Cardiology

Question 1

What is acute coronary syndrome?

Answer 1

Umbrella term that describes ST elevation MI, unstable angina, non-ST elevation MI
All have same pathology - plaque rupture leads to thrombosis and inflammation
Rarely due to emboli, coronary spasm and necrosis

Question 2

What is an ST elevation MI?

Answer 2

Complete occlusion of a major coronary artery previously affected by atherosclerosis
Full thickness damage of heart muscle
Pathological Q waves some time after MI
ST segment is elevated
Tall T waves
May be new LBBB in larger MIs

Question 3

What is unstable angina?

Answer 3

Angina of recent onset
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

Question 4

What is a non-ST elevation MI?

Answer 4

Occurs by developing a complete occlusion of a minor vessel or partial occlusion of a major artery previously affected by atherosclerosis
Retrospective diagnosis made on troponin results
Partial thickness damage of heart muscle
Non-Q wave infarction - ST depression and/or T wave inversion
Thrombus occluding vessel, rise in serum troponin or creatinine kinase

Question 5

What are the 5 types of MI?

Answer 5

Type 1 - spontaneous MI with ischaemia due to a primary coronary event
Type 2 - MI secondary to ischaemia due to increase O2 demand or decreased supply such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension
Type 3,4,5 - MI due to sudden cardiac death, relatd to PCI and related to CABG respectively

Question 6

Name 5 factors that could increase your risk of having an ACS

Answer 6

Age
Male
Family history of IHD - MI in first degree relative below 55
Smoking
Hypertension
DM
Hyperlipidaemia
Obesity, sedentary lifestyle

Question 7

Name 5 causes of ACS

Answer 7

Atheroma/stenosis of coronary arteries impairing blood flow
Valvular disease
Aortic stenosis
Arrhythmia
Anaemia - loss O2 transported to heart muscles

Question 8

What occurs to the heart during an ACS attack?

Answer 8

Death of cardiac myocytes due to myocardial ischaemia
Rupture or erosion of fibrous cap of coronary artery plaque
Leads to platelet aggregation and adhesion, localised thrombus formation, vasoconstriction, and distal thrombus embolisation
Thrombus formation -> fibrotic plaque -> atherosclerotic plaque -> plaque rupture/fissure and thrombosis -> MI or ischaemic stroke or critical leg ischaemia or sudden CVS death
Unstable angina - partial occlusion, plaque has necrotic centre and ulcerated cap
MI - plaque has necrotic core but thrombus results in total occlusion

Question 9

How does unstable angina present?

Answer 9

Chest pain, new onset, at rest with crescendo pattern
Breathlessness
Pleuritic chest pain
Indigestion
Recent destabilisation of pre-existing angina with moderate or severe limitations of daily
exercise
Troponin normal, normal/undetermined ECG

Question 10

How does MI present?

Answer 10

Acute central chest pain lasting more than 20 minutes associated with sweating, nausea, dyspnoea, fatigue, SOB, palpitations
May present w/o chest pain in elderly or diabetics
Distress/anxiety
Pallor
Increased pulse and reduced BP
Reduced 4th heart sound
Signs of HF - increased JVP
Tachy/bradycardic
Peripheral oedema

Question 11

What could be a differential diagnosis of ACS?

Answer 11

Stable angina
Pericarditis
Myocarditis
Aortic dissection
Pulmonary embolism
Pleurisy 
Oesophageal reflux/spasm
Rib fracture, chest trauma, costochondritis
GORD
Anxiety/panic attack

Question 12

How is ACS treated?

Answer 12

Pain relief - GTN spray (angina), IV opioid 
Anti-emetics
Oxygen - if hypoxic
Antiplatelets - aspirin, P2Y12 inhibitors, glycoprotein IIb/IIIa agonists
Beta-blockers
Statins
ACE inhibitors
Coronary revascularisation
Risk factor modifications

Question 13

How does ischaemia present on an ECG?

Answer 13

ST depression and T wave flattening

Question 14

What investigations would you do on a patient with suspected unstable angina?

Answer 14

FBC - anaemia aggravates it
Cardiac enzymes - excludes infarction
ECG - when pain shows ST depression
Coronary angiography

Question 15

What is a myocardial infarction?

Answer 15

Plaque rupture leads to clot formation that occludes one of the coronary arteries causing myocardial cell death and inflammation

Question 16

What are the symptoms of an MI?

Answer 16

Acute central chest pain radiating to jaw or shoulder
Lasting > 20 mins
Nausea
SOB
Plapitations

Question 17

What are the signs of an MI?

Answer 17

Clammy and pale
4th heart sounds
Pansystolic murmur
May later develop peripheral oedema

Question 18

How would you manage an acute MI?

Answer 18

12 lead ECG
O2 if stats < 94%
IV access for bloods and enzymes
Brief history = RFs pulse, BP, JVP, murmurs, signs of congestive cardiac failure
300mg aspirin PO
Morphine 5-10mg IV and an anti-emetic
Refer for PCI or thrombolysis ASAP as long as not contraindicated
B-blocker IV and ACE-I if evidence of HF and patient normotensive

Question 19

What management would you put in place for a patient who had had an acute MI?

Answer 19

Aspirin 75mg OD, reduces risk of repetition
B-blocker - long term, if contraindicated then verapamil
ACE-I if in HF
Statin - reduced cholesterol post-MI beneficial
Address modificable risk factors
Return to work after 2 months
Encorage exercise and no air travel for 2 months

Question 20

What is an acute myocardial infarction?

Answer 20

Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombosis

Question 21

How common are MIs?

Answer 21

5/1000 per annum in UK of STEMI
STEMI most common medical emergency
Worse prognosis in elderly and those with left ventricular failure
Early mortality - 30% outside hospital, 15% in
Late mortality - 5-10% first year, 2-5% annually after

Question 22

What are the 2 types of MI?

Answer 22

STEMI - complete occlusion of major coronary artery previously affected by atherosclerosis
NSTEMI - complete occlusion on minor or partial occlusion of major coronary artery

Question 23

Name 5 risk factors for development of an MI

Answer 23

Increasing age
Male
History of premature coronary heart disease
Premature menopause
Diabetes
Smoking
Hypertension
Hyperlipidaemia
Obesity and sedentary lifestyle
Family history of IHD - MI in first degree relative below 55

Question 24

What pathology occurs in a STEMI?

Answer 24

Sub-endocardial myocardium initially affected but continued ischaemia, infarct zone extends through sub-endocardial myocardium, producing a transmural Q wave MI
Early reperfusion may salvage regions of myocardium - reducing future mortality and morbidity

Question 25

How does an NSTEMI present on an ECG?

Answer 25

Diagnosis made retrospectively after troponin results ST depression and T wave inversion Troponin I or T increased Myoglobin released

Question 26

Name 5 complications of an acute MI?

Answer 26

Sudden death - due to ventricular fibrillation Arrhythmias - electrical instability following infarction Pericarditis - transmural infarct resulting in inflammation of pericardium in STEMI Cardiac rupture Ventricular aneurysm - due to stretching of newly formed collagenous scar tissue

Question 27

What is angina?

Answer 27

Chest pain or discomfort as a result of reversible myocardial ischaemia Usually implies narrowing of one or more of the coronary arteries Tends to be exacerbated on exertion and relieved by rest

Question 28

How common is angina?

Answer 28

More common in men 1.7% deaths per year 7% CV events per year

Question 29

What are the different types of angina?

Answer 29

Stable angina - induced by effort, relieved by rest Unstable angina - crescendo angina, angina of recent onset (less than 24h) or deterioration in previously stable angina with symptoms frequently occurring at rest, occurs on minimal exertion or even at rest Prinzmetal's angina - caused by coronary artery spasm (rare)

Question 30

Give 5 risk factors for developing angina

Answer 30

``` Smoking Sedentary lifestyle Obesity Hypertension DM Family history Genetics Age Hypercholesterolaemia Depression/anxiety Stress - high demand/low control Hostile, competitive behaviour ```

Question 31

Give 5 possible causes of angina

Answer 31

Atheroma/stenosis of coronary arteries impairing blood flow (most common) Valvular disease Aortic stenosis Arrythmia Anaemia - less O2 transported to heart muscle

Question 32

What occurs during angina?

Answer 32

Mismatch between blood supply and metabolic demand Ischaemic metabolites including adenosine stimulate nerve endings producing pain Athersclerosis Plaque continues to encroach upon lumen - increased risk of haemorrhage or exposure to tissue HLA-DR antigens which might stimulate T cell accumulation Drives inflammation reaction against part of plaque contents Complications develop including ulceration, fissuring, calcifcation and aneurysm change

Question 33

How does Ohm's law link to angina?

Answer 33

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

Question 34

How does stable angina present?

Answer 34

Central chest tightness and heaviness Provoked by exertion, especially after meal or in the cold weather or by anger or excitement Relieved at rest or by GTN spray Pain may radiate to one or both arms, neck, jaw or teeth Dyspnoea, nausea, sweatiness, faintness, palpitations, syncope

Question 35

How is stable angina diagnosed?

Answer 35

12 lead ECG - often normal, possible ST depression, flat/inverted T waves, look for signs of past MI Treadmill test - ECG whilst patient running uphill on treadmill, monitor time can exercise for, ST depression, sign of late ischaemia, many patients unsuitable CT scan calcium storing - CT heart if atherosclerosis in arteries calcium will light up white, significant Ca indicates angina SPECT/myoview - radiolabelled tracer injected into patient, taken up into coronary arteries as good blood supply, areas of little blood supply will not light up, no light after exercise indicative of myocardial ischaemia Cardiac catheterisation Bloods - anaemia CXR - heart size, pulmonary vessels Angiogram - shows luminal narrowing

Question 36

Name 5 differential diagnoses of angina

Answer 36

``` Pericarditis/myocarditis PE Chest infection Dissection of aorta GORD Costochondritis ```

Question 37

How is stable angina treated?

Answer 37

Reassure Modify modifiable risk factors Treat underlying conditons Drugs - aspirin, statins, b-blockers, GTN spray, CCB, ivabradine Revascularisation - stents, only when patient not stable on drugs CABG, PCTA

Question 38

What is a coronary artery bypass graft?

Answer 38

``` Bypass surgeries Internal mammary artery for left side Saphenous vein for right side Good prognosis but longer recovery Not for frail ```

Question 39

What is PCTA?

Answer 39

Stenting or ballooning the narrowing, risk of restenosis or thrombosis, less invasive

Question 40

What is atherosclerosis?

Answer 40

Deposition of fatty deposits within inner walls of arteries Causes hardening of arteries Formation of focal elevated lesions in intima of large and medium sized arteries such as coronary arteries Fatty streaks present from around 10 years of age

Question 41

What coronary arteries are most commonly occluded by atherosclerosis?

Answer 41

LAD, circumflex and right coronary

Question 42

Name 5 risk factors for developing atherosclerosis?

Answer 42

``` Age - tends to be over 50s, progressive, chronic disease Tobacco smoking - free radicals damage endothelium High serum cholesterol Obesity - metabolic syndrome, increase systemic lipids Diabetes FHx Hypertension - shearing forces Sex Race Sedentary lifestyle Alcohol consumption Stress ```

Question 43

What is that pathophysiology of atherosclerosis?

Answer 43

Formed of lipid, necrotic core, connective tissue, fibrous cap Injury to epithelial cells leading to endothelial dysfunction Activation of endothelial cells - signals sent to circulating leukocytes which accumulate and migrate into vessel wall - monocytes and T helper cells Inflammation LDL deposited in intima, accumulates in arterial wall, undergoes oxidation and glycation Monocytes -> macrophages that then phagocytose LDLs and become foam cells Foam cells promote migration of SMC from media to intima and SMC proliferation Increase SMC proliferation leads to more collagen synthesis Foam cells die releasing contents driving growth of plaque Growth of plaque increases pressure causing plaque to rupture leading to coagulation cascade in blood vessel leading to thrombosis

Question 44

Name 5 conditions atherosclerosis can cause

Answer 44

MI Angina - stable and unstable Stroke Gangrene

Question 45

How is atherosclerosis treated?

Answer 45

``` Percutaneous coronary artery intervention (PCI) Toxal, sirolimus Aspirin - COX-1 inhibitor Clopidogrel/ticargrelor Statins ```

Question 46

How is an atherosclerotic plaque composed?

Answer 46

Central lipid core Cap of fibrous tissue Covered by arterial endothelium Cap - made of collagen (produced by SMCs), inflammatory cells reside here (macrophages, T lymphocytes, mast cells)

Question 47

What are foam cells?

Answer 47

Macrophages that have phagocytosed oxidised lipoproteins, also release chemokines to attract more macrophages, release IGF1 (growth factor) causing SMC to migrate to intima and to proliferation, proinflammatory cytokines, DNA

Question 48

Why is diabetes a risk factor for atherosclerosis?

Answer 48

Increased free radicals which increases oxidation of LDLs | Less NO so less relaxation of blood vessels

Question 49

What primary prevention methods could you use to prevent atherosclerosis?

Answer 49

Lifestyle changes - Decrease alcohol intake - Improve diet - less fats, salt and sugar - Increase amount of physical activity - Stop smoking - Try to lose some weight

Question 50

What secondary prevention methods could you used to prevent the progression of atherosclerosis?

Answer 50

``` Statin treatment Aspirin Anti-hypertensives Help with nicotine replacement therapies to help stop smoking Lifestyle advice Diabetic clinic and refer to dietician GTN spray Gym voucher Weight loss groups ```

Question 51

What is heart failure?

Answer 51

Inability of heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues despite the normal or increased cardiac filling pressures Impairment of heart contractility - LV systolic dysfunction most common State where heart unable to pump enough blood to satisfy the needs of metabolising tissues Symptomatic condition where breathlessness, fluid retention and fatiuge are associated with a cardiac abnormality that reduces CO

Question 52

What is heart failure with diastolic function?

Answer 52

Heart requires energy to relax, problem with not relaxing (hypertension) Preserved ejection fraction

Question 53

What is ischaemic HF?

Answer 53

Reduced blood supply to heart

Question 54

What is valvular HF?

Answer 54

Damage or defect in one of four valves

Question 55

What is myopathic HF?

Answer 55

Disease of heart muscle, makes it harder to pump blood around body

Question 56

What is hypertensive HF?

Answer 56

Due to overworking of heart

Question 57

What is cor pulmonale?

Answer 57

High BP in pulmonary arteries leading to right sided HF

Question 58

How common is HF?

Answer 58

``` Common 2-20% 2% NHS expenditure Disabiling Deadly 80% HF death within 5 years Treatable Median age 80 Majority chronic ```

Question 59

What are the different types of HF?

Answer 59

Actute HF = acute decompensated CHF - Generally under 70, male, LV ejection fraction < 40% Acute heart failure - 71-76, equally male and female, 50% LVEF > 40% Chronic HF

Question 60

What is the NYHA classification?

Answer 60

New York Heart Association classificaiton Class I - high risk of developing HF Class II - slight limitation (mild HF) Class III - marked limitation (moderate HF) Class IV - inability to carry out any physical activity without discomfort (severe HF)

Question 61

What are the stages of HF?

Answer 61

A - high risk of developing HF B - asymptomatic HF C - symptomatic HF D - end-stage HF

Question 62

Name 5 causes of HF

Answer 62

``` Hypertension Alcohol excess Cardiomyopathy Endocardial Pericardial MI Obesity Superimposed infection AF and arrhythmias Excess alcohol Endocrine NSAIDs ```

Question 63

Name 5 risk factors for developing HF

Answer 63

``` Hypertension Cardiomyopathy Hypertension Coronary artery disease Heart attack Diabetes Certain medications - NSAIDs Congenital heart defects Valvular heart disease Viruses Alcohol, smoking Obesity Irregular heart beats ```

Question 64

What are the symptoms of HF?

Answer 64

``` SOB Fatigue Ankle swelling Non-specific symptoms Cold peripheries ```

Question 65

What are the signs of HF?

Answer 65

Acute - pleural oedema Chronic - ankle oedema and abdominal ascites Crackles and tachycardia non-specific but sensitive Murmurs

Question 66

How is HF diagnosed?

Answer 66

CXR/blood tests - FBC, LFTs, U&Es, BNP, TFTs, B-type natriuretic peptide (raised in HF) Cardiac enzymes - creatinine kinase, troponin I and T ECG Echo (TTE) - done within 48 hours Myocardial perfusion imaging Raised NTproBNP - 72% chance of having HF CXR

Question 67

Name 5 differential diagnoses of HF

Answer 67

``` COPD PE Pneumothorax Anaphylaxis Asthma Pneumonia Foreign body obstruction ACS ```

Question 68

How is HF treated?

Answer 68

Loop diuretics - to treat severe oedema, symptomatic treatment of congestion ACE-I Aldosterone antagonist B-blockers ARB (angiotensin II receptor blockers) - instead of ACEI if contraindicated Calcium glycoside Surgery - mitral/aortic valve repair/replacement Defibrillator Palliative care 1st line - ACEI, low dose, slow uptitration 2nd line - aldsoterone antagonist Digoxin/ivabradine Lifestyle - education, obesity control, diet, smoking cessation, cardiac rehab

Question 69

Give 5 complications of HF

Answer 69

``` Renal dysfunction Rhythm disturbances Systemic thromboembolism DVT and PE LBBB and bradycardia Hepatic dysfunction Neurological and psychological complications ```

Question 70

How is CO calculated?

Answer 70

CO = HR x SV

Question 71

What is the difference between systolic HF and diastolic HF?

Answer 71

``` Sytolic - Failure to contract - EF < 40% - IHD, MI, CM Diastolic - Inability to relax and fill - EF > 50% - Constritive pericarditis, cardiac tamponade (accumulation of fluid in pericardial space), hypertension ```

Question 72

What is the difference between low output HF and high output HF?

Answer 72

Low - Decreased CO, fails to increase with exertion - Could be due to pump failure, excessive pre-load, chronic increased afterload High - Anaemia - Pregnancy - Hyperthyroidism

Question 73

What occurs during HF?

Answer 73

Once heart begins to fail compensatory changes occur | As HF progresses, these compensatory changes become overwhelmed (pathological)

Question 74

What compensatory changes occur in HF?

Answer 74

Sympathetic stimulation - increases afterload by causing peripheral vasoconstriction RAAS - salt and water retention, increases afterload and preload (increases volume and vasoconstriction) Cardiac changes - ventricular dilatation, myocyte hypertrophy Increased preload

Question 75

What are the symptoms of left-sided heart failure?

Answer 75

Exertional dyspnoea Fatigue Paroxysmal noturnal dyspnoea Nocturnal cough - pink, frothy sputum

Question 76

What are the signs of left-sided heart failure?

Answer 76

``` Cardiomegaly (displaced apex beat) 3rd and 4th heart sounds Crepitations in lung bases Weight loss Reduced BP Tachycardia Cool peripheries Heart murmur ```

Question 77

What are the symptoms of right sided HF?

Answer 77

Peripheral oedema Ascites Nausea Anorexia

Question 78

What are the signs of right sided HF?

Answer 78

``` Raised JVP Hepatomegaly Pitting oedema Ascites Weight gain (fluid) ```

Question 79

What can cause right sided HF?

Answer 79

LV failure Pulmonary stenosis Lung disease (cor pulmonale)

Question 80

What can be seen on a CXR in HF?

Answer 80

``` ABCDE Alveolar oedema Kerley B lines (interstital oedema) Cardiomegaly Dilated prominent upper lobe vessels Pleural Effusion ```

Question 81

How do you treat acute HF?

Answer 81

``` 100% oxygen Nitrates - GTN (dilate vessels) IV opiates IV furosemide (to reduce fluid overload) Inotropic drug - to increase contractility of dilated vessels ```

Question 82

How do you treat chronic HF?

Answer 82

ACEI/ARB (valsartan) B-blockers CCB and other vasodilators Diuretics and digoxin (furosemide)

Question 83

What is the difference between primary and secondary hypertension?

Answer 83

Primary - high BP that doesn't have a secondary cause Secondary - high BP that does have a secondary cause eg kidney disease, adrenal disease, thyroid problems, obstructive sleep apnoea, high aldosterone Most cases primary

Question 84

What is the epidemiology of hypertension?

Answer 84

``` Often symptomless - requires screening Major risk factor in CVD Remains under diagnosed, under treated and poorly controlled Prevalence in those older than 35 More common in men ```

Question 85

What is stage 1 hypertension?

Answer 85

More than or equal to 140/90mmHg clinic BP Daytime ABPM greater than or equal to 135/85mmHg Don't need to treat unless increased risk of CVS events due to diabetes/end-organ damage (stroke, TIA, MI) or high QRISK 30-40% increased risk of death per 10mmHg 5 year lower life expectancy on average if untreated

Question 86

What is stage 2 hypertension?

Answer 86

More than or equal to 160/100mmHg clinic BP | Daytime averge ABPM greater than or equal to 150/95mmHg

Question 87

What is stage 3 hypertension?

Answer 87

Clinic systolic BP greater than or equal to 180mmHg and/or diastolic greater than or equal to 110mmHg Start immediate anti-hypertensive drug treatment

Question 88

What are the possible causes of essential/primary hypertension?

Answer 88

``` Primary cause unknown Multifactorial involving Genetic susceptibility Excessive sympathetic nervous system activity Abnormalities of Na/K membrane transport High salt intake Abnormalities in RAAS ```

Question 89

What are the potential causes of secondary hypertension?

Answer 89

Renal disease Pregnancy Endocrine causes - Cushing's (corticosteroids), Conn's (aldosterone), phaemochromocytoma (catecholamines - vasoconstriction, increased cardiac contractility, increased in HR) Coarctation of aorta Drugs - corticosteroids, cyclosporin, erythropoietin, contraceptive pill, SSRIs, NSAIDs, immunosuppressives, cold cures Alcohol, amphetamines, ecstasy, cocaine

Question 90

Name 5 risk factors for developing hypertension

Answer 90

``` FHx Age Race - more common in Afro-Caribbean population Overweight/obese Sedentary lifestyle Smoking Too much salt Alcohol Diabetes Stress ```

Question 91

What vascular changes occur in hypertension?

Answer 91

Accelerates atherosclerosis due to shearing forces exerted on vessel walls Thickening of media of muscular arteries Smaller arteries and arterioles typically affected Results in endothelial cell dysfunction associated with impaired NO mediated dilatation and enhance secretion of vasoconstrictors including endothelins and prostaglandins

Question 92

What is hypertension a major risk factor for?

Answer 92

IHD Intracerebral haemorrhage Renal disease (cause and result) - kidney size often redued, small vessels show intimal thickening and medial hypertrophy, numbers of sclerotic glomeruli increased

Question 93

What is malignant hypertension?

Answer 93

Markedly raised diastolic pressure, usually over 120mmHg and progressive renal disease Rare Renal vascular changes prominent and usually evidence of acute haemorrhage and papilloedema Can occur in previously fit individuals, often black males in 30s-40s

Question 94

How does malignant hypertension present?

Answer 94

Proteinuria - if affecting kidneys | Haemorrhages/papilloedema (swelling of optic nerve) - worse prognosis than cancer

Question 95

How is malignant hypertension diagnosed?

Answer 95

Look for end-organ damage Urinalysis - albumin-creatinine ratio, protein, haematuria Blood tests - serum creatinine, eGFR, fasting glucose, cholesterol Fundoscopy/ophthalmoscopy ECG - LV hypertrophy, past MI Echo - LV hypertrophy 24h ABPM

Question 96

How is hypertension treated?

Answer 96

``` Treatment goal 140/90mmHg Change diet - high consumption of fruit/veg and low fat Regular physical exercise Reduce alcohol intake Reduce salt intake Lose weight if obese Stop smoking - increases CVS risk ACD pathway Lifelong treatment Check BP every 6 months Withhold certain drugs in pregnancy Withhold during surgery ```

Question 97

What is the ACD pathway?

Answer 97

For treating hypertension in under 55s or non-Afro-Caribbeans ACE-I eg ramipril (or ARB if ACE-I contraindicated) CCB Diuretics Beta-blockers if combination of all 3 don't work Also consider addition of spironolactone, high dose thiazide-like diuretic, alpha-blocker

Question 98

How do you treat hypertension in over 55s and Afro-Caribbeans?

Answer 98

CCB 1st line | Add ACEI/ARB after CCB not working

Question 99

What are the potential complications of hypertension?

Answer 99

``` Stroke MI HF Angina T2DM Vascular dementia ```

Question 100

What are the two types of aortic aneurysm?

Answer 100

Abdominal aortic aneurysm - aortic diameter exceeding 3cm | Thoracic abdominal diameter

Question 101

When is AAA more common?

Answer 101

More commonly occurs below renal arteries Incidence increases with age More common in men 5% of population over 60

Question 102

When is TAA more common?

Answer 102

Ascending thoraco-abdominal aneurysms occur more commonly in patients with Marfan's or hypertension Descending/arch TAAs secondary to atherosclerosis

Question 103

Name 5 risk factors for developing AAA?

Answer 103

``` Severe atherosclerotic damage FHx Smoking Male Increasing age Hypertension COPD Trauma Hyperlipidaemia ```

Question 104

Name 5 risk factors for developing TAA

Answer 104

``` Strong genetic link - autosomal dominant trait Certain connective tissue disorders - Marfan's, Ehler's-danlos, Loeys-dietz Mycotic aneurysm endocarditis Aortic dissection Weight lifting, cocaine, amphetamine use - rise in BP Hypertension Increasing age Smoking Bicuspid/unicuspid aortic valves Atherosclerosis COPD Renal failure Previous aortic aneurysm repair ```

Question 105

Why does an AAA occur?

Answer 105

Degradation of elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and SMC loss Dilatation affects all 3 layers of vascular tunic Doesn't then pseudoaneurysm

Question 106

Why does TAA occur?

Answer 106

Inflammation, proteolysis and reduced survival of SMCs in aortic wall Once aorta reaches crucial diameter, loses all distensibility so rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture

Question 107

How does an unruptured AAA present?

Answer 107

Often asymptomatic Picked up via routine examination Pain in abdomen, back, loin or groin Pulsatile abdominal swelling

Question 108

How does a ruputred AAA present?

Answer 108

``` More likely if hypertension, female, smoker, strong FHx Intermittent/continuous abdominal pain (radiating to back, iliac fossa/groin) Pulsatile abdominal swelling Collapse Hypotension Tachycardia Profound anaemia Sudden death ```

Question 109

How does a TAA present?

Answer 109

``` Most asymptomatic Diagnosed incidentally Pain in chest/neck/upper back/mid-back/epigastrium Aortic regurgitation Fever if infective cause Symptoms due to compression of local strucutures Acute pain Collapse, shock, sudden death Cardiac tamponade Haemoptysis ```

Question 110

Give 5 differential diagnoses of AAA

Answer 110

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

Question 111

Give 4 differential diagnoses of TAA

Answer 111

Thoracic back pain Arterial ischaemia Collapse MI

Question 112

How is an AAA diagnosed?

Answer 112

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

Question 113

How is TAA diagnosed?

Answer 113

CT/MRI Aortography - assess position of key branches relative to aneurysm Transoesophageal echo Ultrasound

Question 114

How is an AAA treated?

Answer 114

Small aneurysms below 5.5cm generally monitored Treat underlying causes Modify risk factors Smoking cessation Vigorous BP control Lowering of lipids in blood Surgery - if larger than 5.5cm and expanding yearly and symptomatic - open surgical repair/endovascular repair

Question 115

How is a TAA treated?

Answer 115

``` Immediate urgent surgery required for ruptured Symptomatic - surgery regardless of size Regular CT/MRI monitoring every 6 months Rigorous BP control with B-blockers Smoking cessation Treat underlying cause ```

Question 116

What is an aortic dissection?

Answer 116

Tear in aorta causing inner and middle layer of aortic wall to separate

Question 117

How common is aortic dissection?

Answer 117

Medical emergency that can lead to death Affects more men than women Most common between 50-70, rare below 40 Very rare in children

Question 118

How is aortic dissection classified?

Answer 118

Classified by timing of diagnosis from origin of symptoms Acute - less than 2 wks Subacute - 2-8 wks Chronic - more than 8 wks

Question 119

What are the potential causes of aortic dissection?

Answer 119

Inherited Degenerative eg cystic medial disease (degenerative disease of aortic wall) Atherosclerotic Inflammatory eg giant cell arteritis Trauma eg shearing stresses in RTA Connective tissue disorders eg Marfan's and Ehlers-Danlos

Question 120

What occurs when an aortic dissection happens?

Answer 120

Begins with tear in intima Blood under pressure then penetrates the diseased medial layer and flows between the layers of the aorta, forcing the layers apart resulting in dissection Blood forms a haematoma separating the intima from the adventitia and creating a false lumen False lumen extends for a variable distance in either direction - anterograde/retrograde

Question 121

Where is an aortic dissection most likely to happen?

Answer 121

Within 2-3cm of aortic valve | Distal to left subclavian artery in descending aorta

Question 122

How does an aortic dissection present?

Answer 122

Sudden onset of severe and central chest pain radiating to back and down arms - mimics an MI Pain often described as tearing in nature - may be migratory Hypertension Pain maximal from time of onset - unlike MI where pain gains in intensity Shock Neurological symptoms secondary to loss of blood supply to spinal cord 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

Question 123

Name 5 differential diagnoses for aortic dissection

Answer 123

ACS, MI, aortic regurgitation without dissection, MSK pain, pericarditis, cholecystitis, atherosclerotic embolism

Question 124

How is aortic dissection diagnosed?

Answer 124

CXR - widened mediastinum | Urgent CT, transoesophageal echo or MRI will confirm diagnosis

Question 125

How is aortic dissection treated?

Answer 125

``` If hypertension - urgent anti-hypertensive medication to reduce BP to less than 120mmHg - IV B-blockers or vasodilators Analgesia - morphine Surgery to replace aortic arch Endovascular intervention with stents Long term follow up with CT or MRI ```

Question 126

What is aortic stenosis?

Answer 126

Narrowing of aortic valve resulting in obstruction of left ventricular stroke volume leading to symptoms of chest pain, breathlessness, syncope and fatigue Normal aortic valve 3-4cm2 Symptoms occur when valve area 1/4 of normal

Question 127

What is aortic regurgitation?

Answer 127

Leakage of blood into LV from aorta during diastole due to ineffective coaptation of aortic cusps Can be associated with aortic stenosis

Question 128

What is the classification of aortic stenosis?

Answer 128

Supravalvular Subvalvular Valvular - most common

Question 129

What are the main causes of aortic stenosis?

Answer 129

Calcific aortic valvular - essentially calcification of aortic valve resulting in stenosis Calcification of congenital bicuspid aortic valve Rheumatic heart disease

Question 130

What are the main causes of aortic regurgitation?

Answer 130

Rheumatic fever Congenital bicuspid aortic valve IE

Question 131

What are the risk factors that could lead to aortic stenosis?

Answer 131

Congenital bicuspid aortic valve | Male

Question 132

What are the risk factors that could lead to aortic regurgitation?

Answer 132

Marfan's and Ehlers-Danlos syndrome SLE Aortic dilatation IE or aortic dissection

Question 133

What occurs during aortic stenosis?

Answer 133

Narrowing obstructed LV emptying and pressure gradient develops between LV and aorta resulting in increased afterload Increased LV pressure and compensatory LV hypertrophy Results in relative ischaemia of LV myocardium and consequent angina, arrhythmias and LV failure Obstruction to LV emptying relatively more severe on exercise When compensatory mechanisms exhausted LV function rapidly declines

Question 134

What occurs during aortic regurgitation?

Answer 134

Reflux of blood from aorta through aortic valve into LV during diastole LV dilation and hypertrophy to maintain total volume of blood ejected from LV Progressive dilation leads to HF Diastolic pressure falls due to regurgitation so coronary perfusion decreases Large LV size mechanically less efficient, demand for O2 greater and cardiac ischaemia develops Combined pressure and volume overload

Question 135

How does aortic stenosis present?

Answer 135

``` Syncope Angina HF Dyspnoea on exertion due to HF Sudden death Slow rising carotid pulse and decreased pulse amplitude Heart sounds - soft/absent S2, prominent S4 due to LV hypertrophy, ejection systolic murmur (crescendo-decresendo) Pulsus tardus - late Pulsus parvus - weak ```

Question 136

How does aortic regurgitation present?

Answer 136

``` Asymptomatic for years Exertional dyspnoea Orthopnoea - dyspnoea lying down Paroxysmal nocturnal dyspnoea Palpitations Angina Syncope Wide pulse pressure Apex beat displaced laterally Early diastolic murmur at L sternal border Systolic ejection murmur Collapsing water hammer pulse Quincke's sign - capillary pulsation in nail beds De Musset's sign - head nodding with heart beat Pistol shot femoral - sharp bang heard ```

Question 137

What could be a differential diagnosis for aortic stenosis?

Answer 137

Aortic regurgitation | Subacute bacterial endocarditis

Question 138

What could be a differential diagnosis for aortic regurgitation?

Answer 138

HF IE Mitral regurgitation

Question 139

How is aortic stenosis diagnosed?

Answer 139

Echo - LV size and function, doppler derived gradient and valve area, diagnostic ECG - LV hypertrophy, LA delay, LV strain pattern due to pressure overload - depressed ST segments and T wave inversion in leads orientated towards LV CXR - LV hypertrophy, calcified aortic valve

Question 140

How is aortic regurgitation diagnosed?

Answer 140

Echo - evaluation of aortic valve and aortic root, measurement of LV dimensions and function, cornerstone decision making and follow up evaluation CXR - enlarged cardiac silhouette and aortic root enlargement ECG - LV hypertrophy due to volume overload, tall R waves and deeply inverted T waves in left-sided chest leads, deep S waves in R side leads

Question 141

How is aortic stenosis treated?

Answer 141

Rigorous dental hygiene, IE prophylaxis in dental procedures Limited role for medication as mechanical problem Vasodilators contraindicated in severe as may trigger hypotension and syncope Surgical aortic valve replacement definitive treatment - any patients with severe, decreasing EF, undergoing CABG with moderate/severe Transcatheter aortic valve implantation (TAVI) - if not fit for surgery

Question 142

How is aortic regurgitation treated?

Answer 142

Vasodilators such as ACEi improve stroke volume and reduce regurgitation but only if symptomatic Serial echos to monitor progression Surgery for valve replacement before LV dysfunction

Question 143

What is atrial fibrillation?

Answer 143

Choatic irregular atrial rhythm at 300-600bpm, AV node responds intermittently, hence irregular ventricular rate Mechanically ineffective

Question 144

How common is AF?

Answer 144

Most common sustained cardiac arrhythmia Males more than females 5-15% patients over 75 Paroxysmal (self-terminating) or persistent

Question 145

How is AF classified?

Answer 145

Acute - onset within previous 48h Paroxysmal - stops spontaneously within 7 days Recurrent - 2 or more episodes Persistent - continuous for more than 7 days and not self-terminating Permanent

Question 146

What can cause AF?

Answer 146

``` Idiopathic Any condition resulting in raised arterial pressure, increased muscle mass, atrial fibrosis or inflammation and infiltration of atrium Hypertension HF Coronary artery disease Valvular heart disease especially mitral stenosis Cardiac surgery Cardiomyopathy Rheumatic heart disease Acute excess alcohol intoxication Thyrotoxicosis ```

Question 147

Name 5 risk factors for developing AF

Answer 147

``` Older than 60 Diabetes Hypertension Coronary artery disease Prior MI Structural heart disease ```

Question 148

What occurs during atrial fibrillation?

Answer 148

Continuous rapid activation of atria by multiple re-entry waves 300-600/min Rapidly depolarising automatic foci, located within pulmonary veins Atria respond electrically at this rate, no coordinated mechanical action, only proportion of impulses conducted to ventricles due to refractory period of AVN Ventricular response depends on rate and regularity of atrial activity, entry to AV node, balance between sympathetic and parasympathetic tone CO drops 10-20% as ventricles not primed reliably by atria Higher risk of thrombotic events, blood pools and remains still and clots HR - 120-180bpm

Question 149

How does AF present?

Answer 149

``` Asymptomatic Palpitations Dyspnoea or chest pains Fatigue HF No P waves Rapid and irregular QRS rhythm Apical pulse rate greater than radial rate 1st heart sound variable intensity Irregularly irregular pulse ```

Question 150

How is AF diagnosed?

Answer 150

ECG - absent P waves, irregular and rapid QRS complex

Question 151

What could be a differential diagnosis of AF?

Answer 151

Atrial flutter | Supraventricular tachyarrhythmias

Question 152

How if AF treated?

Answer 152

Acute management - when due to acute precipitating event, cardioversion (conversion to sinus rhythm electrically or pharamcologically), ventricular rate control with drugs that block AV node eg CCB, B-blocker, digoxin, anti-arrhythmic Long term and stable patient management - Rate control - AV nodal slowing agents plus oral coagulation - B-blockers/CCB/digoxin - Rhyhtm control - for younger, symptomatic and physically activate patients, cardioversion and amiodarone, anti-coagulation Calculate stroke risk - 5x risk of stroke (embolism due to thrombus formed in atrium)

Question 153

What is the target INR with treatment with warfarin?

Answer 153

2-3

Question 154

What is atrial flutter?

Answer 154

Organised atrial rhythm with an atrial rate typically between 250-350bpm

Question 155

How common is atrial flutter?

Answer 155

Often associated with atrial fibrillation and frequently require similar initial therapeutic approach Paroxysmal or persistent Much less common than atrial fibrillation

Question 156

Name 5 things that can cause atrial flutter

Answer 156

``` Idiopathic Coronary heart disease Obesity Hypertension HF COPD Pericarditis Acute excess alcohol intoxication ```

Question 157

What is a risk factor for developing atrial flutter?

Answer 157

Atrial fibrillation

Question 158

What occurs during atrial flutter?

Answer 158

Continuous rapid activation of atria by multiple re-entry wavelets Rapidly repolarising automatic foci, located within pulmonary veins Atria respond electrically at this rate, no co-ordinated mechanical action, only proportion on impulses conducted to ventricles Ventricular response depends on rate and regularity of atrial activity, entry to AV node, balance between sympathetic and parasympathetic tone CO drops 10-20% as ventricles not primed reliably by atria Higher risk of thrombotic events, blood pools and remains still and clots

Question 159

How does atrial flutter present?

Answer 159

``` Palpitations Breathlessness Chest pain Dizziness Syncope Fatigue Atrial rate - 300bpm Ventricular rate - 150bpm ```

Question 160

How is atrial flutter diagnosed?

Answer 160

ECG - definitive Regular saw-tooth like atrial flutter waves between QRS complexes due to continuous atrial depolarisation F waves may be unmasked by slowing AV conduction by carotid sinus massage or IV adenosine

Question 161

What could be a differential diagnosis of atrial flutter?

Answer 161

Atrial fibrillation | Supraventricular tachyarrhythmias

Question 162

How is atrial flutter treated?

Answer 162

Electrical cardioversion but anti-coagulated before Catheter ablation - create conduction block IV amiodarone to restore sinus rhythm and use beta-blocker to suppress further arrhythmias

Question 163

How is atrial flutter different to atrial fibrillation?

Answer 163

Atrial flutter - atria beat regularly but more often | Atrial fibrillation - atria beat irregularly and faster

Question 164

What is a cardiac arrhythmia?

Answer 164

Abnormality of cardiac rhythm

Question 165

Give 5 complications of cardiac arrhythmias

Answer 165

``` Sudden death Syncope HF Chest pain Dizziness Palpitations Asymptomatic ```

Question 166

What is bradycardia?

Answer 166

Heart rate slow < 60 bpm during day and < 50 bpm at night Usually asymptomatic unless heart very slow Normal in athletes due to increased vagal tone and thus parasympathetic activity

Question 167

What is tachycardia?

Answer 167

Heart rate fast > 100 bpm | More symptomatic when arrythmia fast and sustained

Question 168

How can tachycardias be further classified?

Answer 168

Supraventricular tachycardia - arise from atrium or AV junction Ventricular tachycardia - arise from ventricles

Question 169

What can cause bradycardia?

Answer 169

Extrinsic (treat underlying cause) - drug therapy BB digoxin, hypothyroidism, hypothermia, raised intracranial pressure Intrinsic (treat with atropine or temporary pacing in acute cases) - acute ischaemia, infarction of SAN, sick sinus syndrome

Question 170

What is long QT syndrome?

Answer 170

ECG where ventricular repolarisation (QT interval) is greatly prolonged

Question 171

What can cause long QT syndrome?

Answer 171

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, tricyclic antidepressants), bradycardia, acute MI, diabetes

Question 172

How does long QT syndrome present?

Answer 172

Syncope Palpitations Polymorphic ventricular tachycardia usually terminates spontaneously but may degenerate to ventricular fibrillation

Question 173

How do you treat long QT syndrome?

Answer 173

Treat underlying cause | If acquires give IV isoprenaline (contraindicated for congenital)

Question 174

What is mitral stenosis?

Answer 174

Obstruction of left ventricle inflow that prevents proper filling during diastole Normal valve area = 4-6cm2 Symptoms begin at less than 2cm2

Question 175

What is mitral regurgitation?

Answer 175

Backflow of blood from LV to LA during sytole | Mild physiological MR seen in 80% normal individuals

Question 176

What can cause mitral stenosis?

Answer 176

Rheumatic heart disease secondary to rheumatic fever (infection with group A beta-haemolytic streptococcus), inflammation leads to commisural fusion and reduction in mitral valve orifice area causing charateristic pattern seen on echo Progresses to valve thickening, cusp fusion, calcium deposition, severely narrowed valve orifice and progressive immobility of valve cusps Prevalence and incidence decreasing due to a reduction of rheumatic heart disease Also - IE, mitral annular clacification, congenital

Question 177

What can cause mitral regurgitation?

Answer 177

Abnormalities of valve leaflets, chordae tendinae, papillary muscles/LV Mitral valve prolapse Ischaemic mitral valve Rheumatic heart disease IE Papillary muscle dysfunction/rupture, dilated cardiomyopathy

Question 178

Name 2 risk factors for developing mitral valve stenosis

Answer 178

History of rheumatic fever | Untreated strep infection

Question 179

Name 5 risk factors for developing mitral regurgitation

Answer 179

``` Female Lower BMI Advanced age Renal dysfunction Prior MI ```

Question 180

What happens to the heart in mitral stenosis?

Answer 180

Thickening and immobility of valve leads to obstruction of blood flow from LA to LV LA pressure increases = LA hypertrophy and dilatation Pulmonary venous, arterial and right heart pressure increases Increase in pulmonary capillary pressure = pulmonary oedema Partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction Pulmonary hypertension leads to RV hypertrophy, dilatation and failure with subsequent tricuspid regurgitation

Question 181

What happens to the heart in mitral regurgitation?

Answer 181

Regurgitation into LA = LA dilatation but little increase in LA pressure in longstanding regurgitation Pure volume overload due to leakage of blood into LA during sytole LA enlargement, LV hypertrophy to maintain CO and increases contractility Progressive LA dilatation and RV dysfunction due to pulmonary hypertension Progressive LV volume overload leads to dilatation and progressive HF

Question 182

How does mitral stenosis present?

Answer 182

No symptoms until 2cm2 Progressive dyspnoea due to LA dilatation (pulmonary congestion) worse with exercise, fever, tachycardia, pregnancy Haemoptysis - rupture of bronchial vessels due to increases pulmonary pressure RHF - pulmonary hypertension, weakness, fatigue, abdominal and lower limb swelling AF - LA dilatation = palpitations Systemic emboli (AF) Mitral facies - bilateral, cyanotic or dusky pink discolouration over upper cheeks due to vasoconstriction in response to lowered CO Heart sounds - diastolic murmur, lower opening S1 snap, tapping non-displaced apex beat Chest pain Low volume pulse

Question 183

How does mitral regurgitation present?

Answer 183

Auscultation - soft S1 and pan systolic murmur at apex radiating to axilla, prominent S3, displaced hyperdynamic apex Exertional dyspnoea - pulmonary venous hypertension Fatigue and lethargy - reduced CO Increased SV felt as palpitation RHF symptoms and eventually congestive HF

Question 184

How is mitral stenosis diagnosed?

Answer 184

CXR - LA enlargement, pulmonary oedema/congestion, calcified mitral valve ECG - AF, LA enlargement Echo - assess mobility, gradient and area

Question 185

How is mitral regurgitation diagnosed?

Answer 185

ECG - LA englargement, AF, LV hypertrophy CXR - LA enlargement, central pulmonary artery enlargement, LV enlargement Echo - estimation of LA and V size and function, valve structure assessment, transoesophageal

Question 186

How is mitral stenosis treated?

Answer 186

``` Mechanical problem B-blocker control HR (if in AF) and prolongue disatole for improved diastolic filling Diuretics for fluid overload Anticoagulate - warfarin Percutaneous mitral balloon valvotomy Mitral valve replacement ```

Question 187

How is mitral regurgitation treated?

Answer 187

``` Vasodilators - ACEI HR control for AF - BBs, CCB, digoxin Anticoagulation for AF and flutter Diuretics for fluid over load Serial echo - Mild 2-3 years - Moderate 1-2 years - Severe 6-12 months Surgery for any symptomatic patient at rest or exercise for repair If asymptomatic EF less than 60%, new onset AF ```

Question 188

What is pericarditis?

Answer 188

Inflammatory pericardial syndrome with/without effusion

Question 189

What can cause pericarditis?

Answer 189

Viral (most) - enterovirus, herpesvirus, adenovirus, parvovirus B19, EBV, mumps, coxsackie B Bacterial - mycobacterium TB, pneumonia, rheumatic fever, staph, strep Autoimmune - Sjorgren's, RA, scleroderma, systemic vasculitis Neoplastic - secondary metastatic tumours, lymphoma Metabolic - uraemia, myoxedema Traumatic and iatrogenic - early onset (rare - direct/indirect injury), delayed onset (pericardial injury syndromes, iatrogenic trauma) Other - amyloidosis, aortic dissecion, pulmonary arterial hypertension, chronic HF, post-MI

Question 190

How does a major pericarditis present?

Answer 190

``` Fever > 38 Subacute onset Large pericardial effusion Cardiac tamponade Lack of response to aspirin/NSAIDs after at least 1 wk therapy ```

Question 191

What can cause a minor pericarditis?

Answer 191

Myopericarditis Immunosuppression Trauma Oral anticoagulation therapy

Question 192

How does pericarditis present?

Answer 192

Chest pain - severe, sharp pleuritic pain, rapid onset, left anterior chest/epigastrium, radiates to arm, relieved by sitting forwards Dyspnoea, cough, hiccups Viral prodrome, antecedent fever Skin rash, joint pain, eye Sx, weight loss

Question 193

How is pericarditis diagnosed?

Answer 193

``` Pericardial rub Sinus tachycardia Tachypnoea Fever Signs of effusion Beck's triad - hypotension, elevated jugualr veins, distant muffled heart sounds ECG Bloods - FBC, CRP, cardiac enzyme CXR Echo ```

Question 194

Name 5 differential diagnoses of pericarditis

Answer 194

``` Pneumonia Pleurisy PE Chostocondritis GORD Myocardial ischaemia/infarction Aortic dissection Pneumothorax Pancreatitis Peritonitis Herpes zoster - shingles ECG pericarditis Blood tests ```

Question 195

How is pericarditis treated?

Answer 195

Sedentary activity until resolution of symptoms and ESR/CRP - mainly for athletes 3 months NSAID (ibuprofen 600mg TDS 2 wks) or aspirin (750-1000mg BD 2wk) large dose for pain and inflammation Colchicine (0.5mg BD 3 wk) limited by nausea and diarrhoea, reduces recurrence Corticosteroids for symptomatic relief Manage complications

Question 196

What does a saddle-shaped ST and PR depression suggest?

Answer 196

Pericarditis

Question 197

What do tall tented T waves and pathological Q waves suggest?

Answer 197

Hyperkalaemia

Question 198

What does ST depression suggest?

Answer 198

Stable angina

Question 199

What do absent P waves suggest?

Answer 199

Atrial fibrillation

Question 200

What does an early diastolic heart murmur suggest?

Answer 200

Mitral stenosis

Question 201

What does and early-systolic click suggest?

Answer 201

Mechanical heart valve

Question 202

What does an ejection systolic crescendo-decrescendo murmur suggest?

Answer 202

Unstable angina

Question 203

What does an end-diastolic heart murmur suggest?

Answer 203

Aortic stenosis

Question 204

What does a pansystolic murmur suggest?

Answer 204

Mitral regurgitation

Question 205

What is peripheral vascular disease?

Answer 205

Partial blockage of leg or peripheral vessels vy an atherosclerotic plaque and/or resulting thrombus in insufficient perfusion of lower limb resulting in lower limb ischaemia Commonly caused by atherosclerosis and usually affects aorta-iliac and infra-inguinal arteries

Question 206

What is acute lower limb ischaemia?

Answer 206

May occur because of embolic or thrombotic disease | Rapid decrease in lower limb blood flow due to acute occlusion of peripheral artery

Question 207

What is thrombotic disease?

Answer 207

Chronic atherosclerotic stenosis in patient who has previously reported symptoms of claudication

Question 208

In whom is peripheral vascular disease more common?

Answer 208

Men

Question 209

Name 5 risk factors for developing peripheral vascular disease

Answer 209

``` Smoking Hypertension Diabetes Hypercholesterolaemia Physical inactivity Obesity ```

Question 210

What occurs in chronic lower limb ischaemia?

Answer 210

Always due to atherosclerosis of arteries distal to aortic arch Symptoms of ischaemia

Question 211

What occurs in mild ischaemia?

Answer 211

Stress induced by physiological malfunction Exercise induced angina Intermitted claudication - cramping pain induced by exercise Pain as a result of lactic acid produciton Leg pulses often absent Pain distal to site of atheroma

Question 212

What occurs in moderate ischaemia?

Answer 212

Structural and functional breakdown Ischaemic cardiac failure Critical limb ischaemia Vascular dementia

Question 213

What occurs in severe ischaemia?

Answer 213

Infarction | Gangrene

Question 214

How does thrombotic disease present?

Answer 214

``` 6Ps Pain Pallor Perishingly cold Pulselessness Paralysis Paraesthesia The more Ps, the more sudden and complete the ischaemia ```

Question 215

Name 3 differential diagnoses for PVD?

Answer 215

Osteoarthritis of hip/knee due to knee pain at rest Peripheral neuropathy - paraesthesia Arteritis

Question 216

How do you diagnose PVD?

Answer 216

Exclude arteritis - ESR/CRP raised in arteritis FBC - Hb to exclude anaemia/polycythaemia ECG - cardiac ischaemia Ankle/brachial pressure index 0.5-0.9 = intermittent claudication, less than 0.5 = critical leg ischaemia Colour duplex ultrasound MRICT

Question 217

How do you treat PVD?

Answer 217

Risk factor modification - smoking cessation. antiplatelets ect Revascularisation for critical ischaemia Bypass procedure Amputation for severe

Question 218

How do you treat acute ischaemia?

Answer 218

Surgical emergency - revascularisation within 4-6hrs to save limb

Question 219

What is intermittent claudication?

Answer 219

Ischaemic pain Tissue not dying just suffering Moderate/mild exercise, O2 debt resulting in lactic acid - pain

Question 220

What is critical ischaemia?

Answer 220

Tissue dying and suffering at rest Blood supply inadequate to allow basal metabolism No reserve available for increased demand Resting pain - typically nocturnal Gangrene/infection risk

Question 221

Give 2 signs/symptoms of critical ischaemia

Answer 221

Severe nocturnal pain in all toes of left foot only relieved by hanging foot over edge of bed (gravity for perfusion) Non-healing painful ulcer on big toe with no trauma

Question 222

Give 3 signs/symptoms of acute ischaemia

Answer 222

Acute MI Loss of use of R side of body Fast, irregular pulse

Question 223

What is shock?

Answer 223

Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised hypoxia and/or an inability of cells to utilise oxygen Low BP systolic < 90mmHg

Question 224

What can cause hypovolaemic shock?

Answer 224

Low blood volume

Question 225

What can cause cardiogenic shock?

Answer 225

Heart not pumping

Question 226

What can cause distributive shock?

Answer 226

Septic shock Anaphylactic shock Neurogenic shock

Question 227

What can cause anaemic shock?

Answer 227

Not enough O2 carring capacity

Question 228

What can cause cytotoxic shock?

Answer 228

Cell poisoned

Question 229

What is 'Tennis score'?

Answer 229

Score for staging of hypovolaemic shock Class 1 - 15% blood loss, pulse below 100bpm, normal BP, PP normal, resp rate 14-20, slightly anxious Class 2 - 15-30% blood loos, pulse greater than 100bpm (tachycardic), BP normal (autonomic response), PP decreased, resp rate 20-30, mildly anxious Class 3 - 30-40% blood loss, pulse above 120bpm, resp rate 30-40, PP decreased, confused

Question 230

What occurs in hypovolaemic shock?

Answer 230

Secondary to haemorrhagic shock Loss of blood due to GI bleed, trauma, peri/post operative, splenic rupture Loss of fluid - dehydration, burns, pancreatitis

Question 231

What can cause cardiogenic shock?

Answer 231

``` Cardiac tamponade - limits CO PE - flow of blood to lungs blocked Acute MI Fluid overload Myocarditis - inflammation of muscle ```

Question 232

What occurs in septic shock?

Answer 232

Shock when infection becomes out of control Disruptive shock Systemic inflammatory response associated with infection Sepsis complicated by persistent hypotension that is unresponsive to fluid resuscitation Acute vasodilation from inflammatory cytokines

Question 233

What occurs in anaphylactic shock?

Answer 233

Release of IgE due to allergic response Intense allergic reaction Massive release of histamine and other vasoactive mediators causing haemodynamic collapse Accompanied by breathlessness and wheeze due to bronchospasm

Question 234

What happens in the heart during shock?

Answer 234

Reduction in ventricular filling leading to a fall in BP and SV reducing hypotension Reduced stimulation of baroreceptors in aortic arch and carotid sinuses resulting in increases sympathetic activity with release of noradrenaline and adrenaline Vasoconstriction and increased myocardial contractility and HR to help restore BP and CO Reduction of perfusion of renal cortex stimulating juxtaglomerular apparatus to release renin Vasopressin released in response to decreased blood volume - aquaporin 2 channels increased water retention Cortisol - fluid retention Glucagon - raised blood sugar levels

Question 235

How does shock present?

Answer 235

``` Skin pale, cold, sweaty and vasoconstricted Pulse weak and rapid PP reduced Reduced urine output Confusion, weakness, collapse, coma ```

Question 236

How does hypovolaemic shock present?

Answer 236

``` Skin cold, pale, clammy, slate grey Drowsiness and confusion - inadequate tissue perfusion Increased sympathetic tone Tachycardia - narrow PP, weak pulse Sweating BP maintained but later hypotension ```

Question 237

How does cardiogenic shock present?

Answer 237

Signs of heart failure Raised JVP Gallop rhythm Basal crackles and pulmonary oedema

Question 238

How does septic shock present?

Answer 238

``` Pyrexia and rigors Nausea and vomiting Vasodilation with warm peripheries Bounding pulse Temp > 38 or < 36 Tachycardia > 90bpm RR > 20 breaths/min WBC > 12 x10^9/L or < 4x10^9/L ```

Question 239

How does anaphylactic shock present?

Answer 239

``` Signs of profound vasodilation Warm peripheries Low BP Tachycardia Bronchospasm Pulmonary oedema ```

Question 240

How is shock diagnosed?

Answer 240

Capillary refill time | More than 3 seconds to refill after 5 seconds compression = bad

Question 241

How is shock treated?

Answer 241

ABC B - 100% O2 and correct immediately if life threatening problems such as congestive HF, bronchospasm, tension pneumothorax C - establish IV access, fluids and blood if acute blood loss, ensure haemostasis In septic shock - take blood cultures before antibiotics

Question 242

What is a potential complication from shock? And where might be most affected?

Answer 242

Organ failure after recovery | Kidneys, lungs, heart, brain

Question 243

What can cause neurogenic shock?

Answer 243

Spinal cord injury Epidural Spinal anaesthesia

Question 244

What is the difference between sepsis, severe sepsis, septic shock and septicaemia?

Answer 244

Sepsis - life-threatening response to organisms that can lead to tissue damage, organ failure and death Severe sepsis - sepsis with sepsis-induced organ-dysfunction or tissue hypoperfusion Septic shock - when sepsis leads to a dangerously low BP and abnormalities in cellular metabolism Septicaemia - blood poisoning

Question 245

What is tachycardia?

Answer 245

HR > 100bpm | Physiological response to exercise and excitement

Question 246

What is AVNRT?

Answer 246

AV-nodal re-entrant tachycardia More common in women Strikes without obvious provocation Attack may stop spontaneously or continue indefinitely

Question 247

What is AVRT?

Answer 247

Atrioventricular re-entrant tachycardia

Question 248

What is supraventricular tachycardia?

Answer 248

Arises from atria/atrioventricular junction AVNRT and AVRT paroxysmal SVTs Presents between 12-30 Young patients with no/little structural heart disease AV node essential component

Question 249

What is ventricular tachycardia?

Answer 249

Pulse of more than 100bpm with at least 3 irregular heartbeats in a row Found in patients with structurally normal hearts - benign condition May lead to cardiomyopathy if untreated Inadequate filling of ventricles due to rapid ventricular beating and less time for filling Reduced CO and decrease in amount of oxygenated blood circulating

Question 250

What is sustained ventricular tachycardia?

Answer 250

Ventricular tachycardia for longer than 30 seconds

Question 251

Name 5 risk factors for AVNRT

Answer 251

``` Exertion Emotional stress Coffee Tea Alcohol ```

Question 252

What is the pathophysiology of AVNRT?

Answer 252

Short refractory period and slow conduction or long refractory period with fast conduction (more common) Atrial impulse occurs early slow pathway toakes over in propagating atrial impulses to ventricles Once propagates fast pathway finished refractory period and transmits pulses again Repeats - re-entrant loop at AV, sends signals through AV node at faster rate tan normal pacemaker so tachycardia Atria contract slowly in first cycle then fast in next

Question 253

What is the pathophysiology of AVRT?

Answer 253

Atrial activation after ventricle activation Prone to AF Wolff-Parkinson-White syndrome Premature beat from SAN -> AVN accessory pathway in refractory period, so travels down IV septum via purkinje cells until meets accessory pathway Out of refractory period conducts impulse back to atria - re-entry circuit leading to tachycardia

Question 254

What is the pathophysiology of Wolff-Parkinson-White syndrome?

Answer 254

Normal AV conduction but with accessory pathway SAN depolarises impulse travels to AVN via atria as well as accessory pathway Accessory pathway - quick conduction, abnormal depolarisation of ventricles Pre-excitation ECG - short PR interval, wide QRS

Question 255

How does AVNRT present?

Answer 255

Rapid regular palpitations with abrupt onset and sudden termination Chest pain and breathlessness Neck pulsations - atrial conductions against closed AV valves Polyuria

Question 256

How does AVRT present?

Answer 256

Palpitations Severe dizziness Dyspnoea Syncope

Question 257

How does VT present?

Answer 257

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

Question 258

How does SVT present?

Answer 258

``` Dizziness Syncope Hypotension Cardiac arrest Pulse rate between 120-220 bpm ```

Question 259

How is AVNRT diagnosed?

Answer 259

ECG - QRS complexes typical BBB, P waves either not visible or seen immediately before or after QRS complex due to simultaneous atrial or ventricular activation

Question 260

How is AVRT diagnosed?

Answer 260

ECG - short PR, wide QRS

Question 261

How is SVT diagnosed?

Answer 261

ECG - rapid ventricular rhythm, broad abnormal QRS complex greater than 0.14 seconds

Question 262

How are AVNRT and AVRT treated?

Answer 262

Emergency cardioversion if haemodynamically unstable Vagal manoeuvres if stable - Breath holding - Carotid massage - Valsalva manoeurvre IV adenosine Surgery - catheter ablation of accessory pathway in AVRT and modification of slow pathway AVNRT

Question 263

How is VT treated?

Answer 263

B-blockers to slow sinus rate

Question 264

How is SVT treated?

Answer 264

Haemodynamically unstable - emergency cardioversion | Stable - IV beta-blocker, IV amiodarone

Question 265

What can also cause tachycardia?

Answer 265

``` Anaemia Fever HF Thyrotoxicosis Acute PE Hypovolaemia Atropine ```

Question 266

What is a supraventricular tachycardia?

Answer 266

Any tachycardia that arises from atrium/atroventricular junction 4 main types - AF, atrial flutter, AVNRT and AVRT

Question 267

What is tetralogy of Fallot?

Answer 267

Most common form of congenital heart disease | Cyanotic cardiac disorder with highest survival to adulthood

Question 268

What occurs in tetralogy of Fallot?

Answer 268

Large, maligned ventricular septal defect Overriding aorta RV outflow obstruction RV hypertrophy Stenosis of RV outflow (pulmonary stenosis) leads to RV being at higher pressure than left Blue blood passes from RV to LV Patients are blue

Question 269

How does tetralogy of Fallot present?

Answer 269

``` Central cyanosis Low birth weight and growth Dyspnoea on exertion Delayed puberty Systolic ejection murmurs Toddler's may squat ```

Question 270

How is tetralogy of Fallot diagnosed?

Answer 270

CXR - boot shaped heart

Question 271

How it tetralogy of Fallot treated?

Answer 271

Full surgical treatment during first 2 yrs of life due to progressive cardiac debility and cerebral thrombosis risk Often get pulmonary valve regurgitation in adulthood and require redo surgery

Question 272

What is ventricular ectopic?

Answer 272

Premature ventricular contraction Most common post-MI arrhythmia Can also occur in healthy patients

Question 273

What is a risk factors for developing a ventricular ectopic?

Answer 273

MI

Question 274

What occurs during a ventricular ectopic?

Answer 274

Extra/missed/heavy beats LV dysfunction if ectopics are frequent Broad and bizzare QRS as arise from abnormal site in ventricular myocardium Complete compensatory pause as AV node or ventricle is refractory resulting in missed beat Can provoke ventricular fibrillation

Question 275

How does a ventricular ectopic present?

Answer 275

Uncomfortable especially when frequent Pulse irregular owing to premature beats Usually asymptomatic Can feel faint/dizzy

Question 276

How is a ventricular ectopic diagnosed?

Answer 276

ECG - widened QRS complex

Question 277

How is ventricular ectopic treated?

Answer 277

Reassure patient | Give beta-blockers if symptomatic - to slow down sinus rate

Question 278

What is an atrial-septal defect?

Answer 278

Abnormal connection between two atria | Patent foramen ovale

Question 279

How common is atrial-septal defects?

Answer 279

Often first diagnosed in adulthood 1/3 congenital heart disease More common in women

Question 280

What occurs in the heart in an atrial septal defect/

Answer 280

Slightly higher pressure in LA than RA L -> R shunt NOT blue Increased flow from R heart to lungs If untreated - R heart overload and dilation, R ventricle dilates to accommodate increased pulmonary flow - RV hypertrophy - Pulmonary hypertension - Eisenmenger's reaction - Increases risk of IE As heart compliance falls with age, the shunt increases Can lead to heart failure and shortness of breath by 40

Question 281

How does an atrial-septal defect present?

Answer 281

``` Dyspnoea Exercise intolerance Atrial arrhythmias from RA dilation Pulmonary flow murmur Fixed split second heart sound ```

Question 282

How in an atrial-septal defect diagnosed?

Answer 282

CXR - large pulmonary arteries, large heart ECG - right BBB due to RV hypertrophy ECHO - hypertrophy, dilation of right side of heart and pulmonary arteries

Question 283

How is an atrial-septal defect treated?

Answer 283

Surgical closure | Percutaneous (keyhole)

Question 284

What is the difference between primum ASD and secundum ASD?

Answer 284

Primum - earlier presentation, may involve AV vales | Secundum - may be asymptomatic until adulthood

Question 285

What is Eisenmenger's complex?

Answer 285

Shunt reversed due to development of pulmonary hypertension -> cyanosis and organ damage

Question 286

What is an atrio-ventricular septal defect?

Answer 286

Hole in very centre of heart Includes - ventricular septum, atrial septum, mitral and tricuspid valves Can be complete or partial Associated with Down's syndrome

Question 287

What occurs in the heart in atrio-ventricular septal defect?

Answer 287

Instead of 2 separate atrio-ventricular valves, just on big malformed one which usually leaks

Question 288

How does a complete atrio-ventricular septal defect present?

Answer 288

Breathlessness as neonate Poor weight gain and feeding Torrential pulmonary flow - Eisenmenger's resulting in cyanosis over time

Question 289

How does a partial atrio-ventricular defect present?

Answer 289

Can present late in adulthood | Presents similar to a ventricular/atrial defect - dyspnoea, tachycardia, exercise intolerance

Question 290

How is an atrio-ventricular defect treated?

Answer 290

Pulmonary artery banding if large defect in infancy - band reduces blood flow to lungs reducing pulmonary hypertension and Eisenmenger's syndrome Surgical repair challenging Partial defect left alone if no R heart dilatation

Question 291

What is a bicuspid aortic valve?

Answer 291

2 cusps aortic valve | Can go undetected, can be severely stenotic in infancy or childhood

Question 292

How common is a bicuspid aortic valve?

Answer 292

Most common form of cogenital heart disease More common in males Degenerate quicker than normal valves Regurgitant earlier than normal valves Associated with coarctation and dilation of ascending aorta May eventually develop aortic stenosis - requires replacement - IE

Question 293

What should patients with a bicuspid aortic valve avoid? Why?

Answer 293

Intense exercise may accelerate complications | Yearly ECHO on affected patients

Question 294

What does a bicuspid aortic valve lead to?

Answer 294

Aortic stenosis +/- aortic regurgitation | Can also pre-dispose individual to IE, aortic dilation, aortic dissection

Question 295

How is a bicuspid aortic valve treated?

Answer 295

Treat surgically with a valve replacement

Question 296

What is coarctation of the aorta?

Answer 296

Narrowing of aorta at or just distal to, to insertion of ductus arteriosis

Question 297

In whom is coarctation of the aorta more common in?

Answer 297

Men

Question 298

What happens in the heart with coarctation of the aorta?

Answer 298

Net narrowing of aorta just after arch, with excessive blood flow being diverted through carotid and subclavian vessels into systemic vascular shunts to supply to rest of the body Stronger perfusion to upper body compared to lower Associated with Turner's syndrome Resultant decreased renal perfusion, leads to systemic hypertension that persists even after surgical correction

Question 299

What can coarctation of aorta lead to?

Answer 299

Berry aneurysms and patent ductus arteriosis | Increased risk of IE

Question 300

How does coarctation of the aorta present?

Answer 300

Often asymptomatic for years Right arm hypertension Bruits over scapulae and back from collateral vessels Murmur Headahces and nose bleeds Hypertension in upper limbs Discreptant blood pressure in upper and lower body Long term - hypertension - early coronary artery disease, early strokes, sub-arachnoid haemorrhage Radio-femoral delay

Question 301

How is coarctation of the aorta diagnosed?

Answer 301

CXR - dilated aorta indented at site of coarctation ECG - LV hypertrophy CT - accurately demonstrate coarctation and quantify flow

Question 302

How is coarctation of the aorta treated?

Answer 302

Surgery Balloon dilatation and stening Risk of aneurysm and at site of repair

Question 303

What is the difference between severe and mild coarctation of aorta?

Answer 303

Severe - block aorta, collapse with heart failure | Mild - raised BP, systolic murmur (best heart over left scapula (scapula briut)

Question 304

What is infective endocarditis?

Answer 304

Infection of endocardium or vascular endothelium of heart | Subacute bacterial endocarditis

Question 305

Who is more at risk of IE?

Answer 305

Valves with congenital or acquired defects R sided IE more common with IV drug users Normal valves with virulent organisms such as streptococcus pneumoniae or S aureus Prosthetic valves or pacemakers

Question 306

Who is more at risk of IE?

Answer 306

``` More common in developing countries Disease of - elderly, those with prosthetic valves, young IV drug user, young with congenital heart disease More common in men Those with poor dental hygiene Dental treatment IV cannula Skin and soft tissue infection Cardiac surgery Pacemaker ```

Question 307

What pathogens cause IE?

Answer 307

S aureus P aeruginosa S viridans

Question 308

What is the pathophysiology of infective endocarditis?

Answer 308

Consequence of 2 factors - presence of organisms in bloodstream and abnormal cardiac endothelium facilitating adherence and growth Poor dental hygiene - bacteria from dental plaques get into blood, IVDU, soft tissue infections Damage endocardium promotes platelets and fibrin deposition allowing organism to adhere and grow, leading to infected vegetation Aortic and mitral valve most affected - IV drug users exception where R Virulent organisms destory valve they are on resulting in regurgitation and worsening heart failure

Question 309

How does infective endocarditis present?

Answer 309

New valve lesion/regurgitant murmur Embolic events unknown origin Sepsis of unknown origin Haematuria, glomerulonephritis, suspected renal infarction Fever plus risk factor Headache, fever, malaise, confusion, night sweats Finger clubbing S aureus - high fever, feel ill rapidly Valve dysfunction Splinter haemorrhages on nail beds of fingers Embolic skin lesions Osler nodes - tender nodules in digits Janeaway lesions - haemorrhages and nodules on fingers Roth spots - retinal haemorrhages with white or clear centres seen on fundoscopy Petechiae

Question 310

How is IE diagnosed?

Answer 310

Dukes criteria Blood cultures - 3 from different sites over 24 hrs, take before antibiotics started If not staph - penicillin - benzylpenicillin and gentamycin If staph - vancomycin and rifampicin Treat complications Surgery - remove valve and replace with prosthetic one - if infection can't be cured, remove infected devices, remove large vegetations before they embolise Good oral health for prevention

Question 311

What is patent arteriosus?

Answer 311

Where ductus arteriosus fails to close after birth

Question 312

What happens to the heart with a patent ductus arteriosus?

Answer 312

Ductus arteriosis persistent communication between the proximal left pulmonary artery and descending aorta Foeatal pulmonary vascular resistance high and right heart pressure exceeded that of left - flow from right to left atrium through foramen ovale and pulmonary artery to aorta via ductus arteriosus Some premature babies and cases of maternal rubella ductus arteriosus doesn't close Remains open then there is abnormal left-to-right sunt and eventually means that lung circulation overload with pulmonary hypertension and right-side cardiac failure subsequently Increases risk of IE

Question 313

How does patent ductus arteriosus present?

Answer 313

Continuous machinery murmurs Bounding pulse Large then large heart and breathlessness Eisenmenger's syndrome with differential cyanosis that is clubbed with blue toes but pink and not clubbed fingers Tachycardia

Question 314

How is patent ductus arteriosus diagnosed?

Answer 314

CXR - large shunt in aorta and pulmonary arterial system may be prominent ECG - demonstrate left arterial abnormality and LV hypertrophy ECHO - dilated LA and LV

Question 315

How is patent ductus arteriosus treated?

Answer 315

Can be surgically or percutaneously Low risk complications Venous approach may require and AV loop Indometacin can be given to stimulate duct closure

Question 316

What is the symptoms of peripheral arterial disease?

Answer 316

Cramping pain in calves, thighs and buttocks relieved by rest

Question 317

What are the signs of peripheral arterial disease?

Answer 317

Absent pulses Punched out ulcers Postural colour change (Bueger's test) 6Ps - pain, pallor, pulselessness, paraesthesis, paralysis, perishingly cold

Question 318

What investigations do you need to do in peripheral arterial disease?

Answer 318

Exclude DM, arteritis, anaemia, renal disease, lipids ABPI - normal is 1-1.2, PAD is 0.5-0.9 Colour duples USS - quick and non-ivasive, can show vessels and blood flow within them MRI/CT angiography - to identify stneoses and quality of vessels Blood tests - raised CK-MM, shows muscle damage

Question 319

How do you manage peripheral arterial disease?

Answer 319

Risk factors modification - quit smoking, treat HTN, lower cholesterol, improve DM control, lower fat diet Medications - antiplatelets, clopidogrel is recommended as 1st line Exercise programmes - reduce claudication by improving blood flow PTA or surgery if severely stenosed

Question 320

How common is structural/congenital heart defects?

Answer 320

1% of all lives births have some form of cardiac defect Vary from all minor to incompatable with life ex-utero Overall male predominance Atrial septal defect and patent dutus arteriosus occur more commonly females

Question 321

Name 5 risk factors for having a structural/congenital heart disease

Answer 321

``` Affected sibling Maternal prenatal rubella infection - persistent ductus arteriosus and pulmonary valvular and arterial stenosis Maternal alcohol misuse Single genes Drugs Diabetes of mother Genetic abnormalities ```

Question 322

When do you get finger clubbing?

Answer 322

Prolonged cyanosis

Question 323

What is a ventricular septal defect?

Answer 323

Abnormal connection between 2 ventricles Many close spontaneously during childhood 20% of congenital heart defects

Question 324

What occurs in the heart with a ventricular septal defect?

Answer 324

Higher pressure in LV then RV L to R shunt - not blue Increased blood through lungs

Question 325

How do large ventricular septal defects present?

Answer 325

``` Pulmonary hypertension Eisenmenger's complex Cyanosis Small, breathless, skinny baby Increased resp rate Tachycardia ```

Question 326

How do small ventricular septal defects present?

Answer 326

Large systolic murmur Thrill (buzzing sensation) Well grown

Question 327

What do large ventricular septal defects look and sound like? What do small ventricular septal defects look and sound like?

Answer 327

Large defects - CXR (big heart), murmurs vary in intensity (pansystolic), cause more problems in infancy Small defects - normal HR, normal size, asymptomatic, increase IE risk, louder murmur/thrill

Question 328

How are ventricular septal defects treated?

Answer 328

Medical initially since many will spontaneously close Surgical closure If small - no intervention required Prophylactic antibiotics Moderately size lesion - furosemide, ACEi

Question 329

What is pulmonary stenosis?

Answer 329

Narrowing of outflow of RV | Can be valvular, subvalvular or supravalvular

Question 330

How does severe pulmonary stenosis present?

Answer 330

``` RV failure as neonate Collapse Poor pulmonary blood flow RV hypertrophy Tricuspid regurgitation ```

Question 331

How do you treat pulmonary stenosis?

Answer 331

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

Question 332

What is cardiomyopathy?

Answer 332

Group of diseases of myocardium that affects the mechanical or electrical function of the heart

Question 333

What are the different types of cardiomyopathy?

Answer 333

Hypertrophic Dialted Restricted Arrhythmogenic right ventricular

Question 334

What is hypertrophic cardiomyopathy?

Answer 334

Ventricular hypertrophy/thickening of muscle Quite common, second most common cardiomyopathy 1/500 Autosomal dominant - familial May present at any age Most common cause of sudden cardiac death in the young

Question 335

What is dilated cardiomyopathy?

Answer 335

Dilated left ventricle which contracts poorly/has thin muscle Most common cardiomyopathy Autosomal dominant Can be caused by ischaemia, alcohol, thyroid disorder, familial/genetic

Question 336

What is restricted cardiomyopathy?

Answer 336

Rare | Caused by amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

Question 337

What is arrhythmogenic right ventricular cardiomyopathy?

Answer 337

Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium Familial form autosomal dominant but can be recessive

Question 338

What can increase your risk of having a cardiomyopathy?

Answer 338

Family history

Question 339

What occurs in hypertrophic cardiomyopathy?

Answer 339

Sarcomeric protein gene mutations eg troponin T and B-myosin All in absence of hypertension and valvular disease Hypertrophic, non-compliant ventricle impair diastolic filling resulting in reduced stroke volume and thus cardiac output Thick powerful heart is disarray of cardiac myocytes so conduction affected

Question 340

What occurs in dilated cardiomyopathy?

Answer 340

Caused by cytoskeletal gene mutations Left ventricle or right ventricle or all 4 chamber dilatation and thus dysfunction Poorly generated contractilve force leads to progressive dilatation of heart with some diffuse interstitial fibrosis

Question 341

What occurs in restrictive cardiomyopathy?

Answer 341

Normal or decreased volume of both ventricles with bilateral enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filling Restrictive physiology Poor dilation of heart restricts its ability to take on blood and pass it to the rest of the body Rigid myocardium restrict diastolic ventricular filling

Question 342

What occurs in arrhythmogenic RV cardiomyopathy?

Answer 342

Desmosome gene mutation RV replaced by fat and fibrous tissue Muscle dies and replaced by fat as part of inflammatory process

Question 343

How does hypertrophic cardiomyopathy present?

Answer 343

``` Hypertrophy of myocardium Sudden death Chest pain, angina, dyspnoea, dizziness, palpitations, syncope LV outflow obstruction Cardiac arrhythmia Ejection systolic murmur Jerky carotid pulse ```

Question 344

How does dilated cardiomyopathy present?

Answer 344

``` SOB and fatigue Heart failure Arrhythmias Thromboembolism Sudden death Increased JVP ```

Question 345

How does restricted cardiomyopathy present?

Answer 345

``` Dyspnoea Fatigue Embolic symptoms Elevated JVP with diastolic collapse and elevation of venous pressure with inspiration Hepatic enlargement Ascites Dependent oedema 3rd and 4th heart sounds ```

Question 346

How does arrhythmogenic cardiomyopathy present?

Answer 346

Cardiac cells held less together Arrhythmia most common Syncope R heart failure

Question 347

How is hypertrophic cardiomyopathy diagnosed?

Answer 347

ECG - abnormal, LV hypertrophy sings, progressive T wave inversion, deep Q waves Echo - ventricular hypertrophy, small left ventricle cavity Genetic analysis

Question 348

How is dilated cardiomyopathy diagnosed?

Answer 348

CXR - cardiac enlargement ECG - tachycardia, arrythmia, non-specific T wave changes Echo - dilated vessels

Question 349

How is restrictives cardiomyopathy diagnosed?

Answer 349

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

Question 350

How is arrhythmogenic cardiomyopathy diagnosed?

Answer 350

ECG - usually normal by may show T wave inversion ECHO - could be normal, advanced disease show right ventricular dilation Genetic testing

Question 351

How is hypertrophic cardiomyopathy treated?

Answer 351

Amiodarone - anti-arrythmatic medication CCB B-blocker

Question 352

How is dilated cardiomyopathy treated?

Answer 352

HF and AF treated in normal way

Question 353

How is restricted cardiomyopathy treated?

Answer 353

No specific treatment with poor prognosis Patients die within a year Cardiac transplantation

Question 354

How is arrhythmogenic cardiomyopathy treated?

Answer 354

B-blockers Amiodarone for symptomatic arrhythmias Occasionally cardiac transplant indicated

Question 355

What is heart block?

Answer 355

Block in either AV node/HIS bundle results in AV block | Block in lower conduction system produces bundle branch block

Question 356

What can cause heart block?

Answer 356

Coronary artery disease Cardiomyopathy Fibrosis of conducting tissues in elderly

Question 357

What are the different types of AV block?

Answer 357

First degree Second degree - type 1 and 2 Third degree

Question 358

What is first degree AV block?

Answer 358

'If the R is far from the P then you have first degree' Prolongation in PR interval greater than 0.22 seconds Every atrial depolarisation followed by conduction to ventricles but with delay Asymptomatic so no treatment

Question 359

What can cause first degree heart block?

Answer 359

Hypokalaemia, myocarditis, inferior MI, AVN blocking drugs eg b-blockers, CCB, digoxin

Question 360

What is second degree heart block?

Answer 360

'Longer longer longer drops, then you have a Wenkebach' (Mobitz I 'If some Ps don't get through, then you have a Mobitz II' When some P waves conduct, others don't

Question 361

What is a Mobitz I heart block?

Answer 361

PR interval before blocked P wave longer than after blocked P wave Light headedness, dizziness, syncope Doesn't require a pacemaker unless poorly tolerated Progressive PR interval prolongation until beat dropped, P wave fails to conduct then cycle restarts

Question 362

What can cause a Mobitz I heart block?

Answer 362

AVN blocking drugs | Inferior MI

Question 363

What is a Mobitz II heart block?

Answer 363

PR interval constant and QRS interval dropped Failure of conduction through His-Purkinje system SOB, postural hypotension, chest pain High risk of developing sudden complete AV block and pacemaker should be inserted

Question 364

What can cause a Mobitz II heart block?

Answer 364

``` Anterior MI Mitral valve surgery SLE Lyme disease Rheumatic fever ```

Question 365

What is a third degree heart block?

Answer 365

'Ps and Qs don't agree, the you have a third degree' Complete AV block Spontaneous escpae rhythm originated below block keeps ventricles going P waves completely independent of QRS

Question 366

What can cause third degree heart block?

Answer 366

Structural heart disease, IHD, hypertension, endocarditis, Lyme disease

Question 367

How is third degree heart block treated?

Answer 367

IV atropine or permanent pacemaker insertion

Question 368

What is bundle branch block?

Answer 368

Usually asymptomatic | Slightly widening of QRS complex - incomplete BBB

Question 369

What is RBBB?

Answer 369

R bundle no longer conducts, ventricles don't get impulses at same time QRS M wave in V1, W in V5 and V6 (MaRRoW)

Question 370

What can cause RBBB>

Answer 370

PE, IHD, A/VSD

Question 371

What is LBBB?

Answer 371

Late activation of LV Deep S wave leads I and V6, tall late R in V1 WiLLiaM - QRS in V1 and 2, M in V4-6

Question 372

What can cause LBBB?

Answer 372

IHD, aortic valve disease

Question 373

What are ACEI used for?

Answer 373

Hypertension, heart failure, diabetic nephropathy

Question 374

Name 3 examples of ACEi's

Answer 374

``` Ramipril Enalapril Perindopril Liniopril Trandolapril ```

Question 375

What are the main adverse effects of ACEI's?

Answer 375

Related to angiotensin II formation - hypotension, acute renal failure (release more renin causing BP to drop further), hyperkalaemia, teratogenic effects in pregnancy (angiotensin II important for baby development) Related to increased kinin production - dry chronic cough (ACE also breaks down bradykinin so inhibited = more bradykinin), rash, anaphylactiod reaction

Question 376

How do ACEi's work?

Answer 376

Block action of ACE enzyme in lungs preventing conversion of angiotensin I to angiotensin II

Question 377

What does angiotensin II do?

Answer 377

Potent vasocontrictor Stimulates aldosterone release Increases peripheral resistance

Question 378

What does aldosterone do?

Answer 378

Increases Na+ Therefore water retention Increased blood volume and BP

Question 379

What are ARBs used for?

Answer 379

Hypertension Diabetic neuropathy heart failure (when ACEI contraindicated)

Question 380

How do ARBs work?

Answer 380

Block AT-1 receptor that angiotensin II works at preventing the action of angiotensin II

Question 381

Name 3 examples of ARBs

Answer 381

``` Candesartan Losartan Valsartan irbesartan Telmisartan ```

Question 382

What are the main adverse effects of ARBs?

Answer 382

``` Symptomatic hypotension Hyperkalaemia Potential renal dysfunction Rash Angio-oedema Contraindicated in pregnancy Generally well tolerated ```

Question 383

What are CCBs used for?

Answer 383

Hypertension, IHD eg angina and arrhythmia

Question 384

Which CCBs have an effect on electrial conductivity?

Answer 384

Diltiazem and verapamil

Question 385

Name 3 examples of CCBs

Answer 385

``` Amlodipine Diltiazem Verapamil Nifedipine Felodipine Lacidipine ```

Question 386

How do L-type CCBs work?

Answer 386

Block calcium ion channels Dihydropyridine - nifedipine, amlodipine, felodipine, lacidipine preferentially affect vascular smooth muscle, peripheral arterial vasodilators Phenylalkylamines - verapamil main effect on heart, reduced HR and force of heart contraction Benzothiozepines - diltiazem, intermediate heart/peripheral vascular effects

Question 387

What are the main adverse effects of CCBS?

Answer 387

Due to peripheral vasodilation - flushing, headache, oedema, palpitations (decreased BP so body tried to correct by increasing HR) Due to -vely chronotropic effects - bradycardia, atrioventricular block, postural hypotension Due to -vely inotrophic effects - worsening of cardiac failure Verapamil causes constipation

Question 388

How to beta-adrenoceptor blockers work?

Answer 388

Block beta-adrenoceptors causing slowing down of heart rate

Question 389

What are b-blockers used for?

Answer 389

IHD - angina, heart failure, arrythmia, hypertension

Question 390

Name 3 examples of B-blockers

Answer 390

``` Bisoprolol Carbvedilol Propranolol Metoprolol Atenolol Nadolol ```

Question 391

Which B-blockers are more B-1 selective?

Answer 391

Metoprolol | Bisoprolol

Question 392

Which B-blocker is in the middle in terms of selectivity?

Answer 392

Atenolol

Question 393

Which B blocker is non-selective?

Answer 393

Propranolol Nadolol Carvedilol

Question 394

Why do you need to be careful with B-blocker selectivity?

Answer 394

Seletive B1 in asthma since non-selective used will also block B-2 resulting in airway constriction and thus worsening of asthma

Question 395

What are the main adverse effects of B-blockers?

Answer 395

``` Fatigue Headache Sleep disturbance/nightmares Bradycardia Hypotension Cold peripheries Erectile dysfunction Bronchospasm Worsening of asthma/COPD by bronchospasm PVD - claudication or raynauds HF is given standard dose acutely - give in small doses and increase slowly ```

Question 396

What are diuretics indicated for?

Answer 396

Hypertension and heart failure

Question 397

What are the different classes of diuretics and give an example for each?

Answer 397

Thiazides - cause Na+ and thus water loss in urine, act on distal tubule, less potent - bendroflumethiazide, hydrochlorothiazide, chlorothalidone Lopp diuretics - act on loop of Henle, more potent, furosemide (blocks Na/K/2Cl transporter), bumetanide Potassium-sparing diuretics - spironolactone, eplerenone Aldosterone antagonists

Question 398

What are the main adverse effects of diuretics?

Answer 398

``` Hypovolaemia (mainly loop) Hypotension (mainly loop) Hypokalaemia Hyponatraemia Hypomagnesaemia Hypocalcaemia Hyperuricaemia - gout Erectile dysfunction (thiazides) Impaired glucose tolerance (thiazides) ```

Question 399

Name an alpha-1 adrenoceptor blocker

Answer 399

Doxazosin

Question 400

Name a centrally acting anti-hypertensive

Answer 400

Moxonidine | Methyldopa - can be used in pregnancy

Question 401

Name a direct renin inhibitor

Answer 401

Aliskiren

Question 402

What are the cardiac natriuretic peptides?

Answer 402

ANP - atria | BNP - brain natriuretic peptide - ventricle

Question 403

When are the natriuretic peptides released?

Answer 403

When stretching of atrial or ventricular muscle cells Raised atrial or ventricular pressures Volume overload

Question 404

What are the main effects of the natriuretic peptides?

Answer 404

Increased renal excretion of sodium and water Relax vascular smooth muscle Increase vascular permeability Inhibit action/release of aldosterone, angiotensin II, endothelin and ADH In HF raised natriuetic peptdes in serum blood

Question 405

How do nitrates work?

Answer 405

Arterial and venous dilators Reduce pre-load and afterload Lower BP

Question 406

What are nitrates used for?

Answer 406

IHD (angina) and HF

Question 407

Give 3 examples of nitrates

Answer 407

Isosorbide mononitrate (long acting) GTN (glyceryl trinitrate) spray - commonly gives headache, potent vasodilator GTN infusion

Question 408

What are the main potential side effects of nitrates?

Answer 408

Headache GTN spray syncope Potential tolerance to drug

Question 409

How are antiarrhythmic drugs classified?

Answer 409

Vaughan Williams classification Classes 1 and 3 - rhythm control Classes 2 and 4 - rate control

Question 410

What are class I antiarrhythmic drugs?

Answer 410

Sodium channel blockers - flecainide

Question 411

What are class II antiarrhythmic drugs?

Answer 411

B-blockers

Question 412

What are class III antiarrhythmic drugs?

Answer 412

Prolong action potential | Amiodarone, sotalol

Question 413

What are class IV antiarrhythmic drugs?

Answer 413

CCBs - verapamil, diltiazem, amlodipine

Question 414

How does digoxin work?

Answer 414

Cardiac glycoside Inhibits Na/K pump - found everywhere Main effect on heart - bradycardia (increased vagal tone), increased ectopic activity, increased force of contraction by increased intracellular Ca2+ Slowing AV conduction Narrow therapeutic range otherwise side effects

Question 415

What are the potential side effects of digoxin?

Answer 415

Nausea, vomiting, diarrhoea, confusion

Question 416

When is digoxin used?

Answer 416

AF to reduce ventricular rate response | Severe HF as positive inotropic

Question 417

How does amiodarone work?

Answer 417

Blocks potassium rectifier current that are responsible for repolarisation of heart

Question 418

What are the potential adverse effects of amiodarone?

Answer 418

``` QT prolongation Polymorphic ventricular tachycardia Interstitial pneumonitis Abnormal liver function Hyperthyroidism/hypothyroidism Sun sensitivity Slate grey skin discolouration Optic neuropathy Multiple drug interacton Large volume of distribution ```