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Outline the conducting pathway of the heart
- Autonomic and endocrine control
- Sinu-atrial node (right atrium)
- Atrioventricular node
- Bundle of His
- Left/Right bundle (left has 2 branches, ant/post)
- Purkinje fibres
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What is preload?
Pressure of blood on the left ventricle after diastole (when passive filling has completed)
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What is afterload?
The amount of systemic pressure that needs to be exceeded by the ventricles to open the aortic/pulmonary valves
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What is stable angina?
- A relatively unchanging reduction in coronary blood flow
- Insufficient blood flow occurs when heart activity increases
- No thrombotic pathogenesis
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What is unstable angina?
- Acute reduction in coronary blood flow
- Typically caused by endothelial rupture in pre-existing stable angina/atheromatous disease
- Symptoms of this angina occur at rest, with rise in troponin due to clotting involvement
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What are the major criteria in the Duke diagnosis of IE?
- Causative organism in 2 separate cultures
- Positive echo OR new valve regurgitation detected in auscultation
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What investigations are required in suspected IE?
- ECG: Ischaemia, conduction delay or arrhythmia
- Blood cultures: S. Viridans/S. Aureaus
- Echo: Valve function and ejection volume
- CXR: Valve calcification
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What is rheumatic fever?
- S. Pyogenes infection
- 'Molecular mimicry' effect
- Autoimmunity against valves and kidneys
- Both stenosis and regurgitation occur
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What is the lower limit for ST segment elevation?
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How is heart axis determined on an ECG?
- Examine QRS in lead I and II
- Normal = Both are mostly positive
- Posterior deviation = I positive and II negative
- Anterior = I is negative, II positive
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Briefly describe the normal metabolism of cholesterols
- Absorbed in GI, enter lymph as chylomicrons
- In liver, converted to cholesterol then either bile, vLDL or LDL
- Transported to tissues, which can return it as HDL (which is then converted to bile)
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Outline the pathogenesis of atheroma
- LDL enters sub-endothelial space when high blood content
- Macrophages consume and oxidise the LDL
- Cytoplasm enlarges and saturates, making "foam cells"
- Apoptotis occurs, causing LDL release and inflammation
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What is the MoA of statins?
- Inhibit HMG-CoA reductase activity in liver
- Reduced cholesterol production from acetyl CoA
- Liver LDL receptors expressed to remove cholesterol from bloodstream
- Cholesterol processed into bile salts, excreted and 95% absorbed by bowel
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What modifiable risk factors can be managed for primary prevention of cardiovascular events? Give 6
- Smoking
- Alcohol consumption
- Blood pressure
- BMI/obesity
- Cholesterol
- Blood glucose
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What are the most common and most dangerous adverse effects of statins?
Side effects: Muscle/joint pain or cramps, malaise, GI features
Complications: Serious drug interactions, rhabdomyolysis, acute renal failure
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What other lipid-lowering therapies are available if statins are not tolerated? What is their MoA? Give 3
Fibrates: Increase liver FFA uptake and converstion to acetyl-CoA
Ezetimibe: Reduced absorption of lipids in small intestine
Resins: Same as ezetimibe
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Describe the anatomy of the coronary arteries
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Outline cardiovascular-related factors in the pathogenesis of heart failure
- Build up of exacerbating factors, especially increased systemic resistance
- Intrinsic changes, e.g. ventricular hypertrophy and frank-starling mechanism, allow compensation
- Injury to heart, acute or chronic increase in preload or afterload cause decompensation and dilation of ventricles
- Loss of systolic output, as sufficient ventricular pressure in systole not able to be maintained
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Outline non-cardiovascular related factors in the pathogenesis of heart failure
- Loss of systolic output causes compensation, relying on frank-starling mechanism
- Systemic modulation via ANS (carotid sinus receptors - medulla - SA node/peripheral constriction)
- ADH secretion from carotid/atrial baroreceptor activation
- RAS system causes vasoconstriction and retention of Na/H20 by aldosterone (juxtaglomerular cells)
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What are the causes of an exacerbation of heart failure?
- HEART FAILED
- Hypertension
- Environment
- Anaemia
- Rheumatic
- Thyroid
- Failed medication
- Arrhythmia
- Infection/infarction
- Lung disease
- Endocrine
- Diet
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Give 5 signs and 5 symptoms of heart failure
- Symptoms:
- - Dypnoea
- - PND
- - Orthopnoea
- - Cough
- - Exercise intolerance
- Signs:
- - Crackles
- - Bilateral effusion
- - Pitting oedema
- - Increased JVP
- - Displaced apex
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What are the investigative findings in heart failure?
- ECG: Axis deviation, evidence of ischaemia/MI (st segment or q wave changes)
- CXR: Cardiomegaly, effusion, oedema, kerley b-lines [<1cm lines in lung peripheriesl], cuffing
- Echo: Dilated ventricle/hypertrophy with poor ejection fraction
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Briefly outline the classification of arrhythmias
- Bradyarrhythmias <60bpm
- Tachyarrhythmias >100bpm
Tachyarrhythmias: Regular or irregular
Regular: Narrow or broad QRS
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What causes bradycardias? List 5 of them
Due to failure of impulse formation or impulse conduction from atria to ventricles (AV block)
- - Sinus bradycardia
- - AV-block escape rhythm
- - Hypothyroidism
- - Infarction
- - Drugs; B-Blockers, CCBs, digitalis
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Describe the use of troponin measurement in suspected MI
- Protein not detectable in normal people (high specificity)
- Also highly sensitive
- Troponin levels can take 9-12 hours to raise, so should be checked on admission AND 12 hours later
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Give 5 medications used in the prevention of MI
- Aspirin
- Lipid lowering therapy (Statin)
- B-Blockers
- CCBs
- Isosorbide mononitrate (symptomatic)
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What ECG leads are:
- Inferior
- Lateral
- Anterior
- II, III and aVF (Bottom left)
- I, aVL
- V3, 4 initially and others if infarction large. Lower leads = anteroseptal, higher means anterolateral
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Give 5 ECG features that might be seen in acute MI
- Hyperacute T wave
- ST segment elevation
- Q waves
- New BBB
- VF/VT
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Give 5 short term or long term complications of MI
- Heart failure
- Myocardial rupture
- Bundle branch block
- Arrhythmias
- VSD
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Outline the pathophysiology of mitral stenosis and the resulting clinical features
- Almost always due to rheumatic fever (foreigners or elderly)
- Left atrial pressure/volume increases and hypertrophy occurs to maintain flow through valve
- Pulmonary venous pressure increases, causing pulmonary artery hypertension
- Right ventricle hypertrophy, dilatation and failure
- Stenosed valve means mid-diastolic murmur as ventricle refills
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Give 5 signs of mitral stenosis
- LOW PITCHED MID-DIASTOLIC MURMUR
- Malar flush
- Weak pulse
- AF
- Increased JVP (RHF)
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Outline the pathophysiology of mitral regurgitation and the resulting features
- Hypertensive or systemic disease causes valve damage
- Compliance of L.A. causes regurgitating blood to increase pressure
- Pulmonary venous pressure rises and oedema occurs
- Ventricular systole pushes blood into atrium causing pan-systolic murmur
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Outline the pathophysiology of aortic stenosis and its resulting features
- Increased resistance leads to left ventricular hypertrophy and ischaemia
- Exercise intolerance, arrhythmia and angina occur in moderate stenosis
- Increased pressure causes ejection systolic murmur
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Outline the pathophysiology of aortic regurgitation and its resulting features
- Reflux of blood means reduction in cardiac ouput, meaning ventricular hypertrophy occurs
- Diastolic run off causes reduction in diastolic BP and reduced coronary perfusion
- Systolic pressure increases to improve perfusion
- "Hyperdynamic" circulation, i.e. difference in sys/dia greater
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Give 5 signs of aortic regurgitation
- Early diastolic AND ejection systolic
- Collapsing pulse
- Pistol shot femorals
- Capillary pulsation
- Head nodding
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Outline the pathophysiology of tricuspid stenosis
- Don't bother with this condition
- Caused by rhematic fever and associated with other valve disease typically
- Features of right heart failure
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Outline the pathophysiology of tricuspid regurgitation and its resulting features
- Don't bother with this condition
- Can be functional due to right ventricle dilation or rheumatic fever
- "Blowing" pan systolic murmur
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Outline the pathophysiology of pulmonary stenosis and its resulting features
- Increase in right ventricle pressure causes hypertrophy and dilation
- Systemic features of heart failure occur; JVP, ascites, oedema
- Ejection systolic murmur
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Outline the pathophysiology of pulmonary regurgitation and its resulting features
- Occurs due to pulmonary hypertension
- Diastolic murmur
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Outline the management of acute heart failure
- Fuck My NOPP
- Frusemide
- Morphine
- Nitrates
- Oxygen
- Positive pressure airway ventilation
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What is a ventricular assist device and when is it used?
- Implanted device which takes blood from the ventricle and pumps it into the corresponding great vessel
- Can be extra or intracorporeal
- Complications include TE, bleeding, infection and malfunction
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Outline the pathophysiology of AF
- Any condition resulting in injury or distension of atria
- Fibrillation of atria, which conducts to AV node but is physiologically slowed
- Ventricles beat quickly but inefficienctly
- Loss of CO and blood stasis causes thrombosis
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What factors aid in deciding between rate or rhythm control in AF?
- Rate:
- - Patient age >65
- - Known IHD
- - AF duration >1yr
- - Anti-arrhythmics contraindicated
- Rhythm control:
- - Young symptomatic patients
- - Correctable aetiology
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How is the stroke risk of AF patients stratified?
- High risk: Previous TE event, >75 with disease or evidence of impaired LV function Warfarin
- Moderate: >65 or <75 with HBP/DM W/A
- Low: Anyone else Aspirin
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Give 5 patient factors which indicate careful monitoring is required when warfarin prescribed
- Over 75
- Concurrent antiplatelet therapy
- NSAIDs
- Uncontrolled hypertension
- History of bleeds; e.g peptic ulcer, cerebral
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What stratergies are used to induce cardioversion and when are they indicated?
- Electrical alone: When little risk of failure
- Sotalol/amiodarone: 4 weeks, then electrical cardioversion
- Drugs: Rhythm control alone
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When are anticoagulants required before/after cardioversion and for how long?
- Before
- - If onset <48 hours then heparin
- - If >48 then 3 weeks of anticoagulation before
- After
- - 4 weeks of anticoagulation unless >48hr onset
- - Further anticoagulation if appropriate
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Outline the drugs used in rhythm control of AF, from first choice onwards
- Standard beta blocker
- Class 1c (flecanide) or sotalol if SHD present
- Amiodarone if SHD present or other drugs fail
- If rhythm control fails, move to rate control or refer for other methods
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What medications are used in the rate control of AF?
- Thromboprophylaxis first
- Beta blocker/rate limiting CCB
- Add digoxin if further control required
- Refer to specialist for amiodarone/other if still required
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Outline the pathophysiology of atrial flutter
- Rapid but regular atrial depolarisation >300bpm
- Caused by a re-entrant rhythm, i.e. 'loop'
- AV node blocks to a ratio of 2:1 (or 3:1) so pulse is 150bpm
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What ECG features are seen in atrial flutter?
- "Sawtooth" in inferior leads
- Valsalva/massage or adenosine can reduce ventricular beats and reveal P-waves
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Give 3 ECG features seen in VT
- Ventricular rate >100bpm
- Monomorphic or polymorphic (life threatening)
- Broad complex
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Give 8 causes of cardiac arrest
- Hypovolemia
- Hyperkalaemia
- Hypothermia
- Hydrogen ions
- Thromboembolism
- Tension pneumothorax
- Tamponade
- Tablets
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Outline the NYHA scoring system
- New York Heart Association
- 1: No symptoms or limitation
- 2: Mild
- 3: Marked limitation but comfortable at rest
- 4: Severe limitations even at rest
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Give 5 causes of sinus bradycardia
- Physiological
- Hypothermia
- Hypothyroidism
- Drugs
- Sick sinus syndrome
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Describe the ECG findings in each type of AV block
- 1st degree: PR interval >200ms
- 2nd type 1: Elongating PR interval until QRS drops
- 2nd type 2: PR interval normal but QRS dropped. Can become 3rd
- 3rd degree: No relation between P and QRS (complete). Bradycardia
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Give 5 signs of heart block seen on chest x-ray
- Cardiomegaly
- Bat-wing mediastinal opacification
- Bilateral pleural effusions/CPh angle blunting
- Kerley B lines
- Bronchoalveolar cuffing
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Give 3 methods of managing chronic heart failure
- Lifestyle: Elevate head at night and secondary prevention
- Symptom management: Domiciliary O2
- Pharmacological: RAAS, IsMN, diuretics, bBs
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Give 5 underlying causes of hypertension
- Essential (likely atherosclerosis)
- Renal disease (e.g. ADPKD, failure)
- Cushing's
- Phaeo
- Pregnancy
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List the steps of drugs in hypertension management
- ACE inhibitors/ARBs (skip step if <55 or black)
- + calcium channel blocker
- + Thiazide
- + increase diuretic, alpha or beta blockers
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Give 4 features typical of pericarditis
- Sudden "sharp" pain
- Pain relieved when leaning forward
- Friction rub
- Excessive sweating
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Give 4 signs on examination found in PVD
- Pallor
- Absent pulses
- Cold
- Low ankle:brachial pressure index
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How might suspected peripheral vascular disease be investigated?
- US doppler to find atherosclerosis
- X-ray angiogram
- CT angiogram
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Outline the acute management of critical limb ischaemia
- Exam and doppler US to assess ischaemia
- WHO ladder analgesia
- Surgical referral for revascularisation with angioplasty/stenting
- If revascularisation contra-indicated, amputation required
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What management options are available for PVD
- Supervised exercise
- Medical: Antiplatelet therapy, thrombolysis
- Surgical: Angioplasty/stenting/bypass/graft when severe
- If above not effective, naftidofuryl oxalate
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Give 5 features suggesting AAA rupture
- MEDICAL EMERGENCY: HIGH INDEX = NO INVESTIGATIONS
- Extreme general abdominal pain
- Hypotension
- Tachycardia
- Flank bruising
- Abdominal mass/rigid
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Give 5 risk factors for abdominal aortic aneurysm
- Male
- Increasing age
- Atherosclerosis
- Connective tissue disorders
- Trauma/surgery
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Outline the screening programme for AAA
- Men >65
- 10 minute US
- Conservative management if <5.5cm
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Outline the management options for AAA
- Lifestyle: Smoking
- Medication: HTN and dyslipidemia
- Surgical: Endovascular stent
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What is the prognosis for a ruptured aortic aneurysm?
- 1 in 3 fail to survive trip to hospital
- Emergency repair mortality 80%
- Compare with 5% mortality for elective repair
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Give 3 management options for varicose veins
- Conservative: Compression stockings, NSAIDs, dry skin
- Stripping: Removal of saphenous vein
- Ablation: Endovascular laser causes contraction
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Give 5 risk factors for varicose veins
- Female
- Increasing age
- Pregnancy
- Obesity
- Family history
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Give 4 features of an arterial ulcer
- 'Punched out' appearance
- Intensely painful
- Distal limb/digits
- Underlying fascia visible
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