Cardio Flashcards

Question

'New widening QRS complexes and an RSR' pattern in V1'

Answer 1

right bundle branch block

Answer 2

hypokalaemia

Answer 3

IV loop diuretics e.g. furosemide or bumetanide oxygen can give nitrates if concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease with resp failure -> CPAP if hypotensive -> inotropic agents eg dobutamine mechanical circulatory assistance e.g. intra-aortic balloon counterpulsation or ventricular assist devices

Answer 4

heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock

Answer 5

massive PE + unstable -> alteplase otherwise -> DOAC (apixaban or rivaroxaban) if significant renal impairment -> LMWH, unfractionated heparin or LMWH followed by vitamin K antagonist eg warfarin if antiphospholipid syndrome -> LMWH followed by VKA

Answer 6

If provoked, stop after 3 months (3-6 months if cancer) if unprovoked, go up to 6 months

Answer 7

Regular assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block) loading dose of amiodarone followed by 24 hour infusion Irregular seek expert help. Possibilities include: atrial fibrillation with bundle branch block - the most likely cause in a stable patient atrial fibrillation with ventricular pre-excitation torsade de pointes

Answer 8

Regular vagal manoeuvres followed by IV adenosine if the above is unsuccessful consider a diagnosis of atrial flutter and control rate (e.g. beta-blockers) Irregular probable atrial fibrillation if onset < 48 hr consider electrical or chemical cardioversion rate control: beta-blockers are usually first-line unless there is a contraindication

Answer 9

hypotension hyponatraemia hypokalaemia, hypomagnesaemia hypochloraemic alkalosis ototoxicity hypocalcaemia renal impairment (from dehydration + direct toxic effect) hyperglycaemia (less common than with thiazides) gout

Answer 10

Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

Answer 11

Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

Answer 12

Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

Answer 13

>=135/85 - only if they are <80 and have one of: -target organ damage -established cardiovascular disease -renal disease -diabetes -10 year cardiovascular risk >=10% >=150/95 - always treat

Answer 14

lifestyle advice: -low salt diet <6g a day ideally 3g -reduce caffeine intake -stop smoking etc If <55 or T2DM start with ACEi or ARB then add CCB or thiazide like diuretic then add both then if K+<4.5 add low dose spironolactone, if >4.5 add alpha or beta blocker If >55 and no T2DM or african/afro caribbean start with CCB add ACEi/ARB or thiazide like diuretic then add both then if K+<4.5 add low dose spironolactone, if >4.5 add alpha or beta blocker

Answer 15

<80 clinic=140/90, ABPM/HBPM = 135/85 >80 clinic=150/90, ABPM/HBPM = 145/85

Answer 16

Used to determine the need to anticoagulate a patient in atrial fibrillation

Answer 17

Heart failure severity scale

Answer 18

Measure of disease activity in rheumatoid arthritis

Answer 19

A scoring system used to assess the severity of liver cirrhosis

Answer 20

Helps estimate the risk of a patient having a deep vein thrombosis

Answer 21

Mini-mental state examination - used to assess cognitive impairment

Answer 22

Hospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptoms

Answer 23

Patient Health Questionnaire - assesses severity of depression symptoms

Answer 24

Used as a screening tool and severity measure for generalised anxiety disorder

Answer 25

Used to screen for postnatal depression

Answer 26

Questionnaire used to detect eating disorders and aid treatment

Answer 27

Alcohol screening tool

Answer 28

Used to assess the prognosis of a patient with pneumonia

Answer 29

Used in the assessment of suspected obstructive sleep apnoea

Answer 30

International prostate symptom score

Answer 31

Indicates prognosis in prostate cancer

Answer 32

Assesses the health of a newborn immediately after birth

Answer 33

Used to help assess the whether induction of labour will be required

Answer 34

Assesses the risk of a patient developing a pressure sore

Answer 35

Risk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture

Answer 36

Acute pancreatitis scoring system

Answer 37

Malnutrition scoring system

Answer 38

syncope heart failure regular bradycardia (30-50 bpm) wide pulse pressure JVP: cannon waves in neck variable intensity of S1

Answer 39

PR interval > 0.2 seconds

Answer 40

type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Answer 41

there is no association between the P waves and QRS complexes

Answer 42

right coronary artery

Answer 43

If STEMI, aspirin 300mg percutaneous coronary intervention (PCI) if presenting <12 hours and can be given within 120 mins of the time that fibrinolysis can be given (basically you want to give PCI but would consider fibrinolysis if you cant give it in time. if fibrinolysis, also give antithrombin drug and do ECG after 60-90 mins to see if changes have resolved) PCI is given with drug eluting stent through radial access preferred over femoral During PCI, unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) is given second antiplatelet should be given with aspirin eg clopidogrel (if taking oral anticoagulant), prasugrel (if not taking oral anticoagulant)

Answer 44

aspirin + fondaparinux (if no immediate PCI) estimate 6 month mortality eg GRACE low risk (<3%) - ticagrelor or clopidogrel (if high risk of bleeding) higher risk (>3%) - Offer PCI (immediately if unstable otherwise within 72 hours) give prasugrel or ticagrelor give unfractionated heparin

Answer 45

IV atropine 5oomcg then use again up to 3mg then transcutaneous pacing then isoprenaline/adrenaline infusion then transvenous pacing with specialist

Answer 46

cough angioedema hyperkalaemia first dose hypokalaemia

Answer 47

pregnancy and breastfeeding - avoid renovascular disease - may result in renal impairment aortic stenosis - may result in hypotension hereditary of idiopathic angioedema

Answer 48

creatinine potassium

Answer 49

acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.

Answer 50

bilateral renal artery stenosis

Answer 51

aspirin + statin for every patient sublingual glyceryl trinitrate to abort angina attacks beta blocker/CCB first line - if CCB used solely, a rate limiting one such as verapamil or diltiazem should be used - if used in combo, use a longer acting dihydropyridine CCB eg amlodipine, modified release nifedipine if poor response, increase to max tolerated dose if still symptomatic after monotherapy add the other thing (ie CCB/beta blocker) then if still symptomatic add one of long acting nitrate ivabradine nicorandil ranozaline

Answer 52

use an assymetric dosing interval if using standard release isosorbide mononitrate which allows a daily nitrate free time of 10-14 hours

Answer 53

chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include a non-productive cough, dyspnoea and flu-like symptoms pericardial rub

Answer 54

widespread changes 'saddle shaped' ST elevation PR depression (most specific for acute pericarditis)

Answer 55

ECG transthoracic echocardiography bloods - inflam markers, troponin for possible myopericarditis

Answer 56

mainly outpatients unless fever >38 or high troponin treat underlying cause avoid physical activity combination of NSAID and colchicine used until symptoms go or inflam markers go down followed by tapering of dose

Answer 57

describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle leading to increased pressure within the left atrium, pulmonary vasculature and right side of the heart

Answer 58

rheumatic fever

Answer 59

dyspnoea - increased left atrial pressure -> pulmonary venous hypertension haemoptysis mid-late diastolic murmur (best heard on expiration) loud S1 opening snap - indicates mitral valve leaflets are still mobile low volume pulse malar flush atrial fib - secondary to increased left atrial pressure -> left atrial enlargement when severe - length of murmur increases, opening snap becomes closer to S2

Answer 60

possible left atrial enlargement

Answer 61

asymptomatic - monitor symptomatic - percutaneous mitral balloon valvotomy, mitral valve surgery associated aFib - require anticoagulation - usually warfarin

Answer 62

give up to 5 back blows give up to 5 abdominal thrusts (pressing forcibly into the upper abdominal area with an upward moment) keep continuing above cycle

Answer 63

you do it when you have a low suspicion (<15% probability) of PE but just want reassurance. All criteria must be negative to rule it out negative test reduces probability to <2%

Answer 64

you do it if PE is suspected >4 points means its likely, <4 means unlikely if likely arrange immediate CTPA if there is a delay in doing this then interim anticoagulation should be given (DOAC) if positive result, PE confirmed if negative, consider proximal leg vein US scan if DVT expected If unlikely arrange a D dimer test if positive arrange immediate CTPA (give anticoag if delay) If negative, PE is unlikely so stop anticoags and consider an alternative diagnosis

Answer 65

if there is renal impairment

Answer 66

S1Q3T3 - large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (RARE) RBBB and right axis deviation sinus tachycardia

Answer 67

usually normal but could see wedge shaped opacification

Answer 68

first line - N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test if high (>2000pg/ml) - arrange specialist assessment including transthoracic echo within 2 weeks if raised (400-2000 pg/ml) do the same within 6 weeks if levels are 'high' arrange specialist assessment (including transthoracic echocardiography) within 2 weeks if levels are 'raised' arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

Answer 69

use CHA2DS2-VASc score C Congestive heart failure 1 H Hypertension (or treated hypertension) 1 A2 Age >= 75 years 2 Age 65-74 years 1 D Diabetes 1 S2 Prior Stroke, TIA or thromboembolism 2 V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1 S Sex (female) 1 0 = no treatment 1 = males - consider treatment, females no >=2 = offer anticoag if no treatment, do transthoracic echo to exclude valvular heart disease Use DOACs, warfarin second line

Answer 70

a succession of rapid atrial depolarisation waves. 'sawtooth appearance'

Answer 71

radiofrequency ablation of the tricuspid valve isthmus is curative

Answer 72

Becks Triad: hypotension raised JVP muffled heart sounds dyspnoea tachycardia absent Y decent on JVP pulsus paradoxus - abnormally large drop in BP during inspiration electrical alternans on ECG

Answer 73

1) JVP CT = Absent Y descent CP = X + Y present 2) Pulsus paradoxus CT = Present CP = Absent 3) Kussmaul's sign CT = Rare CP = Present 4) Characteristic features CP = Pericardial calcification on CXR

Answer 74

urgent pericardiocentesis (pericardial needle aspiration)

Answer 75

systemic features of a vasculitis e.g. malaise, headache unequal blood pressure in the upper limbs carotid bruit and tenderness absent or weak peripheral pulses upper and lower limb claudication on exertion aortic regurgitation (around 20%)

Answer 76

renal artery stenosis

Answer 77

magnetic resonance angiography (MRA) or CT angiography (CTA)

Answer 78

bradycardia 'J' wave (Osborne waves) - small hump at the end of the QRS complex first degree heart block long QT interval atrial and ventricular arrhythmias

Answer 79

Young male smoker with symptoms similar to limb ischaemia - think Buerger's disease extremity ischaemia intermittent claudication ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon

Answer 80

Severe respiratory distress, tracheal deviation, unilateral absent breath sounds, and haemodynamic instability

Answer 81

U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT

Answer 82

leaking of aortic valve causing blood flow in reverse direction during ventricular diastole caused by aortic root disease or valve disease

Answer 83

infective endocarditis

Answer 84

rheumatic fever: the most common cause in the developing world calcific valve disease connective tissue diseases e.g. rheumatoid arthritis/SLE bicuspid aortic valve (affects both the valves and the aortic root)

Answer 85

bicuspid aortic valve (affects both the valves and the aortic root) spondylarthropathies (e.g. ankylosing spondylitis) hypertension syphilis Marfan's, Ehler-Danlos syndrome

Answer 86

aortic dissection

Answer 87

early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre collapsing pulse wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing) mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

Answer 88

echocardiography

Answer 89

medical management of associated heart failure surgery for symptomatic patients or asymptomatic with LV dysfunction

Answer 90

inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Clˆ’ symporter

Answer 91

dehydration postural hypotension hypokalaemia due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions hyponatraemia hypercalcaemia the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones gout impaired glucose tolerance impotence thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis

Answer 92

if patient is unstable electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.

Answer 93

synchronised to R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced

Answer 94

<48 hours - patient is heparinised, put on lifelong anticoagulants if they have risk factors otherwise can be cardioverted using electrical 'DC' cardioversion or pharmacologically with amiodarone >48 hours - anticoags given for >3 weeks prior to cardioversion or do a transoesophageal echo to exclude left atrial appendage thrombus then anticoags for >4 weeks

Answer 95

often asymptomatic exertional dyspnoea angina syncope typically following exercise due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure jerky pulse, large 'a' waves, double apex beat systolic murmurs ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation

Answer 96

MR SAM ASH mitral regurgitation (MR) systolic anterior motion (SAM) of the anterior mitral valve leaflet asymmetric hypertrophy (ASH)

Answer 97

left ventricular hypertrophy non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen deep Q waves atrial fibrillation may occasionally be seen

Answer 98

mitral valve (tricuspid in IVDU)

Answer 99

1 - staph aureus 2 - staph viridans 3 - staph epidermidis

Answer 100

Removing the patient from the cold environment and removing any wet/cold clothing, Warming the body with blankets Securing the airway and monitoring breathing, If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient's body

Answer 101

rapid rewarming

Answer 102

dyspnoea right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent pericardial knock - loud S3 Kussmaul's sign is positive

Answer 103

pericardial calcification

Answer 104

Recent sore throat, rash, arthritis, murmur → ?rheumatic fever erythema marginatum Sydenham's chorea: this is often a late feature polyarthritis carditis and valvulitis (eg, pancarditis) subcutaneous nodules

Answer 105

oral penicillin V NSAIDs

Answer 106

xray to exclude pneumothorax, pleural effusion etc

Answer 107

Amiodarone Beta-blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis*

Answer 108

nitrates ACE-inhibitors inotropes

Answer 109

infancy: heart failure adult: hypertension radio-femoral delay mid systolic murmur, maximal over the back apical click from the aortic valve notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Answer 110

12 lead ecg tfts for thyrotoxicosis u's and e's - potassium FBC then you want to capture episodic arrythmias using Holter monitoring if no abnormality found, can do external loop recorder or implantable loop recorder

Answer 111

A: Adenosine is most commonly used to terminate supraventricular tachycardias.

Answer 112

A: The effects of adenosine are enhanced by dipyridamole (antiplatelet agent).

Answer 113

A: The effects of adenosine are blocked by theophyllines.

Answer 114

A: Adenosine should be avoided in asthmatics due to possible bronchospasm.

Answer 115

A: Adenosine causes transient heart block in the AV node by acting as an agonist of the A1 receptor in the atrioventricular node, inhibiting adenylyl cyclase, reducing cAMP, and causing hyperpolarization by increasing outward potassium flux.

Answer 116

A: The half-life of adenosine is about 8-10 seconds.

Answer 117

A: Adenosine should ideally be infused via a large-calibre cannula due to its short half-life.

Answer 118

A: Adverse effects of adenosine include chest pain, bronchospasm, transient flushing, and enhanced conduction down accessory pathways, resulting in increased ventricular rate (e.g., WPW syndrome).

Answer 119

A: Aspirin (lifelong) & ticagrelor (12 months).

Answer 120

A: Clopidogrel (lifelong).

Answer 121

A: Aspirin (lifelong) & prasugrel or ticagrelor (12 months).

Answer 122

A: Clopidogrel (lifelong).

Answer 123

A: Clopidogrel (lifelong).

Answer 124

A: Aspirin (lifelong) & dipyridamole (lifelong).

Answer 125

A: Clopidogrel (lifelong).

Answer 126

A: Aspirin (lifelong) & dipyridamole (lifelong).

Answer 127

A: Clopidogrel (lifelong).

Answer 128

A: Aspirin (lifelong).

Answer 129

A: Aortic dissection is a rare but serious cause of chest pain characterized by a tear in the tunica intima of the wall of the aorta.

Answer 130

A: Hypertension.

Answer 131

A: Hypertension, trauma, bicuspid aortic valve, Marfan's syndrome, Ehlers-Danlos syndrome, Turner's syndrome, Noonan's syndrome, pregnancy, and syphilis.

Answer 132

A: The pain is typically severe, sharp, and tearing in nature, and it is maximal at onset.

Answer 133

A: Chest pain is more common in type A dissection, while upper back pain is more common in type B dissection.

Answer 134

A: Pulse deficit (weak or absent carotid, brachial, or femoral pulse) and variation in systolic blood pressure (>20 mmHg) between the arms.

Answer 135

A: Coronary arteries can lead to angina, spinal arteries can lead to paraplegia, and distal aorta can lead to limb ischemia.

Answer 136

A: The majority of patients have no or non-specific ECG changes, but a minority may show ST-segment elevation in the inferior leads.

Answer 137

A: Type A involves the ascending aorta (2/3 of cases) and Type B involves the descending aorta, distal to the left subclavian origin (1/3 of cases).

Answer 138

A: Type I originates in the ascending aorta and propagates to at least the aortic arch and possibly beyond; Type II originates in and is confined to the ascending aorta; Type III originates in the descending aorta, rarely extends proximally but will extend distally.

Answer 139

A: Widened mediastinum.

Answer 140

A: CT angiography of the chest, abdomen, and pelvis.

Answer 141

A: A false lumen.

Answer 142

A: Transoesophageal echocardiography (TOE).

Answer 143

A: Surgical management, with blood pressure controlled to a target systolic of 100-120 mmHg while awaiting intervention.

Answer 144

A: Conservative management, including bed rest and blood pressure reduction with IV labetalol.

Answer 145

A: Aortic incompetence/regurgitation and myocardial infarction (often with an inferior pattern due to right coronary involvement).

Answer 146

A: Unequal arm pulses and blood pressure, stroke, and renal failure.

Answer 147

A: Chest pain, dyspnoea, syncope/presyncope (e.g., exertional dizziness), and murmur.

Answer 148

A: An ejection systolic murmur (ESM) that classically radiates to the carotids and is decreased following the Valsalva manoeuvre.

Answer 149

A: Narrow pulse pressure, slow rising pulse, delayed ESM, soft/absent S2, S4, thrill, duration of murmur, and left ventricular hypertrophy or failure.

Answer 150

A: Degenerative calcification.

Answer 151

A: Bicuspid aortic valve.

Answer 152

A: If symptomatic or if asymptomatic with a valvular gradient > 40 mmHg and features such as left ventricular systolic dysfunction.

Answer 153

A: Surgical AVR, transcatheter AVR (TAVR), and balloon valvuloplasty.

Answer 154

A: Surgical AVR.

Answer 155

A: For patients with a high operative risk.

Answer 156

A: ARVC, also known as arrhythmogenic right ventricular dysplasia (ARVD), is an inherited cardiovascular disease that may present with syncope or sudden cardiac death and is the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.

Answer 157

A: Autosomal dominant with variable expression.

Answer 158

A: It is replaced by fatty and fibrofatty tissue.

Answer 159

A: Palpitations, syncope, and sudden cardiac death.

Answer 160

A: T wave inversion in V1-3 and an epsilon wave, which is a terminal notch in the QRS complex, found in about 50% of those with ARVC.

Answer 161

A: Subtle changes in the early stages, but may show an enlarged, hypokinetic right ventricle with a thin free wall.

Answer 162

A: Drugs (sotalol), catheter ablation to prevent ventricular tachycardia, and implantable cardioverter-defibrillator (ICD).

Answer 163

A: Atrial fibrillation (AF).

Answer 164

A: Reducing the increased risk of stroke.

Answer 165

A: First detected episode, paroxysmal, persistent, or permanent.

Answer 166

A: AF that terminates spontaneously and lasts less than 7 days (typically < 24 hours).

Answer 167

A: AF that is not self-terminating and usually lasts greater than 7 days.

Answer 168

A: Continuous AF that cannot be cardioverted or when attempts to do so are deemed inappropriate.

Answer 169

A: Palpitations, dyspnoea, and chest pain.

Answer 170

A: ECG (electrocardiogram).

Answer 171

A: Rate/rhythm control and reducing stroke risk.

Answer 172

A: To slow the rate down to avoid negative effects on cardiac function while accepting an irregular pulse.

Answer 173

A: To get the patient back into, and maintain, normal sinus rhythm through cardioversion.

Answer 174

A: A beta-blocker or a rate-limiting calcium channel blocker (e.g., diltiazem).

Answer 175

A: Any 2 of the following: a beta-blocker, diltiazem, digoxin.

Answer 176

A: For specific situations such as coexistent heart failure, first onset AF, or if there is an obvious reversible cause, and if symptoms/heart rate fail to settle with rate control.

Answer 177

A: To reduce the risk of embolism leading to stroke when the patient switches from AF to sinus rhythm.

Answer 178

A: No treatment.

Answer 179

A: Males: Consider anticoagulation; Females: No treatment (score of 1 is due to gender).

Answer 180

A: Offer anticoagulation.

Answer 181

A: Warfarin and novel oral anticoagulants (NOACs).

Answer 182

Answer: A transthoracic echocardiogram should be done to exclude valvular heart disease, which is an absolute indication for anticoagulation.

Answer 183

Answer: The ORBIT scoring system is used to assess bleeding risk before starting anticoagulation.

Answer 184

0-2: Low risk (2.4 bleeds per 100 patient-years) 3: Medium risk (4.7 bleeds per 100 patient-years) 4-7: High risk (8.1 bleeds per 100 patient-years)

Answer 185

Answer: Apixaban, dabigatran, edoxaban, and rivaroxaban.

Answer 186

Answer: Direct oral anticoagulants (DOACs) are the first-line choice because they do not require regular INR monitoring.

Answer 187

Answer: Warfarin is used second-line, in patients where a DOAC is contraindicated or not tolerated.

Answer 188

Answer: No, aspirin is not recommended for reducing stroke risk in patients with AF.

Answer 189

Answer: Atrial fibrillation is a key risk factor for ischemic stroke, and recognizing and treating it is essential for reducing the risk of future strokes.

Answer 190

Answer: A haemorrhage should be excluded before starting any anticoagulation or antiplatelet therapy.

Answer 191

Answer: NICE recommends warfarin or a direct thrombin or factor Xa inhibitor for long-term stroke prevention.

Answer 192

Answer: Anticoagulation for AF should start immediately following a TIA, once imaging has excluded haemorrhage.

Answer 193

Answer: Anticoagulation therapy should be started 2 weeks after an acute stroke, in the absence of haemorrhage. Antiplatelet therapy should be given in the intervening period.

Answer 194

Answer: Anticoagulation should be delayed if imaging shows a very large cerebral infarction.

Answer 195

Answer: The patient should be electrically cardioverted, following the peri-arrest tachycardia guidelines.

Answer 196

If AF has been present for < 48 hours: rate or rhythm control is used. If AF has been present for ≥ 48 hours or the onset is uncertain: rate control is used. For long-term rhythm control, delay cardioversion until the patient has been maintained on therapeutic anticoagulation for at least 3 weeks.

Answer 197

Answer: Rate control should be the first-line strategy except for patients who: Have a reversible cause for AF. Have heart failure primarily caused by AF. Have new-onset AF (< 48 hours). Have atrial flutter suitable for ablation to restore sinus rhythm. For whom rhythm control is more appropriate based on clinical judgement.

Answer 198

Beta-blockers (contraindicated in asthma). Calcium channel blockers. Digoxin (not first-line due to less effectiveness during exercise, only used if physical exercise is minimal or other options are contraindicated, may be used if heart failure is coexistent).

Answer 199

Beta-blockers. Dronedarone (second-line after cardioversion). Amiodarone (especially if coexisting heart failure).

Answer 200

Answer: Catheter ablation is recommended for patients who have not responded to or wish to avoid antiarrhythmic medications.

Answer 201

Answer: The goal is to ablate the faulty electrical pathways causing AF, typically due to aberrant electrical activity between the pulmonary veins and left atrium.

Answer 202

Answer: The procedure is performed percutaneously, typically via the groin. Radiofrequency (using heat) or cryotherapy can be used to ablate the tissue.

Answer 203

Answer: Anticoagulation should be used 4 weeks before and during the procedure.

Answer 204

Answer: No, catheter ablation controls the rhythm but does not reduce stroke risk. Patients still require anticoagulation according to their CHA2DS2-VASc score.

Answer 205

If CHA2DS2-VASc score = 0: 2 months of anticoagulation is recommended. If CHA2DS2-VASc score > 1: long-term anticoagulation is recommended.

Answer 206

Cardiac tamponade. Stroke. Pulmonary vein stenosis.

Answer 207

Answer: Atrial myxoma.

Answer 208

Answer: 75% occur in the left atrium, most commonly attached to the fossa ovalis.

Answer 209

Answer: Atrial myxomas are more common in females.

Answer 210

Dyspnoea Fatigue Weight loss Pyrexia of unknown origin Clubbing

Answer 211

Answer: Emboli.

Answer 212

Answer: Atrial fibrillation.

Answer 213

Answer: A mid-diastolic murmur, often described as a "tumour plop."

Answer 214

Answer: A pedunculated, heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum.

Answer 215

Answer: Atrial septal defects (ASDs).

Answer 216

Answer: Ostium secundum and ostium primum.

Answer 217

Answer: Ostium secundum.

Answer 218

Answer: An ejection systolic murmur with fixed splitting of S2.

Answer 219

Answer: Embolism may pass from the venous system to the left side of the heart, potentially causing a stroke.

Answer 220

Answer: Heart block is impaired electrical conduction between the atria and ventricles.

Answer 221

Answer: There are three types: First-degree heart block Second-degree heart block (Type 1 and Type 2) Third-degree (complete) heart block

Answer 222

Answer: The PR interval is > 0.2 seconds. Asymptomatic first-degree heart block is relatively common and does not need treatment.

Answer 223

Answer: There is progressive prolongation of the PR interval until a dropped beat occurs.

Answer 224

Answer: The PR interval is constant, but the P wave is often not followed by a QRS complex.

Answer 225

Answer: There is no association between the P waves and QRS complexes.

Answer 226

Answer: BNP is a hormone produced mainly by the left ventricular myocardium in response to strain.

Answer 227

Answer: BNP levels can be raised in heart failure, myocardial ischaemia, valvular disease, and chronic kidney disease (due to reduced excretion).

Answer 228

Answer: Treatment with ACE inhibitors, angiotensin-2 receptor blockers, and diuretics can reduce BNP levels.

Answer 229

Vasodilation Diuretic and natriuretic effects Suppression of sympathetic tone and the renin-angiotensin-aldosterone system

Answer 230

Answer: BNP is used in diagnosing patients with acute dyspnoea. A BNP level < 100 pg/ml makes heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis.

Answer 231

Answer: Beta-blockers are mainly used in the management of cardiovascular disorders.

Answer 232

Angina Post-myocardial infarction Heart failure (certain beta-blockers improve symptoms and mortality) Arrhythmias (used for rate control in atrial fibrillation) Hypertension (role has diminished in recent years) Thyrotoxicosis Migraine prophylaxis Anxiety

Answer 233

Bronchospasm Cold peripheries Fatigue Sleep disturbances (including nightmares) Erectile dysfunction

Answer 234

Uncontrolled heart failure Asthma Sick sinus syndrome Concurrent use with verapamil (may precipitate severe bradycardia)

Answer 235

Answer: Brugada syndrome is an inherited cardiovascular disease that may present with sudden cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of 1:5,000-10,000. It is more common in Asians.

Answer 236

Convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave Partial right bundle branch block

Answer 237

Answer: The ECG changes may become more apparent following the administration of flecainide or ajmaline, which is the investigation of choice in suspected cases of Brugada syndrome.

Answer 238

Answer: Implantable cardioverter-defibrillator (ICD).

Answer 239

Answer: Smoking.

Answer 240

Extremity ischaemia Intermittent claudication Ischaemic ulcers Superficial thrombophlebitis Raynaud's phenomenon

Answer 241

Answer: Myoglobin.

Answer 242

Answer: CK-MB, because it returns to normal after 2-3 days, whereas troponin T remains elevated for up to 10 days.

Answer 243

Answer: Troponin T and Troponin I.

Answer 244

Leading cause of sudden cardiac death in young athletes Usually due to a mutation in the gene encoding β-myosin heavy chain protein Common cause of sudden death Echo findings include mitral regurgitation (MR), systolic anterior motion (SAM) of the anterior mitral valve, and asymmetric septal hypertrophy

Answer 245

Right ventricular myocardium is replaced by fatty and fibrofatty tissue Around 50% of patients have a mutation in genes encoding components of desmosome ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARVD, described as a terminal notch in the QRS complex

Answer 246

Alcohol Coxsackie B virus Wet beriberi Doxorubicin

Answer 247

Amyloidosis Post-radiotherapy Loeffler's endocarditis

Answer 248

Answer: Peripartum cardiomyopathy typically develops between the last month of pregnancy and 5 months post-partum. It is more common in older women, those with greater parity, and multiple gestations.

Answer 249

Also known as "stress-induced cardiomyopathy" Often occurs after a stressful event, such as finding out a family member has died Patients develop chest pain and features of heart failure Characterized by transient, apical ballooning of the myocardium Treatment is supportive

Answer 250

Heavy, central chest pain that may radiate to the neck and left arm Nausea, sweating Elderly patients and diabetics may experience no pain Risk factors for cardiovascular disease

Answer 251

History of asthma, Marfan's syndrome, etc. Sudden dyspnoea and pleuritic chest pain

Answer 252

Sudden dyspnoea and pleuritic chest pain Calf pain/swelling Current combined pill user, malignancy

Answer 253

Sharp pain relieved by sitting forwards May be pleuritic in nature

Answer 254

'Tearing' chest pain radiating through to the back Unequal upper limb blood pressure

Answer 255

Burning retrosternal pain Other possible symptoms include regurgitation and dysphagia

Answer 256

Pain often worse on movement or palpation May be precipitated by trauma or coughing

Answer 257

Answer: Pain often precedes the rash

Answer 258

Occurs when blood tracks into the medial layer of the aorta, creating a false lumen Presents with tearing intrascapular pain Most common in Afro-Caribbean males aged 50-70 Diagnosis suggested by widened mediastinum on chest X-ray and confirmed by CT angiography Type A lesions (proximal) treated surgically, Type B lesions (distal) managed non-operatively

Answer 259

Sudden onset of chest pain, haemoptysis, hypoxia, and small pleural effusions Underlying deep vein thrombosis ECG findings: S waves in lead I, Q waves in lead III, and inverted T waves in lead III Diagnosed by CT pulmonary angiography Treatment with anticoagulation, possible thrombolysis in severe cases

Answer 260

Sudden onset of central, crushing chest pain radiating to the neck and left arm Atypical presentations in the elderly and diabetics Diagnosed by dynamic ECG changes and cardiac enzyme changes Treatment with oral antiplatelet agents, primary coronary angioplasty, and/or thrombolysis

Answer 261

Sudden onset of epigastric abdominal pain, followed by generalized abdominal pain Erect chest X-ray may show free intra-abdominal air Treatment usually with laparotomy, small defects excised and overlaid with an omental patch, larger defects managed with partial gastrectomy

Answer 262

Spontaneous rupture of the oesophagus due to severe vomiting Presents with sudden onset of severe chest pain Severe sepsis secondary to mediastinitis Diagnosed by CT contrast swallow Treatment with thoracotomy and lavage; primary repair if < 12 hours, T-tube for controlled fistula if > 12 hours

Answer 263

Answer: Loop diuretics, such as furosemide, are important for managing fluid overload but have not demonstrated a long-term reduction in mortality.

Answer 264

Answer: The first-line treatment is both an ACE inhibitor and a beta-blocker. Generally, one drug should be started at a time, based on clinical judgement.

Answer 265

Answer: Bisoprolol, carvedilol, and nebivolol are the beta-blockers licensed to treat heart failure in the UK.

Answer 266

Answer: No, ACE inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction.

Answer 267

Answer: The standard second-line treatment is an aldosterone antagonist (mineralocorticoid receptor antagonist), such as spironolactone or eplerenone.

Answer 268

Answer: Potassium levels should be monitored due to the risk of hyperkalaemia.

Answer 269

Answer: SGLT-2 inhibitors, such as canagliflozin, dapagliflozin, and empagliflozin, reduce glucose reabsorption and increase urinary glucose excretion. They have been shown to reduce hospitalisation and cardiovascular death in heart failure with reduced ejection fraction.

Answer 270

Answer: Third-line treatment should be initiated by a specialist.

Answer 271

Answer: Ivabradine is indicated if the patient is in sinus rhythm with a heart rate > 75/min and has a left ventricular ejection fraction < 35%.

Answer 272

Answer: Digoxin has not been proven to reduce mortality in heart failure but may improve symptoms due to its inotropic properties. It is strongly indicated if there is coexistent atrial fibrillation.

Answer 273

Answer: Indications include a widened QRS complex on ECG, such as left bundle branch block.

Answer 274

Answer: Patients should be offered an annual influenza vaccine and a one-off pneumococcal vaccine. Adults with asplenia, splenic dysfunction, or chronic kidney disease need a booster every 5 years.

Answer 275

Answer: The NYHA classification is used to classify the severity of heart failure.

Answer 276

No symptoms No limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea, or palpitations

Answer 277

Mild symptoms Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations, or dyspnoea

Answer 278

Moderate symptoms Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

Answer 279

Severe symptoms Unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

Answer 280

Answer: Dilated cardiomyopathy (DCM), accounting for 90% of cases.

Answer 281

Answer: Idiopathic.

Answer 282

Answer: Myocarditis (e.g., Coxsackie B, HIV, diphtheria, Chagas disease).

Answer 283

Answer: Ischaemic heart disease, peripartum, hypertension, iatrogenic (e.g., doxorubicin), substance abuse (e.g., alcohol, cocaine), inherited conditions (e.g., Duchenne muscular dystrophy), infiltrative diseases (e.g., haemochromatosis, sarcoidosis), nutritional deficiencies (e.g., wet beriberi).

Answer 284

Answer: The majority of defects are inherited in an autosomal dominant fashion, although other patterns of inheritance are seen.

Answer 285

Answer: Dilated heart leading to predominantly systolic dysfunction. All four chambers are dilated, but the left ventricle is more so than the right ventricle. Eccentric hypertrophy (sarcomeres added in series) is seen.

Answer 286

Answer: Classic findings of heart failure, systolic murmur (due to stretching of the valves resulting in mitral and tricuspid regurgitation), S3 heart sound, 'balloon' appearance of the heart on chest x-ray.

Answer 287

Answer: The sum of the S wave in V1 and the R wave in V5 or V6 exceeds 40 mm.

Answer 288

Answer: The criterion for right ventricular hypertrophy is not explicitly given in the prompt. However, RVH can often be identified by a right axis deviation and tall R waves in the right precordial leads (V1 and V2).

Answer 289

Bifid P wave in lead II with a duration > 120 ms. In V1, the P wave has a negative terminal portion.

Answer 290

Tall P waves in both lead II and V1 which exceed 0.25 mV.

Answer 291

Left anterior hemiblock Left bundle branch block Inferior myocardial infarction Wolff-Parkinson-White syndrome with a right-sided accessory pathway Hyperkalaemia Congenital conditions such as ostium primum ASD and tricuspid atresia Minor LAD in obese people

Answer 292

Right ventricular hypertrophy Left posterior hemiblock Lateral myocardial infarction Chronic lung disease leading to cor pulmonale Pulmonary embolism Ostium secundum ASD Wolff-Parkinson-White syndrome with a left-sided accessory pathway Normal in infants under 1 year old Minor RAD in tall people

Answer 293

Down-sloping ST depression (referred to as 'reverse tick' or 'scooped out') Flattened or inverted T waves Shortened QT interval Arrhythmias such as AV block and bradycardia

Answer 294

ECG Features: WiLLiaM Pattern: 'W' shape in lead V1 'M' shape in lead V6 Wide QRS complexes (>120 ms) Causes: Myocardial infarction: Diagnosing MI in patients with existing LBBB is challenging. The Sgarbossa criteria can help diagnose MI in the presence of LBBB. Hypertension Aortic stenosis Cardiomyopathy Rare causes: Idiopathic fibrosis Digoxin toxicity Hyperkalaemia Note: New LBBB is always considered pathological and warrants further investigation.

Answer 295

ECG Changes Considered Normal Variants in Athletes: Sinus Bradycardia A slower than normal heart rate (<60 bpm) due to high vagal tone. Junctional Rhythm Rhythm originating from the atrioventricular (AV) junction, often seen during rest or sleep. First-Degree Heart Block Prolonged PR interval (>200 ms) but with each P wave followed by a QRS complex. Mobitz Type 1 (Wenckebach Phenomenon) Progressive prolongation of the PR interval until a P wave is not followed by a QRS complex (dropped beat).

Answer 296

Causes of a Prolonged PR Interval: Idiopathic Ischaemic heart disease Digoxin toxicity Hypokalaemia (more common association) Rheumatic fever Aortic root pathology (e.g., abscess secondary to endocarditis) Lyme disease Sarcoidosis Myotonic dystrophy Athletes (as a normal variant) Note: Hyperkalaemia can rarely cause a prolonged PR interval, but it is a much less common association compared to hypokalaemia. Condition Associated with a Short PR Interval: Wolff-Parkinson-White syndrome

Answer 297

Differentiating RBBB from LBBB: Mnemonic: WiLLiaM MaRRoW LBBB: 'W' in V1 and 'M' in V6 RBBB: 'M' in V1 and 'W' in V6 Causes of Right Bundle Branch Block (RBBB): Normal variant (more common with increasing age) Right ventricular hypertrophy Chronically increased right ventricular pressure (e.g., cor pulmonale) Pulmonary embolism Myocardial infarction Atrial septal defect (ostium secundum) Cardiomyopathy or myocarditis

Answer 298

Answer: Eisenmenger's syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right shunt leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood flow and pulmonary hypertension.

Answer 299

Ventricular septal defect (VSD) Atrial septal defect (ASD) Patent ductus arteriosus (PDA)

Answer 300

Original murmur may disappear Cyanosis Clubbing Right ventricular failure Haemoptysis Embolism

Answer 301

Answer: Heart-lung transplantation is required.

Answer 302

Answer: Eisenmenger's syndrome develops when a left-to-right shunt caused by a congenital heart defect is left uncorrected. This leads to remodeling of the pulmonary microvasculature, increased pulmonary vascular resistance, and ultimately, pulmonary hypertension, reversing the shunt to right-to-left.

Answer 303

Answer: The original murmur may disappear in Eisenmenger's syndrome.

Answer 304

Answer: Cyanosis occurs in Eisenmenger's syndrome due to the reversal of the shunt from left-to-right to right-to-left, leading to deoxygenated blood entering the systemic circulation.

Answer 305

Answer: Signs of right ventricular failure in Eisenmenger's syndrome include cyanosis, clubbing, and haemoptysis.

Answer 306

Answer: Heart-lung transplantation is required for Eisenmenger's syndrome because of the severe pulmonary hypertension and the irreversible damage to the pulmonary vasculature.

Answer 307

Answer: Acute Heart Failure (AHF) is a life-threatening emergency characterized by the sudden onset or worsening of heart failure symptoms, which can present with or without a history of pre-existing heart failure. AHF without a past history of heart failure is called de-novo AHF.

Answer 308

Answer: De-novo Acute Heart Failure refers to AHF occurring without a past history of heart failure, often caused by increased cardiac filling pressures and myocardial dysfunction, usually as a result of ischemia, which reduces cardiac output and causes hypoperfusion and pulmonary edema.

Answer 309

Answer: Common causes of de-novo AHF include: Ischemia Viral myopathy Toxins Valve dysfunction

Answer 310

Answer: Decompensated Acute Heart Failure is a more common form of AHF that occurs in patients with a background history of heart failure. It often presents with signs of fluid congestion, weight gain, orthopnea, and breathlessness.

Answer 311

Acute coronary syndrome Hypertensive crisis Acute arrhythmia Valvular disease

Answer 312

Answer: Patients with AHF are broadly characterized into one of four groups based on their presentation: With or without hypoperfusion With or without fluid congestion This classification is clinically useful for determining the therapeutic approach.

Answer 313

Symptoms: Breathlessness Reduced exercise tolerance Edema Fatigue Signs: Cyanosis Tachycardia Elevated jugular venous pressure Displaced apex beat Chest signs: bibasal crackles or wheeze S3 heart sound

Answer 314

Answer: Over 90% of patients with AHF have a normal or increased blood pressure.

Answer 315

Blood tests: To identify underlying abnormalities such as anemia, abnormal electrolytes, or infection. Chest X-ray: To detect pulmonary venous congestion, interstitial edema, and cardiomegaly. Echocardiogram: Recommended for new-onset heart failure or suspected changes in cardiac function. B-type natriuretic peptide (BNP): Raised levels (>100 mg/litre) indicate myocardial damage and support the diagnosis.

Answer 316

Answer: Chest X-ray findings in AHF include pulmonary venous congestion, interstitial edema, and cardiomegaly.

Answer 317

Answer: Dyspnoea (shortness of breath).

Answer 318

Answer: A cough that may be worse at night and associated with pink/frothy sputum.

Answer 319

Answer: Orthopnoea.

Answer 320

Answer: It is a sudden onset of severe shortness of breath at night that awakens the patient from sleep.

Answer 321

Answer: A wheezing sound associated with chronic heart failure due to pulmonary congestion.

Answer 322

Answer: Weight loss seen in chronic heart failure patients, occurring in up to 15% of patients, and may be hidden by weight gained due to oedema.

Answer 323

Answer: Bibasal crackles.

Answer 324

Raised jugular venous pressure (JVP) Ankle oedema Hepatomegaly

Answer 325

Answer: IV loop diuretics (e.g. furosemide or bumetanide).

Answer 326

Answer: 94-98%, in line with British Thoracic Society guidelines.

Answer 327

Answer: Nitrates may be used if there is concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease.

Answer 328

Answer: Hypotension.

Answer 329

Answer: Continuous positive airway pressure (CPAP).

Answer 330

Answer: Some treatments for acute heart failure (e.g., loop diuretics and nitrates) may exacerbate hypotension.

Answer 331

Answer: Dobutamine.

Answer 332

Answer: Beta-blockers should only be stopped if the patient has a heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock.

Answer 333

Answer: Heart failure is defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body, usually due to structural or functional heart disease.

Answer 334

Heart failure with reduced ejection fraction (HF-rEF), typically defined as LVEF < 35-40%. Heart failure with preserved ejection fraction (HF-pEF), where LVEF is normal or near-normal.

Answer 335

Answer: Systolic dysfunction is typically caused by conditions such as ischaemic heart disease, dilated cardiomyopathy, myocarditis, and arrhythmias.

Answer 336

Answer: Diastolic dysfunction is typically caused by conditions such as hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade, and constrictive pericarditis.

Answer 337

Answer: Heart failure is typically described as acute or chronic. Acute heart failure often refers to an acute exacerbation of chronic heart failure.

Answer 338

Answer: The most urgent symptoms of acute heart failure are often due to left ventricular failure, resulting in pulmonary oedema.

Answer 339

Answer: Common features of left ventricular failure include pulmonary oedema, dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, and bibasal fine crackles.

Answer 340

Answer: Common features of right ventricular failure include peripheral oedema, ankle/sacral oedema, raised jugular venous pressure, hepatomegaly, weight gain due to fluid retention, and anorexia ('cardiac cachexia').

Answer 341

Answer: High-output heart failure refers to a situation where a 'normal' heart is unable to pump enough blood to meet the metabolic needs of the body.

Answer 342

Answer: Causes of high-output heart failure include anaemia, arteriovenous malformation, Paget's disease, pregnancy, thyrotoxicosis, and thiamine deficiency (wet Beri-Beri).

Answer 343

Answer: Right-sided heart failure is caused by increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).

Answer 344

Answer: Wolff-Parkinson-White syndrome is associated with a short PR interval.

Answer 345

Answer: The first heart sound (S1) is caused by the closure of the mitral and tricuspid valves.

Answer 346

Answer: The first heart sound (S1) is soft if there is a long PR interval or mitral regurgitation.

Answer 347

Mitral stenosis Left-to-right shunts Short PR interval, atrial premature beats Hyperdynamic states

Answer 348

Answer: The second heart sound (S2) is caused by the closure of the aortic and pulmonary valves.

Answer 349

Answer: The second heart sound (S2) is soft in aortic stenosis.

Answer 350

Answer: Splitting of the second heart sound (S2) during inspiration is normal.

Answer 351

Answer: The third heart sound (S3) is caused by the diastolic filling of the ventricle.

Answer 352

Answer: The third heart sound (S3) is heard in left ventricular failure (e.g., dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock), and mitral regurgitation.

Answer 353

Answer: The third heart sound (S3) is considered normal if the individual is under 30 years old (may persist in women up to 50 years old).

Answer 354

Answer: The fourth heart sound (S4) is caused by atrial contraction against a stiff ventricle.

Answer 355

Answer: The fourth heart sound (S4) may be heard in aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM), and hypertension.

Answer 356

Answer: The fourth heart sound (S4) coincides with the P wave on an ECG.

Answer 357

Answer: In hypertrophic obstructive cardiomyopathy (HOCM), a double apical impulse may be felt as a result of a palpable S4.

Answer 358

Hypertension: systemic (loud A2) or pulmonary (loud P2) Hyperdynamic states Atrial septal defect without pulmonary hypertension

Answer 359

Causes of a widely split second heart sound (S2) include: Deep inspiration Right bundle branch block (RBBB) Pulmonary stenosis Severe mitral regurgitation

Answer 360

Causes of a reversed (paradoxical) split second heart sound (S2) include: Left bundle branch block (LBBB) Severe aortic stenosis Right ventricular pacing Wolff-Parkinson-White (WPW) syndrome type B (causes early P2) Patent ductus arteriosus

Answer 361

NICE defines hypertension as: A clinic reading persistently above ≥ 140/90 mmHg, or A 24-hour blood pressure average reading ≥ 135/85 mmHg

Answer 362

Glomerulonephritis Chronic pyelonephritis Adult polycystic kidney disease Renal artery stenosis

Answer 363

Primary hyperaldosteronism Phaeochromocytoma Cushing's syndrome Liddle's syndrome Congenital adrenal hyperplasia (11-beta hydroxylase deficiency) Acromegaly

Answer 364

Glucocorticoids NSAIDs Pregnancy Coarctation of the aorta Combined oral contraceptive pill

Answer 365

Fundoscopy: to check for hypertensive retinopathy Urine dipstick: to check for renal disease ECG: to check for left ventricular hypertrophy or ischaemic heart disease

Answer 366

24-hour blood pressure monitoring Urea and electrolytes HbA1c (for diabetes mellitus) Lipid profile (for hyperlipidaemia) ECG Urine dipstick

Answer 367

ACE inhibitors: Inhibit conversion of angiotensin I to angiotensin II. Common side effects include cough, angioedema, and hyperkalaemia. First-line treatment in younger patients (< 55 years old). Calcium channel blockers: Block voltage-gated calcium channels, relaxing vascular smooth muscle. Common side effects include flushing, ankle swelling, and headache. First-line treatment in older patients (≥ 55 years old). Thiazide diuretics: Inhibit sodium absorption at the beginning of the distal convoluted tubule. Common side effects include hyponatraemia, hypokalaemia, and dehydration. Angiotensin II receptor blockers (A2RB): Block effects of angiotensin II at the AT1 receptor. Common side effects include hyperkalaemia. Used when patients do not tolerate ACE inhibitors due to cough.

Answer 368

Dental procedures Upper and lower gastrointestinal tract procedures Genitourinary tract procedures, including urological, gynecological, and obstetric procedures and childbirth Upper and lower respiratory tract procedures, including ear, nose, and throat procedures and bronchoscopy

Answer 369

Answer: The jugular venous pulse provides information about right atrial pressure and can offer clues to underlying valvular disease.

Answer 370

Answer: Kussmaul's sign describes a paradoxical rise in JVP during inspiration, seen in constrictive pericarditis.

Answer 371

Answer: Cannon 'a' waves are caused by atrial contractions against a closed tricuspid valve. They are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, and single-chamber ventricular pacing.

Answer 372

Answer: The 'v' wave represents passive filling of blood into the atrium against a closed tricuspid valve. Giant 'v' waves are observed in tricuspid regurgitation.

Answer 373

Answer: Mitral regurgitation (MR) occurs when blood leaks back through the mitral valve during systole, leading to reduced efficiency of the heart as less blood is pumped with each contraction.

Answer 374

Answer: Mitral regurgitation (MR) is the second most common valve disease after aortic stenosis.

Answer 375

Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction (MI) Prior mitral stenosis or valve prolapse Collagen disorders (e.g., Marfan's Syndrome, Ehlers-Danlos syndrome)

Answer 376

Coronary artery disease (CAD) or post-MI Mitral valve prolapse Infective endocarditis Rheumatic fever (less common in developed countries) Congenital causes

Answer 377

Answer: Most patients with MR are asymptomatic, especially those with mild to moderate MR. Symptoms, if present, are often due to left ventricular failure, arrhythmias, or pulmonary hypertension.

Answer 378

Answer: Patients with severe MR may experience fatigue, shortness of breath, and edema.

Answer 379

Answer: The murmur of MR is typically a pansystolic murmur described as "blowing" and is best heard at the apex, radiating into the axilla.

Answer 380

Answer: In severe MR, S1 may be quiet due to incomplete closure of the valve, and S2 may be widely split.

Answer 381

Nitrates, diuretics, positive inotropes, and intra-aortic balloon pump to increase cardiac output.

Answer 382

ECG: May show a broad P wave (atrial enlargement) Chest X-ray: May show cardiomegaly with an enlarged left atrium and ventricle Echocardiography: Crucial for diagnosis and assessing the severity of MR

Answer 383

Answer: In heart failure, ACE inhibitors, beta-blockers, and spironolactone may be considered for chronic MR.

Answer 384

Answer: In acute, severe MR, surgery is indicated. Valve repair is preferred over replacement due to better outcomes. If repair is not possible, valve replacement with an artificial or pig valve is considered.

Answer 385

Answer: The most common cause of death following MI is cardiac arrest, usually due to ventricular fibrillation.

Answer 386

Answer: Cardiogenic shock occurs when a large portion of the ventricular myocardium is damaged, resulting in decreased ejection fraction. It is often difficult to treat and may require inotropic support or an intra-aortic balloon pump.

Answer 387

Answer: In chronic heart failure following MI, loop diuretics (e.g., furosemide) are used to reduce fluid overload, while ACE inhibitors and beta-blockers improve long-term prognosis.

Answer 388

Common arrhythmias following MI include: Ventricular fibrillation (most common cause of death) Ventricular tachycardia Bradyarrhythmias such as atrioventricular block (especially after inferior MI)

Answer 389

Pericarditis within the first 48 hours of a transmural MI is common, presenting with: Chest pain (worse when lying flat) Pericardial rub on auscultation Pericardial effusion (detected on echocardiogram)

Answer 390

Dressler's syndrome occurs 2-6 weeks after MI and is thought to be an autoimmune reaction. It presents with: Fever Pleuritic pain Pericardial effusion Raised ESR It is treated with NSAIDs.

Answer 391

Answer: A left ventricular aneurysm occurs when ischemic damage weakens the myocardium, leading to aneurysm formation. It is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form in the aneurysm, increasing the risk of stroke, so anticoagulation is often required.

Answer 392

Answer: Left ventricular free wall rupture occurs in about 3% of MI patients, typically 1-2 weeks after MI. It presents with acute heart failure and cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Answer 393

Answer: A ventricular septal defect (VSD) can occur within the first week after MI, causing acute heart failure and a pan-systolic murmur. It is diagnosed by echocardiography and requires urgent surgical correction.

Answer 394

Answer: Acute mitral regurgitation following MI is more common with infero-posterior infarctions and may be due to ischemia or rupture of the papillary muscle. It presents with acute hypotension and pulmonary edema, and requires vasodilator therapy and often emergency surgical repair.

Answer 395

Answer: Myocarditis is the inflammation of the myocardium, which can have a variety of underlying causes. It should be particularly considered in younger patients who present with chest pain.

Answer 396

Common causes of myocarditis include: Viral: Coxsackie B, HIV Bacterial: Diphtheria, Clostridia Spirochaetes: Lyme disease Protozoa: Chagas' disease, Toxoplasmosis Autoimmune diseases Drugs: Doxorubicin

Answer 397

The typical presentation includes: Young patient with acute history Chest pain Dyspnoea Arrhythmias

Answer 398

Blood tests commonly show: Elevated inflammatory markers (99% of cases) Elevated cardiac enzymes Elevated BNP

Answer 399

ECG findings in myocarditis include: Tachycardia Arrhythmias ST/T wave changes, such as ST-segment elevation and T wave inversion

Answer 400

Management of myocarditis includes: Treating the underlying cause (e.g., antibiotics for bacterial infections) Supportive care for heart failure or arrhythmias

Answer 401

Complications of myocarditis include: Heart failure Arrhythmias, which may lead to sudden death Dilated cardiomyopathy, usually a late complication

Answer 402

Answer: Orthostatic hypotension is a condition characterized by a significant drop in blood pressure (usually >20/10 mm Hg) within three minutes of standing, leading to symptoms such as presyncope or syncope.

Answer 403

Orthostatic hypotension is more common in: Older individuals Patients with neurodegenerative diseases (e.g., Parkinson's disease) Patients with diabetes or hypertension

Answer 404

Iatrogenic causes include: Alpha-blockers (e.g., used for benign prostatic hyperplasia)

Answer 405

Features of orthostatic hypotension include: A drop in blood pressure (>20/10 mm Hg) within three minutes of standing Presyncope or syncope

Answer 406

Treatment options for orthostatic hypotension include: Midodrine (a vasopressor) Fludrocortisone (a corticosteroid that increases blood volume)

Answer 407

Answer: Postural hypotension is defined as a fall in systolic blood pressure > 20 mmHg on standing.

Answer 408

Hypovolaemia (e.g., dehydration, blood loss) Autonomic dysfunction (e.g., diabetes, Parkinson's disease) Drugs: Diuretics Antihypertensives L-dopa (used in Parkinson's disease) Phenothiazines (antipsychotics) Antidepressants Sedatives Alcohol consumption

Answer 409

Pulsus paradoxus is a greater than normal (>10 mmHg) fall in systolic blood pressure during inspiration, causing a faint or absent pulse during inspiration. It is commonly seen in: Severe asthma Cardiac tamponade

Answer 410

Answer: A slow-rising/plateau pulse is characterized by a gradual increase in the pulse, often associated with aortic stenosis.

Answer 411

Answer: A collapsing pulse is a pulse that rises quickly and falls abruptly. It is associated with: Aortic regurgitation Patent ductus arteriosus Hyperkinetic states (e.g., anaemia, thyrotoxicosis, fever, exercise, pregnancy)

Answer 412

Answer: Pulsus alternans is characterized by a regular alternation of the force of the arterial pulse, and it is commonly seen in severe left ventricular failure (LVF).

Answer 413

Answer: A bisferiens pulse is a 'double pulse' with two systolic peaks. It is commonly associated with mixed aortic valve disease.

Answer 414

Answer: A jerky pulse is a quick, abrupt rise and fall in pulse force, and it is typically associated with hypertrophic obstructive cardiomyopathy (HOCM).

Answer 415

Answer: SVT refers to any tachycardia that originates above the ventricles. It is often used to describe paroxysmal SVT, characterized by sudden onset of narrow complex tachycardia. Common types include: Atrioventricular nodal re-entry tachycardia (AVNRT) Atrioventricular re-entry tachycardia (AVRT) Junctional tachycardias

Answer 416

Vagal manoeuvres: Valsalva manoeuvre (e.g., blowing into an empty plastic syringe) Carotid sinus massage Intravenous adenosine: Rapid IV bolus: 6mg If unsuccessful, give 12mg, then 18mg if needed Contraindicated in asthmatics, in which case verapamil is preferred Electrical cardioversion (if the above methods fail)

Answer 417

Beta-blockers Radio-frequency ablation

Answer 418

Answer: Syncope is a transient loss of consciousness caused by global cerebral hypoperfusion, with rapid onset, short duration, and spontaneous complete recovery. It excludes other causes of collapse, such as epilepsy.

Answer 419

Reflex syncope (neurally mediated): Vasovagal: Triggered by emotion, pain, or stress Situational: Triggered by specific actions like cough, micturition, or gastrointestinal issues Carotid sinus syncope Orthostatic syncope: Primary autonomic failure: e.g., Parkinson's, Lewy body dementia Secondary autonomic failure: e.g., diabetic neuropathy, amyloidosis, uraemia Drug-induced: e.g., diuretics, alcohol, vasodilators Volume depletion: e.g., haemorrhage, diarrhoea Cardiac syncope: Arrhythmias: Bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular) Structural causes: e.g., valvular disease, myocardial infarction, hypertrophic obstructive cardiomyopathy Others: e.g., pulmonary embolism

Answer 420

Answer: Reflex syncope (neurally mediated) is the most common cause of syncope in all age groups, although orthostatic and cardiac causes become more common in older patients.

Answer 421

Cardiovascular examination Postural blood pressure readings: A symptomatic fall in systolic BP > 20 mmHg, diastolic BP > 10 mmHg, or a decrease in systolic BP < 90 mmHg is diagnostic of orthostatic syncope. ECG for all patients Other tests depending on clinical features Patients with typical features, no postural drop, and a normal ECG do not require further investigations

Answer 422

Answer: Torsades de Pointes is a form of polymorphic ventricular tachycardia associated with a long QT interval. It may deteriorate into ventricular fibrillation, leading to sudden death.

Answer 423

Answer: Causes of long QT interval include: Congenital: Jervell-Lange-Nielsen syndrome Romano-Ward syndrome Antiarrhythmics: e.g., amiodarone, sotalol, class 1a antiarrhythmic drugs Medications: Tricyclic antidepressants Antipsychotics Chloroquine Terfenadine Erythromycin Electrolyte disturbances: Hypocalcaemia Hypokalaemia Hypomagnesaemia Other causes: Myocarditis Hypothermia Subarachnoid haemorrhage

Answer 424

Answer: The first-line treatment for Torsades de Pointes is IV magnesium sulphate.

Answer 425

Signs of Tricuspid Regurgitation include: Pan-systolic murmur Prominent/giant V waves in the JVP Pulsatile hepatomegaly Left parasternal heave

Answer 426

Causes of Tricuspid Regurgitation include: Right ventricular infarction Pulmonary hypertension (e.g., COPD) Rheumatic heart disease Infective endocarditis (especially in intravenous drug users) Ebstein's anomaly Carcinoid syndrome

Answer 427

Answer: Ventricular Tachycardia (VT) is a broad-complex tachycardia originating from a ventricular ectopic focus. It can lead to ventricular fibrillation and requires urgent treatment. The two main types of VT are: Monomorphic VT: Most commonly caused by myocardial infarction. Polymorphic VT: Includes torsades de pointes, which is caused by a prolonged QT interval.

Answer 428

Answer: Causes of a prolonged QT interval include: Congenital: Jervell-Lange-Nielsen syndrome (includes deafness, due to abnormal potassium channels) Romano-Ward syndrome (no deafness) Drugs: Amiodarone, sotalol, class 1a antiarrhythmic drugs Tricyclic antidepressants, fluoxetine Chloroquine, terfenadine, erythromycin Other: Electrolyte imbalances (e.g., hypocalcaemia, hypokalaemia, hypomagnesaemia) Acute myocardial infarction Myocarditis Hypothermia Subarachnoid haemorrhage

Answer 429

Answer: If the patient has adverse signs (e.g., systolic BP < 90 mmHg, chest pain, heart failure), immediate cardioversion is indicated. In the absence of adverse signs, antiarrhythmics can be used. If these fail, synchronised electrical cardioversion may be needed. Drug Therapy: Amiodarone: Ideally administered through a central line. Lidocaine: Use with caution in severe left ventricular impairment. Procainamide: Another option. Important: Verapamil should NOT be used in VT. If drug therapy fails: Electrophysiological study (EPS). Implantable cardioverter-defibrillator (ICD): Particularly indicated in patients with significantly impaired LV function.

Answer 430

Answer: WPW syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles, leading to atrioventricular re-entry tachycardia (AVRT). This pathway bypasses the normal AV node conduction, which allows rapid conduction and can cause atrial fibrillation (AF), which may degenerate rapidly into ventricular fibrillation (VF).

Answer 431

Short PR interval Wide QRS complexes with a slurred upstroke, called the 'delta wave' Left axis deviation if the accessory pathway is right-sided Right axis deviation if the accessory pathway is left-sided

Answer 432

Type A (left-sided pathway): Dominant R wave in V1. Type B (right-sided pathway): No dominant R wave in V1.

Answer 433

Hypertrophic obstructive cardiomyopathy (HOCM) Mitral valve prolapse Ebstein's anomaly Thyrotoxicosis Secundum atrial septal defect (ASD)

Answer 434

Definitive treatment: Radiofrequency ablation of the accessory pathway. Medical therapy: Sotalol, amiodarone, flecainide. Caution: Sotalol should be avoided in patients with coexistent atrial fibrillation (AF), as it may prolong the refractory period at the AV node, increasing the rate of transmission through the accessory pathway, leading to potential ventricular fibrillation (VF).

Answer 435

pregnancy macrolides

Answer 436

alteplase and fondaparinux

Answer 437

Pulmonary Embolism Severity Index (PESI) score

Answer 438

Stop warfarin. Give intravenous vitamin K 5mg. Administer prothrombin complex concentrate or fresh frozen plasma (FFP) if prothrombin complex concentrate is not available.

Answer 439

Stop warfarin. Give intravenous vitamin K 1-3mg. Repeat the dose of vitamin K if the INR is still too high after 24 hours. Restart warfarin when the INR is less than 5.0.

Answer 440

Stop warfarin. Give vitamin K 1-5mg by mouth (using the intravenous preparation orally). Repeat the dose of vitamin K if the INR is still too high after 24 hours. Restart warfarin when the INR is less than 5.0.

Answer 441

Stop warfarin. Give intravenous vitamin K 1-3mg. Restart warfarin when the INR is less than 5.0.

Answer 442

Withhold 1 or 2 doses of warfarin. Reduce the subsequent maintenance dose.

Answer 443

A: Prothrombin complex concentrate is preferred because FFP can take time to defrost, whereas prothrombin complex concentrate can be administered more quickly.

Answer 444

A: Biological (bioprosthetic) valves and mechanical valves.

Answer 445

A: They are usually bovine (cow) or porcine (pig) in origin.

Answer 446

A: Structural deterioration and calcification over time.

Answer 447

A: Most older patients (> 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve.

Answer 448

A: Long-term anticoagulation is not usually needed, but warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.

Answer 449

A: The bileaflet valve. Ball-and-cage valves are rarely used nowadays.

Answer 450

A: Increased risk of thrombosis, necessitating long-term anticoagulation.

Answer 451

A: Warfarin is still used in preference to DOACs for patients with mechanical heart valves.

Answer 452

A: Aspirin is given only if there is an additional indication, such as ischaemic heart disease.

Answer 453

A: The target INR is 3.0.

Answer 454

A: The target INR is 3.5.

Answer 455

bioprosthetic: aspirin mechanical: warfarin + aspirin

Answer 456

monitoring - regular echocardiogram every 6-12 months

Answer 457

should be initiated following ACEi or ARB wash-out period

Answer 458

ejection systolic murmur. This murmur is typically heard best in the second left intercostal space and may radiate towards the left shoulder.

Answer 459

IV prostaglandins to maintain PDA before corrective surgery is done

Answer 460

visual effects, particular luminous phenomena, are common headache bradycardia, heart block

Answer 461

aortic stenosis hypotension (<90) bradycardia (<50) treatment for erectile dysfunction (eg sildenafil)

Answer 462

strep viridans

Answer 463

sglt2 inhibitor

Answer 464

Current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission Chest pain 12-72 hours ago: refer to hospital the same-day for assessment Chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

Answer 465

Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw, or arms Precipitated by physical exertion Relieved by rest or GTN in about 5 minutes

Answer 466

Typical angina: all 3 features present Atypical angina: 2 of the 3 features present Non-anginal chest pain: 1 or none of the features present

Answer 467

CT coronary angiography

Answer 468

Non-invasive functional imaging (looking for reversible myocardial ischaemia)

Answer 469

Invasive coronary angiography

Answer 470

A: High-grade stenosis in the left anterior descending coronary artery.

Answer 471

A: The patient's pain may have resolved, and cardiac enzymes may be normal or minimally elevated.

Answer 472

Biphasic or deep T wave inversion in leads V2-3 Minimal ST elevation No Q waves

Answer 473

The Levine Scale: Grade 1 - Very faint murmur, frequently overlooked Grade 2 - Slight murmur Grade 3 - Moderate murmur without palpable thrill Grade 4 - Loud murmur with palpable thrill Grade 5 - Very loud murmur with extremely palpable thrill. Can be heard with stethoscope edge Grade 6 - Extremely loud murmur - can be heard without stethoscope touching the chest wall

Answer 474

IV loop diuretics

Answer 475

Very long half-life (20-100 days), requiring loading doses. Should ideally be given into central veins (causes thrombophlebitis). Proarrhythmic effects due to lengthening of the QT interval. Interacts with other drugs (P450 inhibitor), e.g., decreases metabolism of warfarin. Numerous long-term adverse effects.

Answer 476

A: TFT (thyroid function test), LFT (liver function test), U&E (urea and electrolytes), CXR (chest X-ray).

Answer 477

A: Every 6 months.

Answer 478

Thyroid dysfunction (hypothyroidism and hyperthyroidism). Corneal deposits. Pulmonary fibrosis/pneumonitis. Liver fibrosis/hepatitis. Peripheral neuropathy, myopathy. Photosensitivity. 'Slate-grey' appearance. Thrombophlebitis and injection site reactions. Bradycardia. Lengthens QT interval.

Answer 479

transfer for pci

Answer 480

A: Primary ciliary dyskinesia.

Answer 481

Dextrocardia or complete situs inversus. Bronchiectasis. Recurrent sinusitis. Subfertility (due to diminished sperm motility and defective ciliary action in the fallopian tubes).

Answer 482

A: Due to its association with dextrocardia, which can present as 'quiet heart sounds' and 'small volume complexes in lateral leads'.

Answer 483

A: 1972 (II, VII, IX, and X).

Answer 484

A: Mechanical heart valves.

Answer 485

A: 2.5, and if recurrent, 3.5.

Answer 486

A: Liver disease and P450 enzyme inhibitors (e.g., amiodarone, ciprofloxacin).

Answer 487

A: Haemorrhage and skin necrosis.

Answer 488

A: Skin necrosis due to a temporary procoagulant state from reduced protein C biosynthesis.

Answer 489

A: Purple toes syndrome.

Answer 490

tricuspid regurg

Answer 491

pulmonary stenosis

Answer 492

patients may complain of atypical chest pain or palpitations mid-systolic click (occurs later if patient squatting) late systolic murmur (longer if patient standing) complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

Answer 493

congenital heart disease: PDA, ASD cardiomyopathy Turner's syndrome Marfan's syndrome, Fragile X osteogenesis imperfecta pseudoxanthoma elasticum Wolff-Parkinson White syndrome long-QT syndrome Ehlers-Danlos Syndrome polycystic kidney disease

Answer 494

mitral valve prolapse

Answer 495

LFTs at baseline, 3 months and 12 months fasting lipid profile

Answer 496

Pulmonary stenosis and tricuspid insufficiency

Answer 497

ECG after 60-90 mins

Answer 498

complete heart block with broad complex QRS recent asystole Mobitz type II AV block ventricular pause > 3 seconds

Answer 499

radial artery

Answer 500

Give via intraosseous access (proximal tibia)

Answer 501

A: Amoxicillin, consider adding low-dose gentamicin.

Answer 502

A: Vancomycin + low-dose gentamicin.

Answer 503

A: Vancomycin + rifampicin + low-dose gentamicin.

Answer 504

A: Flucloxacillin.

Answer 505

A: Flucloxacillin + rifampicin + low-dose gentamicin.

Answer 506

A: Benzylpenicillin.

Answer 507

Severe valvular incompetence Aortic abscess (often indicated by a lengthening PR interval) Infections resistant to antibiotics/fungal infections Cardiac failure refractory to standard medical treatment Recurrent emboli after antibiotic therapy

Answer 508

PAILS stands for P-posterior A-anterior I-inferior L-lateral S-septal. ST elevations in these leads most commonly create reciprocal ST depressions in the corresponding leads of the next letter in the mnemonic.

Answer 509

Amlodipine, Only non-dihydropyridine calcium channel blockers such as Verapamil can be used due to their atrioventricular node blocking actions

Answer 510

High-output heart failure: 2Ps, 2As, 2Ts Pregnancy and Pagets Anaemia and arteriovenous malformation Thyrotoxicosis and thiamine (wet beri-beri)

Answer 511

atorvastatin 20mg for primary prevention, 80mg for secondary prevention

Answer 512

long straight lines before QRS complex

Answer 513

Hypovolaemia - Cardiac output is lowered in hypovolaemia due to decreased preload. PAP is low (therefore preload is low). Cardiac Output is also low. The main clue as to why the answer is Hypovolaemia is because PAP, and therefore preload is low, and preload is largely determined by venous blood volume. This also explains why CO is low, as if only a little amount of blood is returning to the heart, the heart can only pump that small amount of blood. and SVR is raised. The SVR is raised because in order to maintain blood pressure, the body vasoconstricts the peripheral arteries.

Answer 514

Cardiogenic Shock - In cardiogenic shock pulmonary pressures are often high. This is the basis for the use of venodilators in the treatment of pulmonary oedema. PAP and SVR are raised, but CO is low, and this is just suggesting that the problem lies with the heart, therefore it is cardiogeneic shock. The heart is receiving a good amount of blood (because PAP and thus preload is raised), but because the heart isn't pumping very well, the body is vasoconstricting the peripheral vessels and so SVR is raised once again.

Answer 515

Septic Shock Decreased SVR is a major feature of sepsis. A hyperdynamic circulation is often present. This is the reason for the use of vasoconstrictors. SVR is reduced. This is typically seen in sepsis - endotoxins and the inflammatory response vasodilates the peripheries, and so SVR is low. If the peripheral essels are all loose and leaky, not much blood remains inside the vessels and so the venous blood volume will also be low, hence the preload is low, and this is indicated by the low PAP. And in response, the heart is having to work harder to get blood to the organs because not only is it receiving less blood from the venous system, but the body is also struggling to maintain a blood pressure because of the peripheral vasodilation (BP = CO x SVR). So the heart tries to increase heart rate and stroke volume (adrenergic response etc), and cardiac output is thus high.

Answer 516

thyroid dysfunction - hyperthyroidism