential (primary or idiopathic) hypertension' or known ' secondary HTN'

Answer 116

Majority of cases: genetic susceptibility, excessive sympathetic NS activity, abnormalities of Na+/ K+ membrane transport, high salt intake, abnormalities in RAAS system Renal disease/ pregnancy, other; endocrine causes, coarctation of the aorta and drug therapy

Answer 117

Chronic kidney disease Diabetes Promotion of pheochromocytoma vasoconstriction Chronic glomerulonephritis- less common now

Answer 118

Cushings- hyper secretion of corticosteroids Conn's= adrenal tumour secreting aldosterone Phaemochromocytoma- adrenal tumour secreting catacholamines, rare

Answer 119

Coarctation of aorta In either arm, but not legs Femoral delayed relative to radial HF, hypertensive cerebral haemorrhage or dissecting aneurysm

Answer 120

Corticosteroids e.g. prednisolone, cyclosporin, erythropoietin, some types CP Alcohol, amphetamines, ecstasy, cocaine also

Answer 121

Age, more common in blacks, family history, overweight/ obese, little exercise, smoking, too much salt, alcohol, diabetes, stress

Answer 122

Accelerates atherosclerosis, thickening of media of muscular arteries Smaller arteries and arterioles, impaired NO-mediated vasodilation and enhanced secretion of vasoconstrictors including endothelins and prostaglandins Intracerebral haemorrhage Kidney size reduced, small vessels= intimal thickening and medial hypertrophy, sclerotic glomeruli numbers increased

Answer 123

Raised diastolic BP, usually over 120mmHg and progressive renal disease Renal vascular changes prominent, acute haemorrhage and papilloedema (optic disc swelling caused by increased intracranial pressure) Previously fit individuals, often black males in 30-40s Cardiac failure- LVH 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 124

End-organ damage e.g. LVH, retinopathy, proteinuria Protein, albumin: creatine ratio and haematuria BTs: serum creatinine, eGFR, glucose Retinal haemorrhage/ papilloedema ECG: LVH ECHO= further detect LVH 24 hour ABPM

Answer 125

140/90mmHg | High con of fruit, veg, low-fat diet, regular exercise, reduce alcohol, salt, weight, smoking

Answer 126

A- ace-inhibitor or ARB C- CCB e.g. nifedipine or amlodipine D- diuretics- furosemide= more potent Beta-blocker, consider young if intolerant of ACEi/ ARB

Answer 127

Ramipril/ candesartan + nifedipine + bendroflumethiazide + furosemide Ramipril/ candersatan + nifedipine + bendroflumethiazide + furosemide If higher dose not tolerated- consider beta-blocker

Answer 128

Abnormality of the cardiac rhythm | Sudden death, syncope, heart failure, chest pain, dizziness, palpitations, no symptoms at all

Answer 129

Bradycardia- HR<60bpm and <50bpm at night, usually asymptomatic unless rate slow, normal in athletes owing to increased vagal tone and thus parasympathetic activity Tachycardia- HR>100bpm, more symptomatic when fast and sustained--> supraventricular- from atria/ AV junction, ventricular

Answer 130

MI, coronary artery disease, LV aneurysm, mitral valve disease, cardiomyopathy, pericarditis, myocarditis, aberrant conduction pathways Caffeine, smoking, alcohol, pneumonia, drugs, metabolic imbalance, pheochromocytoma

Answer 131

Palpitation, chest pain, presyncope/ syncope, hypotension, pulmonary oedema FBC, U&E, glucose, Ca2+, Mg2+, TSH ECG: signs of IHD, AF, short PR interval (WPW syndrome), long QT interval, U waves 24h ECG monitoring- several recordings ECHO= any structural heart disease Exercise ECG, cardiac catheterisation, electrophysiological studies

Answer 132

Parasymp reduction/ sympathetic increase--> tachycardia and vice versa Women P waves upright in leads I and II, inverted in AVR and V1

Answer 133

Chaotic irregular rhythm at 300-600bpm; AV node responds intermittently, irregular ventricular rate Males more, 5-15% over 75y/o Idiopathic, hypertension, any condition affecting atria, HTN, HF, coronary artery disease, valvular heart disease, cardiac surgery, cardiomyopathy, rheumatic heart disease, acute excess alcohol intoxication

Answer 134

Older than 60, diabetes, high BP, coronary artery disease, prior MI, structural heart disease Acute: onset within previous 48 hours, paroxysmal: stops spontaneously within 7 days, recurrent- 2 or more episodes, persistent- continuous for more than 7 days and not self terminating, permanent

Answer 135

Maintained by continuous, rapid activation of atria by multiple meandering re-entry wavelets Often driven by rapidly depolarising automatic foci, located predominantly within pulmonary veins Atria respond, no coordinated mechanical action, only proportion conducted--> ventricles CO drops by 10-20% and higher risk of thromboembolic events- blood pooling etc

Answer 136

Highly variable symptoms, may be asymptomatic, palpitations, dyspnoea and chest pains, fatigue, no P waves on ECG, rapid and irregular QRS rhythm, apical pulse rate greater than radial rate, 1st heart sound= variable intensity Atrial flutter, irregular and rapid QRS complex

Answer 137

Acute- treat provoking cause, DC shock--> SR, LMW heparin, IV infusion/ antiarrhythmic drug e.g. flecainide or amiodarone, CCB, beta-blocker, digoxin AV nodal slowing agents plus oral anticoagulation, beta-blocker, CCB, or digoxin and then consider amiodarone Rhythm control- younger, symptomatic and physically active Cardioversion--> SR and use Beta-blockers, Flecainide if no heart defect, IV amiodarone if heart defect Appropriate anti-coagulation e.g. warfarin

Answer 138

Congestive HF= 1 point, HTN= 1 point, Age greater/ equal to 75= 2 points, diabetes mellitus (1 point,) stroke/ TIA etc= 2 points, vascular disease= 1 point, age 65-74= 1 point, female= 1 point More than 1 point= consideration of AC and/ or aspirin 2 and above= oral AC needed

Answer 139

Usually an organised atrial rhythm with an atrial rate typically between 250-350bpm Often associated with AF and frequently require a similar therapeutic approach Either paroxysmal/ persistent, much less common than AF, more common in men, prevalence increases with age Idiopathic, CHD, obesity, HTN, HF, COPD, pericarditis, acute excess alcohol intoxication

Answer 140

AF(also diff diagnosis) as well as supra ventricular tachyarrythmias Breathlessness, chest pain, dizziness, syncope, fatigue

Answer 141

Definitive diagnosis, regular sawtooth-like atrial flutter waves (F waves) between QRS complexes due to continuous atrial depolarisation If F waves not visible- may be able to be unmasked by slowing AV conduction by carotid sinus massage or IV adenosine (AV nodal blocker)

Answer 142

Electrical cardioversion- anticoagulant before e.g. LMW heparin e.g. enoxaparin/ Dalteparin if acute Catheter ablation- creating conduction block to try to restore rhythm and block offending re-entrant wave IV amiodarone- restore SR and use beta-blocker to suppress further arrhythmias

Answer 143

AV node/ His bundle Block lower in conduction system First-degree, second-degree, third-degree- complete

Answer 144

Simple prolongation of the PR interval to greater than 0.22 seconds Hypokalaemia, myocarditis, inferior MI, AVN blocking drugs e.g. Beta blockers, CCBs Asymptomatic so no treatment

Answer 145

When some P waves conduct and others do not, acute MI Mobitz I and Mobitz II Wenckebach phenomenon- progressive PR interval prolongation until beat is 'dropped' and P wave fails to conduct, PR before blocked P wave= longer than PR interval after blocked P wave AVN blocking drugs, inferior MI--> light headiness, dizziness and syncope Doesn't require a pacemaker unless poorly tolerated

Answer 146

PR interval= constant, QRS interval is dropped, failure of conduction through His-Purkinje system Anterior MI, mitral valve surgery, SLE and Lyme disease, rheumatic fever SOB, postural hypotension and chest pain Sudden complete AV block and pacemaker should be inserted

Answer 147

Complete heart block when all atrial activity fails to conduct to ventricles Ventricular contractions= sustained by spontaneous escape rhythm which originates below block P waves independent of QRS complex Structural heart disease, ischaemic HD, HTN, endocarditis/ Lyme disease Depends on aetiology- one option= permanent pacemaker, IV atropine

Answer 148

Narrow-complex= QRS complex less than 0.12 seconds, implies block= originates in His bundle, block more proximal than AV node IV atropine Permanent pacemaker Broad-complex escape rhythm- B= below His QRS complex greater than 0.12 seconds Implies block originates below Bundle of His and region of block lies more distally in His-Purkinje system Dizziness and blackouts= often occur Permanent pacemaker implantation= recommended

Answer 149

Asymptomatic Right and left bundle branches Left--> anterior and posterior Slight widening (0.11 seconds) of QRS complex= incomplete BBB Wider QRS complex (larger than 0.12 seconds) On whether right or left bundle is blocked

Answer 150

Pulmonary embolism, IHD, atrial/ ventricular septal defect Right bundle no longer conducts- 2 ventricles do not get impulses at same time, spread from left--> right Produces late activation of R ventricle Deep S wave in leads I and V6 and tall late R wave in lead V1 MarroW- QRS looks like M in lead V1, W in V5 and V6 Causes wide physiological splitting of second heart sound

Answer 151

IHD, aortic valve disease Late activation of left ventricle Deep S wave in lead V1 and tall late R wave in leads I and V6, abnormal Q waves also wiLLiam- W in leads V1 and V2 and M in leads V4-V6 Causes reverse splitting of second heart sound TCP= temporary method, pacemaker

Answer 152

HR>100bpm Anaemia, anxiety, exercise, pain, HF, pulmonary embolism Treating causes, Beta-blocker

Answer 153

Atria/ AV junction Paroxysmal supraventricular tachycardias Young patients with no or little structural heart disease First presentation= commonly between 12-30 ages AV node

Answer 154

In women than men, strikes suddenly without obvious provocation, may stop spontaneously/ may continue indefinitely until medical intervention Exertion, emotional stress, coffee, tea, alcohol Slow-fast AVNRT, atria contract slowly in one cycle and then fast in next Rapid regular palpitations with abrupt onset and sudden termination, chest pain and breathlessness, neck pulsations, polyuria Sometimes QRS complex will show typical BBB P waves are either not visible/ seen immediately before or after QRS complex due to simultaneous atrial and ventricular activation

Answer 155

From incomplete separation of atria and ventricles during fetal development Normal AV conduction but also accessory pathway From atria--> ventricle (anterograde) or from ventricle back to atria (retrograde) Wolff-Parkinson- White (WPW) syndrome If accessory pathway conducts from atrium to ventricle during SR, conducts quickly over abnormal connection to depolarise part of ventricles abnormally

Answer 156

Short PR interval, wide QRS complex begins as slurred part known as delta wave Premature beat from SAN--> AVN and accessory pathway in refractory period, down via AVN as signal not transmitted, until meets accessory pathway, conducts impulse back into atria, back to AVN= re-entry circuit Palpitations, severe dizziness, dyspnoea, syncope Short PR interval, wide QRS complex starts as slurred delta wave

Answer 157

With haemodyamic instability (pulmonary oedema and hypotension)= emergency cardioversion If stable= breath-holding, carotid massage, valsalva manoeuvre, if unsuccessful= IV adenosine Catheter ablation of accessory pathway in AVRT, modification of slow pathway in AVNRT

Answer 158

Ventricular ectopics, ventricular tachycardia, sustained ventricular tachycardia, ventricular fibrillation, some= channelopathis e.g. long QT syndrome

Answer 159

Premature ventricular contraction Post-MI arrhythmia, also in healthy patients MI Extra, missed or heavy beats, if frequent left ventricular dysfunction may develop and can provoke ventricular fibrillation Usually asymptomatic, can feel faint/ dizzy Broad and bizarre QRS complex- greater than 0.12 seconds Reassure patient, give beta-blockers if symptomatic

Answer 160

Pulse of more than 100bpm with at least 3 irregular heartbeats in a row In patients with structurally normal hearts (idiopathic), usually benign with excellent long-term prognosis Occasionally= pathological- known as Gallavardin's tachycardia, untreated--> cardiomyopathy Decreased CO and oxygenated blood around body Breathlessness, chest pain, palpitations, light headed or dizzy Beta-blockers

Answer 161

Longer than 30 seconds Dizziness, syncope, hypotension, cardiac arrest, pulse rate between 120-220bpm Rapid ventricular rhythm, broad and abnormal QRS complex- greater than 0.14 seconds Haemodynamically unstable= emergency electrical cardioversion, stable= IV beta-blocker, IV amiodarone Prevented by use of BBs and implantable cardiac defibrillator

Answer 162

Very rapid and irregular ventricular activation with no mechanical effect- no CO Pulseless patient and becomes unconscious and respiration ceases Shapeless, rapid oscillations and no hint of organised complexes By ventricular ectopic beat Electrical defibrillation Increased risk of sudden death, implantable cardioverter-defibrillators= first-line therapy

Answer 163

Prolonged QT interval on ECG Congenital: Jervell-Lange-Nielsen syndrome, Romano-ward syndrome Acquired: hypokalaemia, hypocalcaemia, amiodarone and tricyclic antidepressants, bradycardia, acute MI, diabetes Syncope, palpitations, polymorphic ventricular tachycardia- usually terminate spontaneously may degenerate to VF Treat underlying cause, if acquired long QT- IV isoprenaline

Answer 164

Obstructs LV inflow during diastole, when area less than 2cm2 Rheumatic carditis, infective endocarditis, mitral annular calcification LA dilatation--> pulmonary congestion and oedema, partially countered by pulmonary arterial vasoconstriction--> right ventricular hypertrophy, dilatation and failure with tricuspid regurgitation

Answer 165

Progressive dyspnoea due to left atrial dilation, haemoptysis- rupture of bronchial vessels, right heart failure, AF- left atrium dilation--> palpitations, systemic emboli- AF, 'a' wave in jugular venous pulsations, mitral facies/ molar flush- pinkish purple cheeks Diastolic murmur prominent at apex, heart best when lying on left side, loud opening S1 snap, more severe= longer murmur and closer opening snap is to S2

Answer 166

CXR: left atrial enlargement, pulmonary oedema, calcified mitral valve ECG: AF, left atrial enlargement ECHO= gold standard for diagnosis, assess mitral valve mobility, gradient and mitral valve area Beta-blockers prolong diastole, diuretics for fluid overload, percutaneous mitral balloon valvotomy- catheter into RA via femoral vein, intertribal septum punctured--> LA, balloon inflated opening valve Mitral valve replacement

Answer 167

Abnormalities of valve leaflets, chordae tendinae, papillary muscles or left ventricle, myxomatous degeneration (MVP), ischaemic mitral valve, rheumatic heart disease, infective endocarditis, papillary muscle dysfunction, dilated cardiomyopathy Females, lower BMI, advanced age, renal dysfunction, prior MI

Answer 168

Left atrial dilatation but little increase in left atrial pressure if regurg longstanding since accommodated by large left atrium--> left atrial enlargement, left ventricle hypertrophy, right ventricular dysfunction due to pulmonary hypertension

Answer 169

Soft S1 and pan systolic murmur at apex radiating to axilla, prominent S3 in congestive heart failure/ left atrium overload, intensity does not correlate with severity Exertion dyspnoea, fatigue, lethargy, increased SV= palpitation, symptoms of right heart failure, HF may increase with pregnancy, infection/ AF 60%

Answer 170

ECG= left atrial enlargement, AF, left ventricle hypertrophy in severe MR, but not diagnostic CXR: left atrial enlargement and central pulmonary artery enlargement ECHO= estimation of left atrium and left ventricle size and function, valve structure assessment, transoesophageal= helpful

Answer 171

ACE-inhibitors, Beta blockers, anticoagulation in AF and flutter, diuretics for fluid overload Serial ECHO- mild= 2-3 years, moderate= 1-2 years, severe= 6-12 months Symptoms at rest/ exercise, if EF<60%, if new onset AF

Answer 172

Narrowing--> obstruction to left ventricular stroke volume, symptoms= area= 1/4th of normal Supravalvular- congenital fibrous diaphragm above aortic valve Subvalvular- fibrous ridge below valve Valvular- most common Calcific aortic valvular disease (CAVD)-calcification, most in elderly Calcification of congenital bicuspid aortic valve (BAV)- most common congenital heart disease Rheumatic heart disease- rare, due to eradication= low

Answer 173

BAV, in males Increased after load, increased LV pressure and compensatory left ventricular hypertrophy--> angina, arrhythmias, LV failure, more severe on exercise Syncope- usually exertion, angina, HF, dyspnoea, sudden death, slow rising carotid pulse and decrease pulse amplitude Soft/ absent 2nd heart sound, prominent 4th heart sound, ejection systolic murmur-crescendo-decrescendo character

Answer 174

Aortic regurgitation, subacute bacterial endocarditis ECHO= left ventricular size and function, Doppler derived gradient and valve areas (AVA) ECG: left ventricular hypertrophy, left atrial delay, left ventricular 'strain' pattern due to pressure overload, depressed ST segments and T-wave inversion CXR: left ventricular hypertrophy, calcified aortic valve

Answer 175

Dental hygiene due to increased risk of IE Vasodilators= contraindicated in severe aortic stenosis Any symptomatic, decreasing EF, undergoing CABG with moderate/ severe TAVI- minimally invasive, catheter up aorta, inflate to crack calcification, another catheter with new valve

Answer 176

Can be associated with aortic stenosis Congenital bicuspid aortic valve, rheumatic fever, IE SLE, Marfan's and Ehlers- Danlos syndrome, aortic dilatation, IE or aortic dissection

Answer 177

Left ventricular size increases--> dilatation and hypertrophy--> HF, diastolic pressure falls and coronary perfusion decreases, cardiac ischaemia develops Chronic= asymptomatic for many years, exertion dyspnoea, palpitations, angina, syncope, wide pulse pressure, apex beat displaced laterally Diastolic blowing murmur at left sternal border, systolic ejection murmur Collapsing water hammer pulse, Quincke's sign- capillary pulsation in nail beds, de Musset's sign- head nodding with each HB, pistol shot femoral- sharp bang heard on auscultation

Answer 178

HF, IE, mitral regurgitation ECHO= evaluation of aortic valve and 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 LVH due to volume overload, tall R waves and deeply inverted T waves in left-sided chest leads and deep S waves in right-sided

Answer 179

IE prophylaxis ACE-inhibitors improve SV- only if symptomatic or has HTN Serial ECHOs to monitor progression Valve replacement if symptoms increasing, enlarging heart on CXR/ ECHO, ECG deterioration (T wave inversion in lateral leads)

Answer 180

Infection of endocardium or vascular endothelium of heart, known as subacute bacterial endocarditis Valves with congenital/ acquired defects, right-sided more common in IV drug addicts, normal valves with virulent organisms, prosthetic valves and pacemakers

Answer 181

More common in developing countries, disease of elderly with prosthetic valves, young IV drug user, young with congenital heart disease More common in males Staph aureus, pseudomonas aeruginosa, streptococcus viridans- gram +ve, alpha haemolytic and optochin resistant

Answer 182

IV drug use, poor dental hygiene, skin and soft tissue infection, dental treatment, IV cannula, cardiac surgery, pacemaker Usually consequence of 2 factors- organisms in bloodstream, abnormal cardiac endothelium facilitating adherence and growth Bacteraemia= poor dental hygiene, IV drug use, soft tissue infections, dental treatment, IV cannula, cardiac surgery, permanent pacemakers Damaged endocardium= platelet and fibrin deposition, aortic and mitral valves most commonly involved also

Answer 183

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 heart, risk factor for IE, newly developed ventricular arrhythmias or conduction disturbances Headache, malaise, confusion, night sweats, finger clubbing Staph aureus= quickly developed, embolisation of vegetations, valve dysfunction--> arrhythmia and HF

Answer 184

Splinter haemorrhages on nail beds of fingers, embolic skin lesions- black spots on skin, Osler nodes- tender nodes in digits, Janeway lesions- haemorrhages and nodules in fingers, Roth spots- retinal haemorrhages with white/ clear centres seen on fundoscopy, petechiae- small red/ purple spots caused by bleeds in skin

Answer 185

Dukes criteria Blood cultures- 3 sets from different over 24 hours, before antibiotics started, identifies in 75% of cases CRP and ESR raised, normochromic, normocytic anaemia, neutrophilic, haematuria- urinalysis, CXR= cardiomegaly, ECG= long PR interval at regular intervals Transthoracic echo-safe, non invasive, no discomfort, poor images, negative does not exclude IE Transoesophageal- sensitive but uncomfortable, good for visualising mitral lesions and development of aortic root abscess

Answer 186

Antibiotics for 4-6 weeks, Benzylpenicillin and gentamicin if not staph If staph= vancomycin and rifampicin if MRSA Treat complications Surgery- removing valve, replace with prosthetic one, if not cure with ABs, remove infected devices, large vegetations before embolism Recommend good oral health and inform patients of symptoms that may indicate IE

Answer 187

``` Intellectual disability in 10% Psychosocial issues Transition Explaining the lesion and prognosis Building independence/ self-reliance ```

Answer 188

2.2%, 5.7%, 3%, 10-14%, 18-22 weeks One child with defect increases the chance of the second child having another defect Maternal prenatal rubella infection- persistent ductus arterioles and pulmonary valvular and arterial stenosis Maternal alcohol misuse- septal defects Singles genes associated Drugs- thalidomide, amphetamines and lithium Diabetes of mother Genetic abnormalities

Answer 189

Central cyanosis- because of R--> L shunting of blood/ mixing of systemic and pulmonary blood flow--> poorly oxygenated blood, skin= bluish, seen in Tetralogy and tricuspid atresia Pulmonary HTN- from L--> R shunts, pulm arteries thicken, resistance--> right ventricular pressure increases causing reversal of shunt to right-to-left--> patient blue= Eisenmenger's complex Clubbing of fingers, growth retardation, syncope- severe right/ left ventricular outflow tract obstruction

Answer 190

Endocarditis- in smaller ventricular septal defects/ 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 191

R-->L side shunting associated w/ R side cardiac failure and R side cardiac hypertrophy Increased pulmonary pressure due to VSD, can't leave--> increase lung resistance and RV pressure-->LV pressure--> blood moves to left again

Answer 192

10% Large maligned VSD, overriding aorta, RV outflow obstruction and RV hypertrophy Stenosis of RV outflow leads to RV being higher pressure than left Blue blood RV--> LV, patients= blue

Answer 193

Central cyanosis, low birthweight and growth, dyspnoea on exertion, delayed puberty, systolic ejection murmurs, CXR= boot shaped heart Full surgical Tx during first 2 years life, often pulmonary valve regurgitation in adulthood and require redo surgery

Answer 194

1-2% of live births- most common form, more common in males, 2 instead of 3 cusps, can be severely stenotic in infancy or childhood Degenerate quicker than normal valves Associated with coarctation and dilation of ascending aorta May develop aortic stenosis with/ without aortic regurgitation, predisposing IE Intense exercise may accelerate, so yearly ECHOs on athletes

Answer 195

Often first diagnosed in adulthood and represents 1/3 CHD, more common in women, probe can be passed through primum and secundum of foramen vale Slightly higher pressure in LA, shunt= L-->R, not blue Right ventricle easily dilates, can result in: RV hypertrophy, pulmonary HTN, increased IE risk

Answer 196

Dysponea, exercise intolerance, may develop atrial arrhythmias from right atrial dilatation, pulm flow murmur, fixed split second heart sound CXR= large plum arteries, large heart ECG: RBBB due to RV dilatation ECHO= hypertrophy and dilation of right side of heart and pulmonary arteries Tx= surgical closure, percutaneous

Answer 197

20% Higher pressure in LV, left--> R shunt Does not go blue Increased blood flow through lung

Answer 198

Pulmonary HTN and eventual Eisenmenger's complex, when RV pressure higher--> shunt R to left, small breathless skinny baby, increased resp rate, tachycardia, CXR: big heart, murmur varies in intensity Large systolic murmur, thrill, well grown, normal HR and size Medical Tx initially since many will spontaneously close, surgical close, small= no intervention, prophylactic antibiotics Moderately sized lesion= furosemide, ACE inhibitor

Answer 199

Ventricular, atrial septum and mitral and tricuspid valves, hole in very centre, can be complete/ partial, one large malformed AV valve Downs Syndrome

Answer 200

Complete= breathlessness as neonate, poor weight gain and feeding, torrential pulm flow--> Eisenmenger's over time Partial= can present in late adulthood Pulm artery banding if large defect in infancy, surgical repair= challenging, partial may be left alone if no right heart dilatation

Answer 201

Proximal left pulm artery and descending aorta, foetal life= pulm vas resistance is high, flow is from right to left atrium, normally closes within few hours of birth In e.g. premature babies and maternal rubella, ductus persists Remains open= abnormal left-to-right shunt--> pulm HTN, right side cardiac failure, increased IE risk

Answer 202

Continuous 'machinery' murmurs, bounding pulse, if large then large heart and breathless, Eisenmengers, tachycardia, CXR: aorta and pulm art prominent, ECG: left atrial abnormality and left ventricular hypertrophy, ECHO= dilated left atrium and left ventricle Closed surgically/ percutaneously, low risk of complications, venous approach may require an AV loop, indometacin- stimulate duct closure

Answer 203

Narrowing of aorta at/ just distal to insertion of ductus arteriosus--> excessive blood flow through carotid and subclavian vessels into systemic vascular shunts Turner syndrome, berry aneurysms, patent ductus arteriosus Decreased renal perfusion--> systemic HTN that persists after surgical correction

Answer 204

Often asymptomatic for many years, right arm HTN, bruits over scapulae and back from collateral vessels, murmur, headaches and nose bleeds, HTN in upper limbs, discrepant BP in upper and lower body Early coronary heart disease, early strokes, sub-arachnoid haemorrhage CXR: dilated aorta indented at site of coarctation, ECG: left ventricular hypertrophy, CT: can accurately demonstrate the coarctation and quantity flow

Answer 205

Surgery, balloon dilatation and stenting, risk of aneurysm formation at site of repair

Answer 206

``` Narrowing of the outflow of the RV Can be valvar, sub valvar or supravalvar Severe= right ventricular failure as neonate, collapse, poor pulm blood flow, RV hypertrophy, tricuspid regurgitation Moderate/ mild= well tolerated for many years, RV hypertrophy ```

Answer 207

Balloon valvoplasty- catheter with balloon through femoral vein then inflate balloon Open valvotomy Shunt- to bypass the blockage

Answer 208

Involves the aorta coming off the right ventricle and pulm trunk off the left ventricle 2 closed circulations result More common in men and associated with diabetes Survival only possible if communication between 2 circuits- all= some form atrial septal defect with blood mixing Tx= atrial switch operation with good results

Answer 209

Partial blockage of leg/ peripheral vessels by an atherosclerotic plaque and or resulting in insufficient perfusion of lower limb--> lower limb ischaemia From atherosclerosis Aorta-iliac and infra-inguinal arteries Men than women

Answer 210

Aorta--> common iliac at L4, external iliac, internal iliac, common femoral, superficial femoral, popliteal, anterior tibial, posterior tibial, perineal

Answer 211

Smoking, diabetes, hypercholesterolaemia, HTN, HTN, physical inactivity, obesity Atherosclerosis of the arteries distal to the aortic arch Normal O2 pressures in different activities Mild ischaemia- stress induces malfunction, angina, intermittent claudication (cramping pain relieved by rest distal to atheroma, absent leg pulses, cold feet) Moderate- structural and functional breakdown, ischaemic cardiac failure, critical limb ischaemia

Answer 212

Rest pain= typically nocturnal, risk of gangrene and/ or infection, chronic and most severe manifestation, low O2 pressures in different activities, vascular dementia Infarction, gangrene Absent femoral, popliteal or foot pulses, cold/ white legs Osteoarthritis of hip/ knee due to knee pain at rest, peripheral neuropathy- tingling

Answer 213

Exclude arteritis by looking at ESR/ CRP- would be raised FBC- Hb to exclude anaemia/ polycthaemia ECG: cardia ischaemia Severity from ankle/ brachial pressure index (ABPI)- cuff pressure at which blood flow is detectable by Doppler in posterior/ anterior tibial arteries compared to brachial artery Colour duplex US- first line test MR/ CT angiography to assess extent and location of stenoses and quality of distal vessels- if considering intervention

Answer 214

Embolic/ thrombotic disease Cardiac thrombus and cardiac arrhythmias Rheumatic fever Aneurysm thrombus or thrombus on atherosclerotic plaques

Answer 215

On a chronic atherosclerotic stenosis in pt who has previously reported symptoms of claudication Also in normal vessels in individuals who are hyper coagulable because of malignancy/ thrombophilia defects Popliteal aneurysms

Answer 216

Pale, pulseless, painful, paralysed, paraesthetic and 'perishingly cold' Fixed mottling Sudden deterioration of symptoms w/ deep duskiness of the limb- due to extensive pre-existing collaterals

Answer 217

Surgical emergency requiring revascularisation within 4-6 hours to save limb Intra-arterial thrombolysis, surgical removal of embolus if present- surgical embolectomy (Fogarty catheter) or local thrombolysis e.g. tissue plasminogen activator (t-PA)- balance risks of surgery w/ haemorrhage complications of thrombolysis Anticoag w heparin after procedure Aware of post-op reperfusion injury and compartment syndrome

Answer 218

Smoking cessation- small vessels in muscles heart to ischaemia provide 'back up supply' contract in response to nicotine and tobacco Treat HTN, hyperlipidaemia and diabetes Antiplatelet agent, exercise and weight loss

Answer 219

Percutaneous transluminal angioplasty- squashes plaque and increases perfusion, bypass procedure, amputation if severe Carotid arterial disease Symptomatic patients w/ ipsilateral stenosis >70%

Answer 220

Local complications of atherosclerotic plaque, in other areas due to presence of atherosclerotic plaques Progression, haemorrhage, plaque rupture, overlying thrombosis, dissection, aneurysm

Answer 221

True and false A permanent dilatation of the artery to twice the normal diameter 2cm Abnormal dilatations that involve all layers of the arterial wall, most frequent= abdominal aorta, iliac, popliteal and femoral arteries, thoracic aorta

Answer 222

Known as pseudoaneurysm, involves collection of blood in outer layer only (adventitia)- communicates with the lumen e.g. after trauma from femoral artery puncture Abdominal or thoracic

Answer 223

Most commonly occur below renal arteries (infra-renal) Incidence increases with age, more in men, aortic diameter exceeding 3cm Most= no specific identifiable causes, severe atherosclerotic damage, family history, tobacco smoking, male, increasing age, HTN, COPD, trauma, hyperlipidaemia

Answer 224

Degradation of elastic lamellae resulting in leucocyte infiltrate, causing proteolysis and smooth muscle cell loss, dilatation affects all 3 layers Unruptured= asymptomatic often, picked up via examination or plain X-ray, pain in abdomen, back, loin or groin, pulsatile abdominal swelling (less pronounced) Ruptured= more likely if increased BP, female, smoker, strong family history, intermittent or continuous abdominal pain, pulsatile abdominal swelling, collapse, hypotension, tachycardia, profound anaemia, sudden death

Answer 225

GI bleed, ischaemic bowel, MSK pain, perforated GI ulcer, pyelonephritis, appendicitis Abdo US, CT and or MRI angiography scans Small aneurysms below 5.5cm= monitored, treat underlying causes, modify risk factors, smoking cessation, vigorous BP control, lowering lipids Patients tend to do better if aneurysm is symptomatic and expanding yearly, open surgical repair, endovascular repair- stent via femoral/ iliac arteries

Answer 226

Normal size of mid-descending= 26-28mm Ascending, arch or descending thoracic aorta Marfan syndrome or hypertension Secondary to atherosclerosis and are now rarely due to syphilis

Answer 227

Strong genetic link- autosomal dominant trait in some families, Marfan's, Ehlen- Danlos syndrome, Loeys- dietz syndrome, mycotic aneurysm= endocarditis, aortic dissection in some cases Weight lifting, cocaine and amphetamine use= large rise in BP HTN, smoking, increasing age, smoking, bicuspid/ unicuspid aortic valves, atherosclerosis, COPD, renal failure, previous AA repair

Answer 228

Inflammation, proteolysis and reduced survival of smooth muscles cells in aortic wall, when aorta reaches crucial diameter= loses all distensibility Asymptomatic, may be diagnosed incidentally, pain in chest, neck, upper back, mid-back, epigastrium, aortic regurgitation, fever, symptoms due to compression of local structures, acute pain, collapse, shock and sudden death, cardiac tamponade, haemoptysis

Answer 229

Thoracic back pain, arterial ischaemia, collapse, MI CT/ MRI for TAA assessment, aortography- assessing position of key branches, transoesophageal ECHO for aortic dissection, US Immediate urgent surgery for ruptured, symptomatic= surgery, regular monitoring by CT/ MRI every 6 months, BP control with beta-blockers, smoking cessation, treat underlying cause

Answer 230

Begins with a tear in the intima (inner wall,) blood penetrates diseases medial layer and flows between aorta layers forcing layers apart Medical emergency, most common affecting aorta, affects men more Most common= 50-70 Classified according to timing of diagnosis from origin of symptoms- acute< 2 weeks, subacute- 2-8 weeks, chronic> 8 weeks Inherited, degenerative, atherosclerotic, inflammatory, trauma e.g. shearing stresses in RTA

Answer 231

Tear in intimal lining of aorta, column of blood under pressure enters aortic wall--> haematoma separating intimal from adventitia--> false lumen Extends for variable distance in either direction; anterograde= towards bifurcations, retrograde= towards aortic root Most common= within 2-3 cmm of aortic valve, distal to left SC artery in descending aorta

Answer 232

Sudden onset of severe and central chest pain--> back and down arms, pain= tearing in nature, HTN, pain is maximal from time of onset, may be shocked and have neurological symptoms, aortic regurgitation, coronary ischaemia, cardiac tamponade Acute KF, acute lower limb ischaemia, absent peripheral pulses

Answer 233

Acute coronary syndrome, MI, aortic regurgitation, MSK pain, pericarditis, cholecystitis, atherosclerotic embolism CXR= widened mediastinum, urgent CT scan, transoesophageal ECHO or MRI will confirm Urgent HTN meds to less than 120 mmHg- IV beta-blockers, adequate analgesia, surgery to replace aortic arch, endovascular intervention with stents, long-term follow-up with CT/ MRI

Answer 234

Acute circulatory failure with inadequate/ inappropriately distributed tissue perfusion- inadequate substrate--> generalised hypoxia and/ or inability of cells to utilise oxygen

Answer 235

Skin= pale, cold, sweaty and vasoconstricted Weak, rapid pulse Pulse pressure reduced- MAP may be maintained, reduced urine output, confusion, weakness, collapse, coma BP<90mmHg--> organ failure after recovery from acute event- may be linked to inflammatory response CRT- capillary refill time, not good if takes longer than 3 seconds to turn pink after 5 seconds compression= earliest and most accurate sign of shock

Answer 236

``` Hypovolaemic- low BV Cardiogenic- heart isn't pumping Distributive: septic, anaphylactic, neurogenic Anaemic- not enough O2 carrying capacity Cytotoxic- cells poisoned ```

Answer 237

Haemorrhagic shock Acute GI bleeding, trauma, peri/ post operative, splenic rupture Dehydration- diarrhoea and vomiting, burns- heat damage increases capillary permeability so plasma leaks, pancreatitis

Answer 238

Cardiac tamponade- blood in pericardial sack placing pressure on heart limiting CO Pulmonary embolism, acute MI, fluid overload, myocarditis

Answer 239

Distributive shock When systemic inflammatory response associated with infection, when sepsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation

Answer 240

Release of IgE= intense allergic reaction, massive release of histamine and other vasoactive mediators--> haemodynamic collapse Accompanied by breathlessness and wheeze due to bronchospasm

Answer 241

15% blood loss, pulse below 100bpm, BP normal, pulse pressure normal, resp rate; 14-20, urine output greater than 30ml/hr, slightly anxious 15-30% blood loss, pulse above 100bpm, BP normal due to autonomic response, pulse pressure decreased, resp rate; 20-30, urine output: 20-30ml/ hr, mental status: mildly anxious 30-40% blood loss, pulse above 120bpm, BP decreased, pulse pressure decreased, resp rate; 30-40, urine output: 5-15ml/hr, mental status= confused

Answer 242

Reduction in ventricular filling--> fall in BP and SV--> hypotension Reduced baroreceptors in aortic arch and carotid sinuses--> increased symptoms activity with NAD and adrenaline release Vasoconstriction with increased myocardial contractility and HR helps restore BP and CO Autotransfusion= reduced capillary BP--> greater fluid movement into vascular component from tissues Reduction in renal cortex perfusion--> renin released--> Na+ and H20 retention and thirst Cortisol= fluid retention, glucagon= raises blood sugar

Answer 243

Hypovalaemic= cold skin, drowsiness and confusion Increased sympathetic tone, tachycardia, sweating, BP may be maintained but later hypotension, bradycardia Cardiogenic= signs of myocardial failure, raised JVP, Gallop rhythm, basal crackles and pulmonary oedema Septic= pyrexia and rigors, nausea and vomiting, vasodilation with warm peripheries, bounding pulse Anaphylactic shock= signs of profound vasodilation, warm peripheries, low BP, tachycardia, bronchospasm, pulmonary oedema

Answer 244

Kidneys- acute tubular necrosis, lung- ARDs, heart- myocardial ischaemia and infarction, brain- confusion, irritability and coma ABC: A- airway (ensure patency,) B- breathing- give 100% O2 and correct immediately life threatening problems like: congestive cardiac failure, bronchospasm, tension pneumothorax C- circulation: establish secure IV access, give fluid quickly and blood if acute blood loss, ensure haemostats i.e. stop bleeding

Answer 245

Impaired oxygenation, bilateral pulmonary infiltrates, no cardiac failure, normal pulmonary arterial pressure (PAOP) Extra= shock of any cause, head injury, drug reaction, sepsis Pulm= pneumonia, chemical pneumonitis, smoke inhalation, near drowning

Answer 246

Alveolar capillary membrane injury results in leakage of fluid into alveolar spaces--> neutrophil invasion--> more neutrophils= exudative phase Eventually fibroblasts initiate healing= proliferative phase Make scar tissue= fibrotic phase--> stiff lungs and severe difficulty in ventilation and O2 blood perfusion Cyanosis, tachypnoea (quick breathing,) tachycardia and peripheral vasodilation

Answer 247

Age, sex, ethnicity, genetics Smoking, diet and alcohol, inactivity HTN, high lipids, diabetes, kidney disease, obesity Behaviour pattern, depression/ anxiety, work, social support

Answer 248

Odds given exposure compared to absence of exposure | Based on event frequency rather than cumulative total outcomes

Answer 249

``` Increases in poorer SE class apoB/ ApoA1 ratio, increased apoldprotein ratio= bad MI risk reduced with reduced risk factors ```

Answer 250

Population affected eliminated if exposure removed Reduced smoking, cholesterol, BP, deprivation, AMI treatments, secondary prevention, revascularisation, aspirin and HTN therapy Increasing obesity, diabetes and reduced exercise

Answer 251

4% 2% 1% 0.25%

Answer 252

Factors influencing psychological responses--> social environment and pathophysiological changes Cognitive, behavioural, emotional, social---> poverty, inequalities/ deprivation

Answer 253

Competitive, hostile, impatient Questionnaires, self-report, interview, speech, answer content, psychomotor Risk factor--> anger, annoyance, resentment, verbal/ physical aggression, evidence= ambiguous

Answer 254

``` Stronger for depression Links between depression and deprivation 3.4X MMPI, BDI and questionnaires 6- month follow-up More of a depressing behavioural pattern ```

Answer 255

MI associations and psychological demands, control and social support in relation to stress and adverse coronary health outcomes 11+ hours a day Quan and qual--> morbidity and mortality= coping with life events, motivation to carry out healthy behaviours

Cardiology Flashcards

(279 cards)