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Year 3 Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

CVS DDx for chest pain

A
  • acute coronary syndrome
  • angina
  • aortic dissection
  • arrhythmia
  • valve disease
  • acute pericarditis (pleuritic)
  • cardiac tamponade
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2
Q

DDx for pleuritic chest pain

A
  • pneumonia
  • PE
  • pneumothorax
  • pericarditis
  • viral pleurisy
  • lung cancer
  • pleural effusion
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3
Q

GI DDx for chest pain

A
  • GORD
  • Peptic ulcer disease
  • gallstones
  • pancreatitis
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4
Q

Other DDx for chest pain (apart from CVS, pleuritic, GI)

A
  • MSK: trauma, costochondritis
  • anxiety: panic attack
  • functional: chest wall syndrome
  • shingles. Pain may come before rash
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5
Q

DDx for bilateral leg swelling

A
  • venous insufficiency
  • right heart, liver or renal failure
  • dependent oedema: effect of gravity when sitting for a prolonged period
  • pregnancy
  • calcium channel blockers
  • hypothyroidism
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6
Q

DDx for unilateral leg swelling

A
  • venous insufficiency
  • DVT
  • Cellulitis
  • lymphoedema
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7
Q

Causes of atrial fibrillation

A

PIRATES
* Pulmonary: PE, pleural effusion, COPD, lung cancer, pneumonia
* Ischaemic heart disease: HTN, HF, cardiomyopathy, pericardial disease, myxoma
* Rheumatic valve disease and mitral stenosis
* Alcohol, smoking, caffeine
* Thyrotoxicosis
* Electrolyte abnormalities
* Sugar (diabetes), sepsis

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8
Q

Epidemiology of atrial fibrillation

A
  • most common arrhythmia, affecting 10% over 80 years old
  • more common in men
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9
Q

Symptoms of atrial fibrillation

A
  • palpitations
  • syncope
  • SOB
  • angina, reflecting age-related ischaemia
  • 20% are asymptomatic
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10
Q

Signs of atrial fibrillation

A
  • tachycardia
  • irregularly irregular pulse
  • hypotension
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11
Q

Investigations in atrial fibrillation

A

ECG
* absent P waves
* irregularly irregular RR interval

Blood
* FBC: anaemia may exacerbate HF
* U+E and TSH to look at cause
* Investigate other CV risk factors: lipids, glucose
* LFT and coag pre-warfarin

Imaging
* trans-thoracic echo
* CXR: may show HF

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12
Q

Indications for thrombophylaxis in atrial fibrillation

A
  • consider in all patients with chronic AF with a CHA2DS2-VASc >= 1 and weigh against bleeding risk with ORBIT score
  • important in any patient undergoing cardioversion
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13
Q

What drugs are used for thrombophylaxis in AF

A
  • Direct oral anticoagulants
  • Warfarin
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14
Q

Mechanism of action of DOACs

A
  • thrombin inhibitor: dabigatran
  • factor Xa inhibitors: rivaroxiban, apixaban, edoxaban
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15
Q

Indication for DOACs

A
  • non-valvular AF
  • DVT
  • PE
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16
Q

Mechanism of action of warfarin

A
  • vitamin K antagonist which works by inhibiting vitamin K1 reductase = reduces hepatic synthesis of clotting factors 2, 7, 9 & 10
  • onset takes a few days as clotting factors have half-life up to 80 hrs
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17
Q

Management of patients on warfarin

A
  • check FBC, LFT and coag at baseline
  • check INR initially after 48 hrs, then daily until in range (aim for 2.5 - 3.5)
  • monitor INR monthly
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18
Q

Contraindications for warfarin

A
  • bleeding disease
  • haemorrhagic stroke
  • active PUD
  • pregnancy
  • severe HTN
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19
Q

Drug interactions with warfarin

A

**Agents which raise levels
* abx: macrolides, metronidazole, ciprofloxacin, isoniazid
* CV: statins, amiodarone
* Psych: SSRIs, valproate
* omeprazole
* liver disease
* diet: acute alcohol, grapefruit, cranberry juice

Enzyme inducers lower levels (PC-BRAS)
* Phenytoin
* Carbamezapine
* Barbiturates
* Rifampicin
* Chronic Alcohol
* St Johns wort and smoking

Aspirin and NSAIDs
* increased bleeding due to antiplatelet effect**

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20
Q

Side effects of warfarin

A
  • bleeding
  • GI: nausea, vomiting, diarrhoea
  • hepatic: jaundice, hepatic jaundice
  • skin necrosis, especially with protein C or S deficiency
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21
Q

Rate control management in AF

A

1st line options
* beta blocker: metoprolol, bisobrolol
* rate-limiting CCB: verapamil, diltiazem
* consider digoxin if they are stationary

2nd line. combine any 2 of
* beta blocker, diltiazem, and/or digoxin

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22
Q

Rhythm control management in AF

A

Electrical cardioversion
* preferred choice if there is haemodynamic instability: SBP<90, syncope, acute HF, MI
* shock carried out under short-acting general anaesthetic, followed by second shock with higher joules if no success with first

Pharmocological cardioversion
* indications: if symptoms are milder and situation is less urgent. Bolus followed by infusion if AF continues. Again anticoagulate first.
* Flecainide or propafenone IV (class IC) if there is no structural heart disease.
* Amiodarone (class 3) if there is structural or IHD. given through central line

Maintaining long term rhythm control post cardioversion
* 1st line = beta blocker
* other options: amiodarone, sotalol, flecainide, propafenone

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23
Q

Complications of AF

A
  • stroke
  • acute HF and pulmonary oedema
  • cardiomyopathy and heart failure
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24
Q

What is a supraventricular tachycardia

A

tachycardia due to faulty impulse formation or conduction which is sustained by tissue about the ventricle

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25
Q

signs and symptoms of SVT

A
  • palpitaions
  • dizziness
  • SOB
  • chest pain
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26
Q

Investigations for SVT

A

ECG
* HR>100 bpm
* QRS: narrow complex. wide in WPW
* P waves: sinus tachy = +ve in all leads except aVR; atrial tachy = inverted (ectopic), varying morphology (multifocal), sawtooth (atrial flutter), or absent (AF); junctional tachy = inverted, hidden within QRS and/or following QRS

Echo
* usually normal
* if there is LVF, then increased risk of sudden cardiac death and class 1 drugs are contraindicated

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27
Q

Acute management of SVT

A
  • Vagal maneuvers: carotid sinus massage
  • IV drugs: 1st line adenosine, 2nd line verapamil, 3rd line beta blocker, flecainide, or amiodarone
  • if haemodynamically unstable or atrial flutter, 1st line synchronised electrical cardioversion
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28
Q

ECG findings in ventricular tachycardias

A
  • HR is usually 150-250
  • broad QRS (>0.12s)
  • QRS complex can be monomorphic or polymorphic
  • signs of AV dissociation
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29
Q

Management of ventricular tachycardia

A

In cardiac arrest
* VF and pulseless VT are shockable rhythms

If there is a pulse VT is treated with
* synchronised DC shocks if unstable, followed by amiodarone 300mg IV over 20 mins, further shock, then amiodarone 900mg over 24h
* straight to amiodarone IV if stable

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30
Q

What is sinus bradycardia?

A

sinus rhythm <60 bpm

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31
Q

Causes of sinus bradycardia

A
  • myocardial: inferior MI, myocarditis
  • CV drugs: beta blockers, alpha agonists, rate limiting CCBs, digoxin, amiodarone
  • CNS drugs: opioids, benzodiazapine
  • sick sinus syndrome
  • metabolic: hyperkalaemia, hypothyroidism, hypothermia
  • physiological staes: high levels of fitness, pain
  • anorexia nervosa
  • cushings reflex: response to increased ICP
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32
Q

What is sick sinus syndrome

A
  • aka sinus node dysfunction
  • usually due to idiopathic SA node fibrosis
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33
Q

Presentation of sinus bradycardia

A

often asymptomatic. otherwise:
* syncope
* fatigue
* palpitations

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34
Q

Causes of atrioventricular (AV) block

A
  • idiopathic
  • RCA infarct (as this supplies the AV node)
  • myocarditis
  • drugs: beta blockers, CCBs, adenosine, digoxin, cholinesterase inhibitors
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35
Q

how does type 1 heart block present on an ECG

A

Prolonged PR interval (>0.2 seconds = 5 small squares)
NOTE: no treatment required

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36
Q

How does 2nd degree heart block - Mobitz type 1 present on an ECG

A

Progressively prolonged PR interval until a P wave fails to transmit to the ventricles
NOTE: no treatment required

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37
Q

How does 2nd degree heart block - Mobitz type 2 present on an ECG

A

constant PR interval but intermittent failure to transmit to the ventricles
NOTE: high risk of progression to 3rd degree block so often requires pacemaker treatment

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38
Q

How does 3rd degree heart block present on an ECG

A
  • No transmission of P waves into ventricles, with a ventricular escape rhythm taking over
  • QRS is usually wide
  • HR 20-40

NOTE: this requires a pacemaker

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39
Q

Causes of left bundle branch block

A
  • anterior MI (LAD)
  • HTN
  • myocarditis
  • cardiomyopathy
  • aortic valve disease
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40
Q

How does left bundle branch block present on ECG

A
  • broad QRS (>120ms)
  • Dominant S wave in V1
  • Broad monophasic R in lateral leads (I, aVL, V5-6)
  • Absence of Q waves in lateral leads
  • Prolonged R wave peak time >60ms in leads V5-6
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41
Q

Causes of right bundle branch block

A
  • increased RV pressure: primary pulmonary HTN, cor pulmonale
  • acquired heart disease: anterior MI (LAD), myocarditis, cardiomyopathy
  • congenital
  • iatrogenic e.g. cardiac catheterisation
  • can also be a normal ECG variant in healthy individuals
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42
Q

How does right bundle branch block present on an ECG

A
  • QRS duration >120ms
  • RSR’ pattern in V1-3 (M shaped QRS complex)
  • Wide slurred S wave in lateral leads (I, aVL, V5-6)
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43
Q

Acute management of bradycardia

A
  1. atropine 500 mcg IV if there is cardiac ischaemia, syncope, SBP <90, or HF
  2. Further measures if there is inadequate response or risk of asystole: further atropine (up to 3mg), transcutaneous pacing, adrenaline infusion, or isoprenaline infusion
  3. Definitive management with transvenous and/or permanent pacemaker (PPM)
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44
Q

Pathophysiology of stable angina

A
  • cardiac chest pain due to ischaemia
  • usually caused by atherosclerosis
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45
Q

Epidemiology of stable angina

A
  • affects 1/10 over 65 years old
  • more common in men
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46
Q

Signs and symptoms of stable angina

A

intermittent, stable chest pain with 3 classic features (ECG)
* Exertion as a precipitant
* Constricting discomfort of anterior chest, which may radate to neck, shoulders, jaw, or arms
* GTN or rest provides relief within 5 minutes

3/3 = typical angina, 2/3 = atypical angina, 1/3 = not angina

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47
Q

Investigations in stable angina

A

Basic tests:
* bloods: FBC (rule out anaemia), U&E (co-morbid CKD, ACEi baseline), and CVD risk factor investigations including BP, lipids, and glucose
* ECG: often normal, but may show ischaemic changes (Q waves or ST-T changes)

Diagnostic testing for IHD should be offered to all those with typical/atypical angina or an ischaemic ECG
* CT coronary angiogram (CTCA) is 1st line
* functional imaging using stress agent if CTCA is non-diagnostic: stress echo, myocardial perfusion scintigraphy, MR perfusion
* invasive angiography if functional imaging if functional imaging non-diagnostic

For those with known IHD with chest pain of unknown cause, consider:
* functional imaging
* exercise ECG. NOTE this is NOT recommended by NICE for initial diagnosis of IHD

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48
Q

Management of stable angina

A

Anti-anginals
* 1st line: beta blockers and/or CCBs. Use both if one is insufficient
* 2nd line: isosorbide mononitrate, nicorandil, ivabradine, ranolazine. Can be used as a monotherapy or in combination with 1st line
* consider revascularisation if not controlled by 2 drugs. PCI for 1 or 2 vessels; CABG for left main or triple vessel disease.

Short-acting nitrate
* GTN spray or sublingual tablet
* use before planned activity and when symptomatic
* if pain continues for 5 minutes after 1st dose, call ambulance and take 2nd dose
* side effects: headache, flushing and light headedness

CVD prevention
* aspirin for all (clopidogrel 2nd line), and consider statins and ACEi
* lifestyle changes, through simple advice as part of cardiac rehab, including exercise (30 mins per day but below anginal threshold), healthy weight, stop smoking, and Mediterranean diet

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49
Q

Pathophysiology of acute coronary syndrome

A

rupture of atheromatous plaque in coronary artery –> thrombus formation –> vessel occlusion locally or elsewhere in the heart

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50
Q

Types of acute coronary syndrome

A
  • unstable angina: prolonged severe angina, usually at rest, possibly with ECG changes.
  • NSTEMI: raised troponins and ischaemic symptoms or ECG changes
  • STEMI: raised troponins and ST elevation on ECG
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51
Q

Symptoms of acute coronary syndrome

A

Evaluate chest pain using SOCRATES
* Site: central
* Onset: usually sudden, but can be more gradual
* Character: tight, crushing, but not sharp
* Radiation: left arm, neck, jaw
* Associated symptoms: sweating, clamminess, SOB, dizziness, faint, angor animin (impending sense of doom)
* Timing: duration >15 mins
* Exacerbating factors: exertion, emotion, eating.
* Severity: high

Atypical presentation seen in elderly or diabetics
* little or no chest pain
* SOB
* sweating
* nausea and vomiting
* sometimes no symptoms at all

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52
Q

Signs of acute coronary syndrome

A
  • HR and BP may be increased or decreased
  • pallor
  • S3 or S4 heart sounds (especially in STEMI)
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53
Q

Investigations in acute coronary syndrome

A

ECG
* Do immediately, and if negative repeat after 20mins if pain continues or suspicion high

Troponin T or I
* test on admission and at 3-6 hrs. troponin peaks at 12-24 hrs, then declines over 10 days
* values >99th centile are diagnostic of acute MI. STEMI diagnosis is initially from the ECG alone so as not to delay treatment

Other investigations
* FBC: anaemia may exacerbate heart strain, and baseline Hb and PLT needed before anticoagulation
* U+E: baseline before anticoagulants and ACEi, and screens for co-morbid renal disease from HTN
* Glucose: tight control improves outcomes
* Lipids: check on admission, as cholesterol can dip 24hrs post-MI
* CXR: rule out other causes and check for HF
* Exercise tolerance test: consider in low risk patients

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54
Q

ECG findings in STEMI

A

Changes over time
* Acute: peaked T waves (<5 mins) then ST elevation (<20 mins). Resolve in hours to days.
* Within days: Q waves then T wave inversion
* Long term: Q waves, ST changes

Leads affected based on territory
* inferior MI (RCA): II, III, aVF
* anterior MI (LAD): V1-4
* lateral MI (circumflex): I, aVL, V5-6

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55
Q

ECG findings in NSTEMI or unstable angina

A
  • ST depression and/or T-wave inversion
  • unlike STEMI, difficult to localise lesion based on ECG
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56
Q

Management of acute coronary syndrome

A

Initial medical treatment
* dual antiplatelet therapy: aspirin and P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel). Loading doses for both
* analgesia PRN: morphine IV and/or nitrates
* other therapies: oxygen if hypoxemic, beta blockers IV if tachycardic/hypertensive (but not if unstable)

Anticoagulation
* unfractionated heparin in those going gor immediate or early angiography
* fondiparineux or enoxaparin SC for those without angiograpyh planned

Reperfusion for STEMI presenting within 12 hrs of onet
* immediate (within 90-120 mins) primary PCI
* if PCI not available within 120 mins, consider thrombolysis (alteplase, reteplase) and transfer to PCI centre
* patients presenting beyond 12 hrs are essentially managed like NSTEMI

Reperfusion in NSTEMI or unstable angina
* angiography +/- revascularisation within 72 hrs if 6 month mortality risk >3% as per GRACE or TIMI score. Revascularisation is usually PCI, but sometimes CABG if left main or triple vessel disease
* immediate PCI if unstable, refractory chest pain, or acute severe heart failure
* conservative management otherwise

Further management - start BAGS within 24 hrs
* Beta blocker PO, metoprolol, atenolol
* ACEi
* maintain Glucose <11mmol/L
* Statin

Further management - Other issues
* anticoagulation is usually stopped post-PCI, or continued until discharge in those managed without reperfusion. However, it is continued for 3 months in anterior MI
* Discharge on CVD secondary prevention medication and offer cardiac rehab
* avoid NSAIDs, especially diclofenac

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57
Q

Prognosis of acute coronary syndrome

A

1/3 MIs are fatal: 20% pre-hospital, and a further 10% within 30 days

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58
Q

Complications of acute coronary syndrome

A

Electrical
* heart block or sinus bradycardia post anterior MI
* Bundle branch block
* ventricular fibrillation

Structural
* acute mitral regurg
* papillary muscle rupture
* ventricular septal rupture
* ventricular aneurysm

Inflammatory
* peri-infarction pericarditis
* Dressier’s syndrome: pericarditis weeks later

Heart failure

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59
Q

CVD risk calculation

A
  • 10 year risk of MI or stroke can be quantified using QRISK2 or the Framingham risk equation
  • Those with previous CVD automatically have a 10 year risk >30%
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60
Q

CVD prevention - lifestyle

A
  • weight loss and dietary change. The Mediterranean diet (fruit, veg, olive oil, fish). Also recommend reducing sugar intake and replacing starch with wholegrains
  • Physical activity: 150mins/week moderate activity
  • smoking cessation
  • reduce alcohol intake: =<14 units/week
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61
Q

CVD prevention - medical

A

Secondary prevention post-ACS
* Beta blocker
* ACEi, aiming for BP 140/90
* Aspirin for life
* Clopidogrel or ticagrelor for 1 year after an ACS
* Statin: high dose e.g. atorvastatin 80mg

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62
Q

What is heart failure

A

1/70

63
Q

What is heart failure

A

it is when the heart fails to provide adequate blood flow to meet body’s needs

64
Q

Types of heart failure

A
  • LEFT VENTRICULAR FAILURE
    1. heart failure with reduced ejection fraction (HFrEF)
    2. heart failure with preserved ejection fraction (HFpEF)
  • RIGHT VENTRICULAR FAILURE
  • CONGESTIVE HEART FAILURE
  • HIGH OUTPUT HEART FAILURE
65
Q

What is HFrEF

A
  • left ventricular ejection fraction <40%
  • also known as systolic heart failure
66
Q

Causes of HFrEF

A
  • IHD/MI
  • HTN
  • Diabetes
  • Dilated cardiomyopathy
  • valve disease
  • arrhythmias
  • drugs or alcohol
67
Q

What is HFpEF

A
  • LV relaxation failure –> inadequate filling –> decreased stroke volume despite normal ejection fraction (>= 50%)
  • also known as diastolic heart failure
68
Q

Causes of HFpEF

A
  • HTN
  • diabetes
  • constrictive pericarditis
  • cardiac tamponade
  • restrictive cardiomyopathy
69
Q

Causes of right ventricular failure

A
  • cor pulmonale: primary lung disease (e.g. COPD) –> vasoconstriction in poorly ventilated lung tissue to correct lower V/Q –> pulmonary HTN –> RVF
  • LVF –> pulmonary HTN –> RVF
  • pulmonary valve stenosis
70
Q

What is congestive heart failure

A

heart failure with fluid overload, especially pulmonary oedema

71
Q

What is high output heart failure

A

Normal heart but increased needs. Due to:
* anaemia
* pregnancy
* hyperthyroidism

72
Q

Respiratory symptoms of LVF

A
  • SOB
  • Orthopnea. Aksk how many pillows they sleep with
  • paroxysmal nocturnal dyspnoea and nocturnal cough
  • pink frothy sputum
  • wheeze
73
Q

non-respiratory symptoms of LVF

A
  • Palpitations
  • poor exercise tolerance
  • fatigue
  • reduced weight (cachexia) or increased weight (fluid retention)
74
Q

signs of LVF

A
  • crackles
  • S3 heart sound, S4 more common in diastolic HF
  • Murmurs
  • cachexia
  • cold peripheries
  • displaced apex
75
Q

Symptoms of RVF

A
  • liver congestion leads to nausea, anorexia, early satiety, right upper quadrant pain
  • epistaxis
  • nocturia: on lying flat, fluid builds up from legs to kidneys
76
Q

signs of RVF

A
  • raised JVP
  • peripheral oedema
  • ascites
  • hepatomegaly
  • right ventricular heave due to pulmonary HTN
77
Q

Investigations for diagnosis of heart failure

A
  • Screen with BNP or NT-proBNP, and proceed to transthoracic echo if elevated. Consider going straight to echo if there is a prior history of MI
  • If diagnosis not clear after echo, consider further tests: cardiac MRI, transoesophageal echocardiography
  • HFrEF diagnosis: {signs and symptoms of HF} + {echo or MRI evidence of EF <40%}
  • HFpEF diagnosis: {signs and symptoms of HF}+{EF>=50%}+{raised BNP/NT-proBNP} + {structural or functional heart disease such as left ventricular hypertrophy or left atrial enlargement}
78
Q

Investigations in heart failure

A

Bloods
* FBC: anaemia may mimic or exacerbate symptoms
* U+E and LFTs: liver and kidney function can be affected in HF, and they are a differential for fluid retention
* TFT: thyrotoxicosis can cause high output failure, while hypothyroidism may cause symptoms of fatigue and oedema
* investigate cardiac RFs: cholesterol, blood glucose

CXR
* may show cardiomegaly and pulmonary oedema

ECG
* abnormal in 80%
* usually non-specific changes
* LVF: ST depression and T inversion in V5-6
* RVF: ST depression or T inversion in V1-3

79
Q

Lifestyle and preventative measures in heart failure

A
  • refer all stable patients to cardiac rehab
  • stop smoking
  • flu and pneumococcal vaccination
  • monitor weight and fluid balance, advise moderate fluid restriction. Get help if rapid gain
  • treat comorbidities such as IHD, AF, and dyslipidaemia
80
Q

Pharmacological management for HFrEF

A

Most patients are on four agents, all of which except diuretics have a mortality benefit
* ACEi - any one should be offered to all, and titrated to evidence-based dose. ARB if intolerant
* beta blockers - bisoprolol, metoprolol - should also be offered to all and titrated to evidence-based dose
* diuretics - loop (furosemide) or thiazides - if there is fluid overload
* mineralcorticoid receptor antagonists - spironolactone should be added if patient remains symptomatic. Given to block effects of aldosterone on the heart as opposed to diuretic effect

81
Q

Interventional and surgical management in HFrEF

A
  • cardiac resynchronisation therapy
  • implantable cardioverter defibrillator
  • LV assist devices
  • transplant if end-stage and no other options
82
Q

Management of RVF and HFpEF

A
  • Symptomatic relief with diuretics, management of co-morbidities, and lifestyle changes
  • long term oxygen therapy is beneficial in cor pulmonale
83
Q

Drug contraindications in HF

A
  • NSAIDs, especially diclofenac. Low dose aspirin is OK
  • Steroids
  • Most CCBs, especially rate-limiting
  • Pioglitazone
  • TCAs
  • beta agonists
84
Q

Prognosis of heart failure

A

Death
* usually due to arrhythmia or pump failure
* 30% in 1 year, 50% in 5 years

85
Q

Epidemiology of Aortic stenosis

A
  • most common valve disease
  • affects 4% of elderly
86
Q

Causes of aortic stenosis

A
  • calcification
  • congenital: bicuspid valve
  • rheumatic valve disease
87
Q

Symptoms of aortic stenosis

A

SAD
* Syncope, which may occur on exertion
* Angina
* Dyspnoea on exertion

88
Q

Signs of aortic stenosis

A
  • ejection systolic murmur: best heard in aortic and left sternal area, radiating to carotids, loud on expiration
  • slow rising pulse
  • narrow pulse pressure
  • non-displaced but sustained/heaving apex, lasting >50% of systole
  • aortic thrill
89
Q

Initial tests in aortic stenosis

A
  • Echo with doppler: confirms diagnosis and assesses severity
  • ECG: LVH, LBBB, poor R wave progression
  • CXR is usually normal, otherwise: LVH, calcified valve, dilated ascending aorta
90
Q

Further investigations in aortic stenosis

A
  • Cardiac MRI, stress testing, angiography or catheterisation if indicated
  • Multi-slice CT can help evaluate severity
  • BNP may proved prognostic information
91
Q

Medical management of aortic stenosis

A
  • modify cardiovascular risk factors
  • treat any secondary heart failure
  • 6 monthly echo if severe
92
Q

Surgical management of aortic stenosis

A
  • Surgical aortic valve replacement
  • transcatheter aortic valve implantation
  • balloon valvuloplasty
93
Q

Complications of aortic stenosis

A
  • LVF or CHF
  • Aortic root dilation due to haemodynamic changes around valve
  • infective endocarditis
  • sudden cardiac death
94
Q

Prognosis of aortic stenosis

A
  • asymptomatic: 1 year mortallity 1%
  • symptomatic: 1 year mortality 25% or 50% if high risk
  • poor prognostic factors: age, IHD, raised BNP
95
Q

Chronic causes of aortic regurgitation

A
  • congenital: bicuspid valve
  • aortic root dilation: Marfan’s, Ehlers-Danlos
  • Inflammatory: SLE, RA or seronegative arthritis, rheumatic heart disease, syphilis
  • appetite suppressants
  • HTN
96
Q

Acute causes of aortic regurgitation

A
  • infective endocarditis
  • aortic dissection
97
Q

Symptoms of aortic regurgitation

A
  • LVF symptoms: SOB, orthopnea, PND
  • Sense of pounding heart beat, worse on lying down on left side
98
Q

Signs of aortic regurgitation

A
  • murmur: high-pitched early diastolic murmuer, aortic and left sternal area
  • collapsing pulse
  • wide pulse pressure
  • hyperdynamic apex beat
  • eponymous signs: visible carotid pulsation (Corrigan’s sign), head nodding with beat (de Musset’s sign), capillary pulsation in nail bed (Quincke’s sign)
99
Q

Investigations in aortic regurgitation

A
  • echo is diagnostic
  • ECG: LVH
  • CXR: LVH, dilated ascending aorta
  • multi-slice CT may help visualise aortic root dilation in Marfan’s
100
Q

Management of aortic regurgitation

A
  • Manage LVF if present: ACEi (especially in HTN), beta blockers (especially in Marfan’s)
  • Monitor: regular echo, 6 monthly if severe or every 2 years if mild-moderate
  • Surgery indications: severe AR with symptoms or LVF. Threshold is lover if there is underlying disease such as Marfan’s or bicuspid valve
101
Q

Primary causes of mitral regurgitation

A
  • mitral valve prolapse (causes 50%)
  • calcification
  • rheumatic heart disease
  • infective endocarditis
  • congenital
  • papillary muscle rupture due to MI
  • appetite suppressants
  • trauma
102
Q

secondary causes of mitral regurgitation

A
  • LV dilation due to IHD
  • Dilated cardiomyopathy
  • HCM
  • Aortic regurgitation
103
Q

symptoms of mitral regurgitation

A
  • SOB
  • fatigue
  • chest pain
  • LVF symptoms
  • symptoms of AF
104
Q

Signs of mitral regurgitation

A
  • pansystolic murmur heard at apex, radiates to axilla
  • hyperdynamic apex beat
  • systolic thrill over apex
  • soft S1
  • LVF signs: S3, crackles
105
Q

Investigations for mitral regurgitation

A
  • Echo is diagnostic

ECG
* AF
* P-mitrale if in sinus rhythm
* LVH

CXR
* enlarged left ventricle and atrium: double right heart border
* valve calcification

Further tests
* cardiac MRI, angiography, and cathetisation, if indicated
* BNP may be provide prognostic information

106
Q

Medical management of mitral regurgitation

A
  • manage AF and HF if present
  • manage acute MR as acute heart failure with the addition of sodium nitroprusside to reduce afterload, and intra-aortic balloon pump if hypotensive
  • 6-monthly follow up and annual echo if severe
107
Q

Surgical management of mitral regurgitation

A
  • indications: symptomatic MR, acute severe MR, or MR complications
  • Procedure: open repair is 1st choice. Valve replacement or percutaneous repair are other options
  • anticoagulation: 3 months after valve repair or bioprosthetic replacement, lifelong after metallic replacement
108
Q

Complications of mitral regurgitation

A
  • structural changes: left ventricular and atrial enlargement, CHF
  • pulmonary HTN
  • AF
  • infective endocarditis
109
Q

Prognosis of mitral regurgitation

A

5 year mortality in severe asymptomatic MR: 20%

110
Q

causes of mitral stenosis

A
  • rheumatic valve disease
  • calcification
  • autoimmune: RA, SLE
  • carcinoid syndrome
  • congenital
111
Q

Symptoms of mitral stenosis

A
  • SOB, orthopnoea, PND
  • Haemoptysis
  • pink frothy sputum
  • fatigue
  • features of AF
  • RVF symptoms
  • hoarseness from recurrent laryngeal nerve compression
112
Q

signs of mitral stenosis

A
  • mid-diastolic murmur heard at apex with bell. Follows opening snap in early diastole
  • loud S1
  • Tapping apex beat
  • Malar flush
  • RVF signs
113
Q

Investigations in mitral stenosis

A
  • Echo is diagnostic

ECG
* AF
* P-mitrale if in sinus rhythm
* RVH

CXR
* enlarged left atrium: double right heart border
* valve calcification

114
Q

Medical management of mitral stenosis

A
  • anticoagulation if there is AF, thrombus in left atrium or prior thrombus
  • diuretics or long-acting nitrates for SOB, and beta blockers or rate-limiting CCBs to improve exercise tolerance
  • annual echo
115
Q

Surgical management of mitral stenosis

A
  • indications: severe symptoms or complications
  • percutaneous balloon mitral commissurotomy is 1st line
  • other options: valve replacement
116
Q

Complications of mitral stenosis

A
  • left atrial enlargement –> oesophageal and recurrent laryngeal nerve compression, AF
  • pulmonary HTN, RVF, tricuspid or pulmonary regurgitation
  • infective endocarditis
117
Q

Location of pain and affected arteries in peripheral vascular disease

A
  • upper 2/3 of calf = superficial femoral artery
  • buttock and hip = aortic and iliac artery
  • Thigh = iliac or common femoral artery
  • Lower 1/3 of calf = popliteal artery
  • foot = tibial or peroneal artery
118
Q

Signs and symptoms of chronic PVD

A

Claudication
* predictable, unrelieved pain on exertion caused by ischaemia of the muscles, which is relieved by rest

Critical limb ischaemia
* rest pain, unrelieved by medication for >= 2 weeks and/or evidence of tissue loss (ulcer or gangrene)
* pain is in the feet and toes rather than calves. Worse at night due to reduced gravitational pull

119
Q

Fontaine classification for chronic PVD

A
  1. asymptomatic
  2. intermittent claudication. 2a if stop >200m, 2b if <200m
  3. rest or nocturnal pain
  4. necrosis/gangrene
120
Q

Signs and symptoms of acute limb ischaemia

A

Presents with 6 Ps
* Pain at rest
* Pulseless
* Pale
* Paraesthesia
* Perishingly cold
* Paralysis is a late feature suggesting irreversible damage

121
Q

Investigations for PVD

A

Diagnose with ankle-brachial pressure index (ABPI)
* the ratio of systolic blood pressure at the ankle and arm, measured using doppler US
* procedure: take after 10 mins at rest, and use the sides with the highest measurements
* Results: roughly<0.9 is claudications, <0.6 is rest pain, <0.3 is impending gangrene

Cardiovascular examinations
* ECG
* Lipids
* glucose
* BP

Duplex US
* combines usual grayscale US image with colour-doppler US to visualise flow
* helps determine site of disease

Angiography if surgery considered
* MR angio is good choice when available
* CT angio is better for showing wall abnormalities
* Intra-arterial digital subtraction angiogram (invasive) = gold standard

122
Q

Conservative and medical management of PVD

A
  • Advise patient to keep active. Can refer to exercise rehabilitation programme
  • CVD prevention. Clopidogrel is 1st line antiplatelet therapy in PVD
  • Foot care
  • vasodilator naftidrofuryl can slightly increase walking distance
123
Q

Surgical managetment of PVD

A

Revascularisation
* surgical bypass, radiological angioplasty and stenting
* acute limb ischaemia: heparin IV and then embelectomy

Amputation
* last resort, considered in patients with ulceration and gangrene

124
Q

Complications of PVD

A
  • arterial ulcers
  • gangrene
  • amputation
125
Q

Pathophysiology of cardiac tamponade

A

fluid in pericardial sac accumulates until increased pressure causes reduced ventricular filling and reduced cardiac output

126
Q

Causes of cardiac tamponade

A

TAMP
* Trauma
* Aortic dissection
* Medical (iatrogenic)
* Pericardial effusion

127
Q

Signs and symptoms of cardiac tamponade

A
  • Beck’s triad: hypotension, reduced heart sounds, raised JVP
  • tachycardia
  • pulsus paradoxus: hypotension with inspiration
128
Q

Investigations in cardiac tamponade

A
  • ECG: tachycardia, low voltage
  • CXR: large cardiac sillhouette
  • Echo
129
Q

Management of cardiac tamponade

A

urgent pericardiocentesis

130
Q

Causes of HTN

A

Primary
* essential HTN
* Non-pathologically raised during pain or anxiety

Kidney disease
* chronic kidney disease
* renal artery stenosis

Endocrine
* Conn’s
* Cushing’s
* Phaemochromocytoma
* Acromegaly
* Hyperparathyroidism

Other
* obstructive sleep apnoea
* pregnancy or pre-eclampsia
* aoarctation of the aorta

Medication (CE-LESS)
* Cyclosporin
* Estrogen (OCP)
* Liquorice
* EPO
* Steroids
* Sympathomimetics

131
Q

Signs and symptoms of HTN

A
  • Symptoms of HTN itself are rare, and only occur in severe disease: headache, blurred vision

Symptoms suggesting secondary cause
* postural hypotension
* palpitations
* sweating

Only notable signs is hypertensive retinopathy

132
Q

How is hypertensive retinopathy graded

A
  1. Silver wiring and tortuosity
  2. AV nipping
  3. Cotton wool spots and flame haemorrhages
  4. Papilloedema
133
Q

Investigations for HTN

A
  • Measure BP

Check for organ effects:
* eyes
* heart: LVF on ECG. CXR and echo are optional
* kidney: urine dip, U+E, protein:creatinine ratio

Calculate 10 year CVD risk by checking
* glucose
* lipids
* using clinic BP measurement

If age<40, investigate underlying causes
* renal artery stenosis: kidney duplex USS
* CKD: urinalysis, U+E
* Endocrine: metadrenalines, cortisol, renin/aldosterone

134
Q

Stage 1 HTN criteria

A

Clinic BP >=140/90 and A/HBPM >=135/85

135
Q

Stage 2 HTN criteria

A

Clinic BP >=160/100 A/HBPM >=150/95

136
Q

Severe HTN criteria

A

Clinic BP >=180 systolic or >= 120 diastolic

137
Q

Stepwise medical treatment in hypertension

A

Step 1: ACEi or ARB or CCB
* ACEi/ARB if <55 yrs old and non-black, or diabetic. Switch to ARB if ACEi causes cough
* CCB if >55yrs and non-diabetic or black
* common drug choices: lisinopril (ACEi), losartan (ARB), amlodipine (CCB)

Step 2: ACEi/ARB +CCB
* ARB not ACEi if black
* Thiazide-like diuretic is an alternative 2nd agent

Step 3: ACEi/ARB + CCB + thiazide-like diuretic
* thiazide-like (indapimide) is preferred to thiazide

Step 4: Diagnose resistant HTN, consider spironolactone
* confirm BP using A/HBPM, check for postural hypotension, check adherance
* spironolactone if K+ =<4.5, alpha or beta blocker if K+ >4.5

138
Q

Other considerations for HTN management

A
  • monitor BP annually in clinic
  • HTN during pregnancy: labetalol, methyldopa, nifedipine
139
Q

BP targets in HTN

A
  • <80 yrs: 140/90
  • > = 80 yrs: 150/90
140
Q

Complications of HTN

A
  • All major CVD: MI, stroke, PVD, HF, AF
  • hypertensive crisis
  • aortic aneurysm +/- dissection
  • hypertensive nephropathy
141
Q

Signs of hypertensive crisis

A
  • papilloedema
  • retinal haemorrhage
142
Q

Management of hypertensive crisis

A
  • labetalol IV or nitroprusside IV
143
Q

Causes of primary dyslipidaemia

A
  • familial hyperchylomicronaemia (T1)
  • familial hypercholesterolaemia (T2a)
  • familial combined hyperlipidaemia (T2b)
  • familial remnant hyperlipidaemia (T3)
  • familial hypertriglyceridaemia (T4)
144
Q

Causes of secondary dyslipidaemia

A
  • obesity
  • sedentary lifestyle
  • diabetes
  • endocrine: hypothyroidism, hypopituitarism
  • hepatic: alcohol excess, cholestasis
  • renal: nephrotic syndrome, CKD
  • others: pregnancy, anorexia, gout, antipsychotics
145
Q

Signs of dyslipidaemia

A
  • eyelids: xanthelasma
  • eyes: corneal arcus and retinal deposits
  • tendon xanthoma
  • palmar xanthoma
146
Q

Investigations in dyslipidaemia

A

Lipid profile
* non-fasting sample is acceptable
* measured variables = total cholesterol, HDL, TG
* apolipoprotein levels may also help assess risk and guide treatment

Other = exclude secondary cause
* kidney disease: U+E, urinalysis
* Others: LFT, TFT, glucose, uric acid

147
Q

Management of dyslipidaemia

A
  • First consider and treat secondary cause: excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease, nephrotic syndrome
  • Consider a familial syndrome
  • Carry out a full CV risk assessment e.g. with QRISK
  • For primary prevention discuss benefits of lifestyle changes, and amange other CV risk factors before offering a stain
  • After these steps are taken, most patients still require a statin e.g. atorvastatin 20mg in primary prevention
148
Q

Mechanism of action of statins

A

HMG-CoA reductase inhibitor –> reduced cholesterol synthesis and increased cholesterol uptake into liver via LDL receptor

149
Q

Examples of statins

A
  • simvastatin
  • atorvastatin (1st line)
  • rosuvastatin
150
Q

Indications for statins

A

Isolated high cholesterol is not sufficient, they need factors for increased CVD risk or a familial syndrome
* existing CVD: IHD, stroke, TIA, PVD
* >=10% 10 year risk (QRISK2)
* T1DM and any one of: >40 yrs, >10 yrs duration, nephropathy or other CVD risk factors
* T2DM and >10% 10 year risk (QRISK2)
* CKD

151
Q

Management when using statins

A
  • start once daily in the evening, since that is when most cholesterol is synthesised

LFTs
* check at baseline and 3 and 12 months
* only stop if LFT rise 3x upper limit

Lipid levels
* check at 3 months, aiming for 40% reduction in non-HDL
* Consider increasing dose if not achieved

Myalgia:
* before starting stain: check CK if patient is complaining of muscle pain 7 if 5x upper limit, dont start on statin
* check CK if complaining of muscle pain after starting statin, rule out other causes and stop statin if 5x upper limit

152
Q

Side effects of statins

A
  • myalgia (increased CK)
  • hepatitis
  • rash
  • GI symptoms
  • altered sleep
  • diabetes
153
Q

Contraindications and interactions of statins

A
  • macrolides
  • azoles. stop statins if course is required
  • for simvastatin, max 20mg daily if on amlodipine or rate-limiting CCBs
  • Grapefruit juice

Year 3 Medicine (3 decks)

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