Cardiology Flashcards
1
Q
What is heart failure?
A
Definition – the inability of the heart to supply the needs of the body despite adequate filling pressure
2
Q
What is the New york heart association classification of heart failure?
A
Classification – New York Heart Association
1. NYHA Class I
• No symptoms
• No limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea, or palpitations
2. NYHA Class II
• Mild symptoms
• Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations, or dyspnoea
3. NYHA Class III
• Moderate symptoms
• Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
4. NYHA Class IV
• 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
3
Q
What is the difference between systolic and diastolic failure?
A
Systolic failure – inability of the ventricle to contract normally, resulting in reduced cardiac output. EF <40%. Caused by IHD, MI and cardiomyopathy
Diastolic failure – inability of the ventricle to relax and fill normally, causing increased filling pressure. Typically, EF>50% - HFpEF. Caused by ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity.
4
Q
Which side of the heart is most often involved in heart failure?
A
Most commonly this occurs in the left ventricle however it can occur in the right.
RVF and LVF can occur independently or together as CCF.
5
Q
What causes right heart failure?
A
Causes of RVF = LVF, pulmonary stenosis and lung disease (cor pulmonale).
6
Q
What signs and symptoms might you find in someone with chronic heart failure?
A
Chronic
• Dyspnoea
• Cough that may be worse at night associated with pink/frothy sputum
• Orthopnoea – breathlessness when lying flat
• Paroxysmal nocturnal dyspnoea- severe attack of breathlessness and coughing at night
• Wheeze
• Weight loss (may be hidden by weight gained from oedema)
• Bi-basal crackles on examination
• Displaced apex beat
• Low BP with narrow pulse pressure
7
Q
What signs and symptoms does right sided heart failure specifically cause?
A
Specific right sided HF Features = Raised JVP, hepatomegaly, peripheral oedema, ascites, nausea, facial enlargement, and epistaxis.
8
Q
What is acute heart failure?
A
Life-threatening worsening of HF can be de novo or decompensated HF. Precipitated by ACS, hypertensive crisis, acute arrhythmia and valvular disease.
9
Q
What symptoms might someone in acute heart failure present with?
A
- Breathlessness
- Reduced exercise tolerance
- Ankle swelling and general oedema
- Fatigue
- Elevated JVP
- Cyanosis
- Tachycardia
- Displaced apex beat
- Wheeze
- S3 heart sounds
- Pulmonary fine crackles
10
Q
How should someone with heart failure be investigated?
A
N-terminal pro-B-type natriuretic peptide (NT-proBNP) – always first line
• If ‘high’ then arrange specialist assessment and transthoracic echo within 2w
• If ‘raised’ then arrange specialist assessment and transthoracic echo within 6w
BNP produced by LV in response to strain and associated with poor prognosis
Routine bloods especially looking at eGFR
Chest X-ray
ECG
Cardiac MRI helps if echo not easily interpreted
Angiogram if suspicion of new coronary artery disease
11
Q
What can influence a BNP level to be higher or lower than normal other than heart failure?
A
BNP can however be influenced by other factors
Increased levels – LVH, ischaemia, tachycardia, RV overload, hypoxaemia, GFR <60ml/min, Sepsis, COPD, diabetes, Age > 70 and liver cirrhosis
Decreased levels – obesity, diuretics, ACEi, beta blockers, ARB and aldosterone antagonists
12
Q
How should someone in acute heart failure be managed?
A
- Sit up and give high flow oxygen
- IV access and monitor ECG – treat any arrhythmias
- Investigations as above
- Opiates pain medication, IV diamorphine
- IV Loop diuretics (no change in mortality)
- GTN spray unless systolic BP < 90
- If Systolic > 100 start infusion of isosorbide dinitrate
Consider Inotropic agents, CPAP and discontinue beta blockers
Once stable and improving – daily weights, change to oral furosemide, consider adding thiazide if on high dose and reassess chronic management
13
Q
How are patients with chronic heart failure with reduced ejection fraction managed, including general, pharmacological and surgical?
A
Lifestyle factors – better diet such as less salt, fat, and sugars
Annual flu vaccine and one-off pneumococcal vaccine
Treat cause if possible and exacerbating factors such as anaemia, thyroid and infections
Avoid NSAIDS and verapamil which worsen HF
Heart failure with reduced ejection fraction
1st line – ACE-I and/or beta blockers
2nd line – Aldosterone antagonists – spironolactone (be aware this and ACEi can cause hyperkalaemia)
3rd line – Ivabradine (inhibits the SAN) – criteria = sinus rhythm > 75 and LVEF < 35%
– Digoxin – does not improve mortality only symptoms, but useful if coexistent AF
– Hydralazine in combination with nitrate – useful in afro-Caribbean patients
– Cardiac resynchronization therapy – criteria = widened QRS
Defibrillator or ICD – due to tendency for VT and VF
Cardiac Transplant if suitable
14
Q
What is different about the management of heart failure with preserved ejection fraction?
A
Heart failure with preserved ejection fraction
Diuretics and treatment of hypertension, diabetes, AF and coronary artery disease
Cardiac Transplant if suitable
15
Q
What is acute coronary syndrome?
A
Umbrella term covering presentations of ischaemic heart disease (also known as coronary artery disease and coronary heart disease). This occurs as a result of build up of fatty plaques within the walls of the coronary arteries leading to gradual narrowing and the risk of rupture and clot formation.
16
Q
How is ACS classified into 3 types?
A
• Unstable Angina - no troponin release and no myocardial infarction
- Crescendo angina where increasing severity of symptoms over a few days provoked by decreasing exertion
- Angina that presents recurrently and unpredictably both at rest and at exertion
- Unprovoked and prolonged episodes of angina
- NSTEMI – troponin positive without ST elevation, caused by incomplete block/complete block with collateral supply but troponin rise
- STEMI – complete block without collateral supple troponin rise
17
Q
What are the risk factors for ACS?
A
Increasing age Male gender Family History Smoking Diabetes Hypertension Hypercholesterolaemia Obesity
18
Q
What are the clinical features of someone with ACS?
A
Tight/crushing/heavy/constricting, central/left-sided chest pain that can radiate up to the jaw or down to the arms (can be no pain in female patients, elderly or diabetics) Sweating, pale and clammy Tachycardia Nausea and Vomiting Shortness of breath (dyspnoea) Palpitations Cardiac failure Mitral regurgitation if papillary muscles affected
19
Q
How should someone with suspected ACS be investigated?
A
ECG and Cardiac enzymes (Troponin I and T and creatinine kinase)
In the ECG you should look for evidence of ischaemia
• New ST segment elevation (can only assess if in sinus rhythm and no BBB)
• New LBBB with broadened QRS
• Pathological Q waves
Echocardiogram evidence of new loss of viable myocardium
Coronary angiogram showing new intracoronary thrombus
LAD syndrome ECG shows deep T-wave inversion and biphasic T-waves (start positive then go negative)
20
Q
How does the location of ST elevation in an ECG suggest the location of a narrowing or occlusion?
A
Left anterior descending infarct = anterior territory = V1- V4
Left circumflex artery infarct = lateral territory = 1, aVL V5 and V6
Right coronary artery = inferior territory = 2, 3 and aVF
Note posterior MI may present with reciprocal ST depression and tall R waves in V1-2
21
Q
How is ACS managed acutely?
A
First line treatment follows the acronym MONAC:
Morphine 1-10 mg titrate to pain
Oxygen (if <94% sats)
Nitrates – Glyceryl Trinitrate (GTN given IV)
Aspirin 300mg and one of
• Clopidogrel 600mg if already on an anticoagulant
• Ticagrelor 180mg if undergoing fibrinolysis
• Prasugrel 60mg if undergoing PCI
Reperfusion therapy
PCI (percutaneous coronary intervention) = angioplasty followed by a stent
Thrombolysis with a fibrinolytic drug as well as antithrombin therapy to prevent further thrombus formation, for this use LMWH or fondaparinux unless angioplasty likely in the next 24 hours or creatinine >265umol/l then give unfractionated heparin.
22
Q
Once identified how are STEMIs managed?
A
PCI is gold standard if <12hrs since onset and available within 2hrs
If less than 12 hours from presentation and PCI not available within 2 hours, then thrombolysis followed by maintenance in hospital medications. After 90 minutes repeat ECG looking for 50% resolution in ST elevation. If inadequate resolution, then rescue PCI is superior to repeat thrombolysis. If successfully treated a follow up PCI is still beneficial.
23
Q
Once identified how are NSTEMIs and UA managed?
A
All patients should receive Aspirin
If unstable then immediately start MONA and proceed to PCI and high risk management
Add fondaparinux if no IMMEDIATE PCI planned, if creatinine > 265 or immediate PCI planned then give unfractionated heparin instead. Following this calculate the 6-month mortality GRACE score.
If low risk GRACE (= 3%) then conservative management, add in ticagrelor if not at high risk of bleeding or clopidogrel if they are
If high risk (>3%) then offer PCI within 72 hours (or immediately if unstable). Give unfractionated heparin regardless of whether they had fondaparinux or not. Add in prasugrel or ticagrelor if not taking an oral anticoagulant or clopidogrel if they are
24
Q
How should blood glucose levels be managed during ACS?
A
Hyperglycaemia should be managed with sliding scale insulin infusion with regular CBG monitoring to levels <11.1mmol/l.
25
What are the rules regarding driving in the following heart conditions and procedures?
```
ACS
ACS successfully treated by PCI
Elective angioplasty
Angina
CABG
Pacemaker insertion
ICD
Catheter ablation
Heart transplant
```
* No driving for 4 weeks unless successfully treated by angioplasty then it is 1 week
* Elective angioplasty – 1 week off driving
* Angina – cease driving if symptoms occur at rest/at the wheel
* CABG – 4 weeks off driving
* Pacemaker insertion – no driving for 1 week
* ICD – if for sustained Ventricular arrhythmia then stop driving for 6 months. If prophylactically then stop for 1 month. Group 2 driving not allowed with ICD.
* Catheter ablation – 2 days off driving
* Heart transplant – do not drive for 6 weeks
26
How do we prevent further ACS events in the future?
Aspirin (75mg) indefinitely and another antiplatelet for 12 months either Ticagrelor for if medically managed or Ticagrelor or Prasugrel if PCI
Anticoagulation until discharge
Beta blocker (If contraindicated Ca+ channel blocker such as verapamil or diltiazem)
ACEi if LV dysfunction, HTN or diabetes
Statin
Cardiac Rehabilitation
27
What is stable angina?
Constricting discomfort in the chest, neck, shoulders, jaw or arms precipitated by physical exertion and relieved by rest or GTN spray within 5 minutes. All 3 features = typical, 2 features = atypical.
28
How should suspected stable angina be investigated?
If diagnosis cannot be excluded by clinical assessment then 1st, 2nd and 3rd line investigations should be:
1. CT coronary angiography
2. Non-invasive functional imaging (e.g. myocardial perfusion scintigraphy/single photon emission computed tomography MPS/SPECT, stress echocardiography, contrast enhanced MRI or MRI imaging for stress-induced wall motion abnormalities
3. Invasive coronary angiography
29
What lifestyle modifications should patients make to managed stable angina?
```
Lifestyle modifications
Reduce weight
Reduce saturated fats and healthy diet
Stop smoking and drinking alcohol
Control diabetes, hypertension and cholesterol levels
Exercise regularly
```
30
How is stable angina managed pharmacologically?
Pharmacology
1. Aspirin
2. Statin
3. Sublingual GTN (tolerance often generated)
4. Beta blockers OR calcium channel blocker and increase to max dose as required
5. If no control gained, then use dual therapy.
For Ca+ blocker if used alone then use negative ionotropic and rate limiting such as verapamil or diltiazem, if used in combination with beta blocker then use long acting dihydropyridine such as MR nifedipine, amlodipine and felodipine DO NOT prescribe verapamil AND beta-blocker due to risk of complete heart block.
6. Long acting nitrate, ivabradine (reduced HR), nicorandil (vasodilator) or ranolazine.
Only add in 3rd drug with dual therapy whilst awaiting PCI or CABG
31
What side effects can patients expect from Ca+ blockers, beta blockers, nitrates, Ivabradine and Nicorandil?
Calcium channel blockers – headaches, flushing, ankle oedema and verapamil = constipation
Beta blockers – bronchospasm, fatigue, cold peripheries, sleep disturbance and dizziness
Nitrates – headache, postural hypotension and tachycardia
Ivabradine – visual effects, headache, bradycardia, and heart block
Nicorandil – headache, flushing and anal ulceration (CI in left ventricular failure)
32
What surgery can be used to managed stable angina?
Percutaneous coronary intervention
33
What is hypertension?
Definition – blood pressure above 140/90 that stays persistently high across multiple readings or a 24-hour average blood pressure reading > 135/85 measured by ABPM or HBPM
34
How are ambulatory and home blood pressure monitoring done?
Ambulatory blood pressure monitoring (2 measurement per hour whilst awake) or home blood pressure monitoring (BP measured morning and evening with 3 readings each time, repeat for 4-7 days, discard first measurement then use average of the rest).
35
What causes hypertension?
Primary – cause unknown (95% of cases)
Secondary
• Renal diseases e.g. glomerulonephritis, chronic pyelonephritis, PCKD and renovascular disease
• Endocrine disorders such as: primary hyperaldosteronism Conn’s syndrome (5-10%), Cushing’s, pheochromocytoma, acromegaly and congenital adrenal hyperplasia , Liddle’s syndrome and hyperthyroidism.
• Others e.g. coarctation of the aorta, pregnancy, NSAIDs, glucocorticoids, and drugs such as the COCP
36
How does hypertension present?
Asymptomatic unless >200/120 in which case headache, visual disturbance, and seizures
Hypertensive retinopathy, CKD, IHD
37
What investigations should be done on someone with hypertension?
U&E, Ca+ and urine dipstick looking for proteinuria and potassium levels
Fasting blood glucose or HbA1c and lipid levels to gauge overall risk
ECG, echo and renal US
Fundoscopy
38
When should patients be managed based on their stage of hypertension?
Stage 1 = ABPM/HBPM >/= 135/85 – treat <80yrs only if end organ damage, CVD, renal disease, diabetes, or 10-year cardiovascular risk >/= 10%. Consider treating all under 60yrs with stage 1 as Q risk may underestimate at this age group.
Stage 2 = ABPM/HBPM >/=150/95 – treat all patient regardless of age
Severe hypertension – clinical systolic >/= 180 or diastolic >/= 120 – admit to hospital if signs of retinal haemorrhage, papilloedema or life-threatening symptoms such as confusion, chest pain, heart failure or AKI. Also consider phaeochromocytoma. If none of these then arrange urgent investigations for end organ damage, if found start management immediately otherwise repeat BP measurement in 7 days
39
What lifestyle modifications should patients with hypertension be advised for?
Lifestyle Changes – eating more healthy foods, less salt, less caffeine, more exercise, stop smoking and drinking, less cholesterol and lose weight.
40
How is hypertension managed pharmacologically?
Pharmacological
1. Ace inhibitor or Angiotensin II receptor blockers (i.e. candesartan or losartan)
2. Add in a calcium channel blocker or a thiazide diuretic
3. Use all 3 (ACEi/A2RB, Ca+ blockers, and thiazide diuretic)
4. If K+ < 4.5 add in spironolactone if K+ > 4.5. add an alpha or beta blocker
If over 55 or Afro-Caribbean, then start on with calcium channel blocker and add A2RB later.
41
What are the common side effects of the 3 main drug classes used in hypertension?
Side effects
ACEi – cough, hyperkalaemia, and angioedema
Calcium channel blockers – flushing, ankle swelling and headache
Thiazide diuretics – hyponatraemia, hypokalaemia, hypercalcaemia, gout, impaired GTT, impotence and dehydration
A2RB – hyperkalaemia
42
What treatment target should we aim for in patients with hypertension?
Blood pressure targets
Age<80yrs = <140/90 or ABPM/HBPM < 135/85
Age > 80yrs = <150/90 or ABPM/HBPM < 145/85
43
What is Aliskiren?
Note new drug Aliskiren – direct renin inhibitor preventing conversion of angiotensin to angiotensin I. Similar affect on BP as ACEi but fewer SE, no mortality data yet.
44
What is malignant hypertension?
Rapid increase in blood pressure resulting in vascular damage. Typically seen with bilateral retinal haemorrhages and papilloedema. Very high mortality rate if not treated. Patients present with severe headaches, visual disturbances, BP over 200/130.
45
What complications can malignant hypertension lead to if left untreated?
This can precipitate AKI, heart failure, cerebral infarction, MI and encephalopathy. This is much more common in younger people and black people.
46
How should malignant hypertension be managed?
Patients should be treated immediately with IV labetalol or sodium nitroprusside with the aim of reducing their blood pressure by 15-20% within minutes to an hour and have a target BP of 160/120
47
What are the common cardiac and non-cardiac causes of arrhythmias?
Cardiac – IHD, structural changes, cardiomyopathy, pericarditis, and myocarditis
Non-cardiac – caffeine, smoking, alcohol, pneumonia, drugs and metabolic disturbance
48
How can arrhythmias present?
```
Palpitations
Chest pain
Syncope or pre-syncope
Hypotension
Pulmonary oedema
SOB
Asymptomatic
Exercise induced symptoms are concerning
```
49
What investigations should you order in someone you think has an arrhythmia?
12-lead ECG -stand alone
24-hour Holter monitor plus patient diary of when they feel palpitations. Can step up to external loop recorder or implantable loop recorder if still find nothing
Blood tests U&Es including Mg+ and Ca+, TFTs and FBC
Echocardiogram
Provocation tests
50
What are tachyarrhythmias?
These are arrhythmias (i.e. not sinus) that occur with a HR >100bpm.
51
How are tachyarrhythmias assessed and managed acutely?
```
Assess patient using ABCDE
Are adverse features present?
• Shock
• Syncope
• Myocardial infarction
• Heart failure
If yes, then unstable and require up to 3 Synchronised DC shocks
If this fails seek expert help. Give amiodarone 300mg IV over 10-20minutes then repeat a shock following this give Amiodarone 900mg over 24 hours.
```
If adverse features are not present, then must assess whether QRS complex is narrow (<0.12s) or broad (>0.12s).
52
How are regular narrow complex tachyarrhythmias managed?
In these the ventricles are being depolarised via the normal conduction pathway.
Attempt vagal manoeuvres such as:
• Carotid sinus massage whilst lying patient with head below their legs
• The Valsalva manoeuvre (blowing out against a closed airway i.e. shut mouth, pinch nose and attempt to expel air)
• Forced cough (pressure in chest stimulates vagus nerve)
• Push knees against the chest
• Stimulate the gag reflex
• Cold water treatment on the face
Failing this Adenosine is used to help visualize the underlying rhythm. Monitor ECG constantly and give rapid IV bolus followed by flush, start with 6mg, followed by 12mg and if still nothing can attempt with 12mg again.
If any of the above resolves the tachyarrhythmia, then it was likely a re-entry paroxysmal SVT such as Atrioventricular re-entry tachycardias AVNT like Wolf Parkinson White or Atrioventricular nodal re-entry tachycardia (AVRNT) which are circuits from within the AVN. A 12 lead should be recorded whilst they are in sinus rhythm, if they return back to the SVT then consider prophylactic anti-arrhythmic drugs
If sinus rhythm is not achieved, then seek expert help as this I likely Atrial flutter and needs rate controlling.
53
How are irregular narrow complex tachycardias managed?
This indicates it is probably AF in which case rate control should be achieved with a beta-blocker or diltiazem. If in heart failure consider digoxin or amiodarone. Assess risk of stroke and anticoagulate appropriately.
54
How are broad complex tachyarrhythmias managed?
In these the ventricles are being depolarised via the an abnormal conduction pathway.
Regular
If VT or the rhythm us unclear, then give amiodarone300mg IV over 20-60 minutes following by 900mg over 24 hours. If patient known to be SVT with a bundle branch block treat as for regular narrow complex tachycardia.
Irregular
Seek expert help and opinion. Possibilities include AF with bundle branch block in which case treat as for irregular narrow complex. If pre-excited AF then consider amiodarone. If Torsade’s de pointes (VT with a varying axis) long QT is a predisposing factor so give IV magnesium.
55
What are ventricular ectopics and when should they be investigated?
Define: bigeminy, trigeminy , couplet and triplet
Ventricular ectopics – common and can be symptomatic, pulse may feel irregular If frequently missing beats. On ECG the ectopic will appear as a broad complex QRS. Occasional ventricular ectopic very common in healthy individuals, if >60/hr require further investigation
1. Bigeminy – ectopic every other beat
2. Trigeminy – every third beat
3. Couplet – two ectopic together
4. Triplet – three ectopics together
56
What is atrial fibrillation?
Atria are beating in non-synchronous random way meaning there is a lack of P-waves and the ventricles only respond randomly when a signal gets through causing an irregular pulse. Cardiac output will decrease by 10-20% as ventricles are not primed by the atria.
57
What causes atrial fibrillation?
Cardiac: Ischaemic Heart Disease, hypertension, heart failure, and mitral valve disease
Other: PE, pneumonia, hyperthyroidism, caffeine, alcohol and post-op.
58
What are the clincial features of atrial fibrillation?
AF can be paroxysmal only occurring periodically, but this eventually becomes constant.
Asymptomatic or painful, palpitations, dyspnoea, feeling faint and LV failure
ECG findings – Irregularly irregular beat, lack of P waves and Tachycardic (Fast AF)
59
How should atrial fibrillation be managed acutely?
Acute
If haemodynamically unstable then electrical cardioversion should be given as an emergency
If <48 hours anticoagulate with heparin
Rhythm control with DC cardioversion or pharmacologically with amiodarone/flecainide if successful further anticoagulation is unnecessary
If > 48hours rate control with bisoprolol or diltiazem. Rhythm control can only be used >48hours if patient has been anticoagulated for >3 weeks first or a transoesophageal echo has been performed to exclude thrombus, then patient can be treated as if <48 hours.
Following DC cardioversion in AF >48 hours patients must be anticoagulated for at least 4 weeks, and then a decision is made based on individual risk.
60
How should atrial fibrillation be managed chronically?
Chronic AF can be paroxysmal (self-terminating), persistent (not self-terminating), or permanent (cannot be cardioverted or attempts to do so are inappropriate). Rate control and anticoagulation are the main treatment options. Use rhythm control only if younger than 65, symptomatic, first presentation, congestive heart failure or AF from corrected precipitant
Rate control – beta-blocker or rate limiting calcium channel blocker (diltiazem) 1st choice. If this fails, then add digoxin and then consider amiodarone. Aim for resting heart rate of <90bpm. Digoxin first line if co existent heart failure.
Rhythm control – Elective DC cardioversion, must do echo first to check for clots or anticoagulate for 3 weeks prior. Can also use elective pharmacological cardioversion with flecainide or amiodarone.
Catheter Ablation – use in those where medication is not acceptable or has not worked. Performed percutaneously and aims to ablate faulty electrical pathways. Requires anticoagulation 4 weeks prior and at least 2 months after.
61
Who needs long-term anticoagulation in atrial fibrillation and how is this decided?
Decision based on score from CHA2DS2-VASc for stroke risk and HAS-BLAD for bleeding. If CHADS-VAS score is 2 or more then anticoagulate everyone, in males with a score of 1 consider anticoagulation. A score of 0 indicates low risk of stroke and no anticoagulation is required however a transthoracic echo should be done to rule out valvular disease – which in combination with AF is an absolute indication for anticoagulation. A HAS-BLAD score >3 indicates a high bleeding risk.
62
What is atrial flutter?
Underlying atrial rate is 300 so ventricular rate will be a factor of 300 dependant on the level of AV block.
63
How is atrial flutter treated?
Treated in similar way to fibrillation except that DC cardioversion preferred to pharmacological. Recurrence also high so ablation is recommended for long term control.
64
How should you assess someone for atrial flutter?
Important to assess after slowing ventricular rhythm down to visualise the atrial depolarisations either with carotid sinus massage or adenosine.
65
What are heart blocks?
In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles.
66
Describe first-degree heart blocks
First-degree heart block
| PR interval > 0.2 seconds. Aasymptomatic first-degree heart block is relatively common and does not need treatment
67
Describe the two types of second-degree heart block
Second-degree heart block
1. Mobitz I, Wenckebach: progressive prolongation of the PR interval until a dropped beat occurs
2. Mobitz II: PR interval is constant, but the P wave is often not followed by a QRS complex
68
Describe the third-degree type of heart block or complete heart block
There is no association between the P waves and QRS complexes. The right coronary artery most commonly supplies AV node. Complete heart block is usually due to a degenerative disease in the elderly but can also be due to right coronary artery disease.
If SA node is not working, then a junctional rhythm from AV nodes takes over generally at about 30-50bpm in a regular bradycardia. You may not see a p wave as atria will contract at the same time as the ventricles.
69
How are heart blocks treated?
Heart blocks are treated using a dual lead pacemaker, one lead detects the atrial contraction the second stimulates the ventricles to contract as a result.
70
What is wolf parkinson white disorder?
Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF
71
What ECG features might you see in WPW disorder?
Possible ECG features include:
• Short PR interval
• Wide QRS complexes with a slurred upstroke - 'delta wave'
• Left axis deviation if right-sided accessory pathway most common
• Right axis deviation if left-sided accessory pathway rare
72
How can you differentiate between Type A and B WPW?
```
Differentiating between type A and type B
Type A (left-sided pathway): dominant R wave in V1
Type B (right-sided pathway): no dominant R wave in V1
```
73
What conditions is WPW associated with?
```
Clinical Associations of WPW
• HOCM
• Mitral valve prolapse
• Ebstein's anomaly (low insertion of tricuspid valve)
• Thyrotoxicosis
• Secundum ASD
```
74
How is WPW managed?
Definitive treatment: radiofrequency ablation of the accessory pathway
Medical therapy: amiodarone and flecainide
75
What is hypertrophic obstructive cardiomyopathy?
Most common cause of sudden cardiac death in the young and has an estimated prevalence of 1 in 500. Autosomal dominant mutation in Beta-myosin protein. Causes diastolic dysfunction and left ventricular hypertrophy.
76
What clinical features does HOCM present with and what will the echo findings be?
Usually asymptomatic, can get exertional dyspnoea, angina, syncope, sudden death due to ventricular arrhythmias, jerky pulse and ejection systolic murmur.
Echo findings = mitral regurgitation, systolic anterior motion of the anterior mitral valve leaflet and asymmetric hypertrophy (MR SAM ASH)
77
What is supraventricular tachycardia?
Technically supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.
78
What is bradycardia and when do we treat this?
This is any HR < 60bpm. After completing an A-E assess their risk of asystole and the presence of adverse signs.
```
Adverse signs
• Shock
• Syncope
• Myocardial Ischaemia
• Heart failure
Risk of asystole
• Recent asystole
• Mobitz type II AV block
• Complete heart block with broad complex QRS
• Ventricular pause > 3 seconds
```
79
How is bradycardia managed if needs be?
Atropine 0.5mg IV is first line
If unsatisfactory response, then atropine up to maximum of 3mg
Seek expert help if non resolving and consider other options such as:
• Transcutaneous pacing
• Isoprenaline/adrenaline infusion titrated to response.
80
How should you assess an ECG?
1. First assess Rate and Rhythm
2. Axis deviation (I+II reaching = right, I+II leaving = left)
3. Are all the P waves association with QRS complex
4. Intervals
• PR interval – 0.12-0.2 seconds (3-5 small boxes)
• QRS interval – less than 0.12 seconds (less than 3 small boxes)
• QT interval – must be corrected with heart rate and charts should be available for this but the correct interval should be roughly less than half the cycle
5. Width of the QRS complex
81
How can you recognise the two different types of bundle branch blocks?
Look at Leads V1 and V6 and remember the acronym WilliaM and MarroW.
In Left Bundle branch block the V1 QRS will look like a W and the V6 like an M
In Right Bundle branch block the V1 QRS will look like an M and the V6 like a W
82
What causes a LBBB and when is it worrying?
```
LBBB causes
• IHD
• Hypertension
• Aortic stenosis
• Cardiomyopathy
A new LBBB is always pathological and could be a sign of an MI. If an existing LBBB is present diagnosing an MI form an ECG can be difficult
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83
What causes a RBBB?
```
RBBB Causes
• Normal especially with increasing age
• Right ventricular hypertrophy
• PE
• MI
• Atrial septal defect
• Cardiomyopathy
```
84
What is infective endocarditis?
Definition – infection of the endocardium of the heart most commonly the heart valves/ Occurs in previously normal valves 50% of the times and the mitral valve is the most commonly affected.
85
What are the risk factors for developing endocarditis?
```
Previous episode of endocarditis
Rheumatic fever
Prosthetic valves
Congenital heart defects
IVDU (typically causing tricuspid lesion)
Recent piercing
```
86
What organisms commonly cause endocarditis?
With heart prothesis up to 2 months after – Staphylococcus Epidermidis
Developing world – Streptococcus Viridans
Developed world – Staphylococcus Aureus
Candida Albicans – Immunocompromised
Streptococcus bovis associated with colorectal cancer
If culture is negative causes could be Coxiella burnetiid, bartonella, brucella or HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella and kingella)
87
What signs and symptoms are suggestive of infective endocarditis?
```
Fever and new heart murmur = infective endocarditis until proven otherwise
Acute heart failure
Breathlessness
Malaise
Weight loss
Clubbing
Emboli may be thrown off and cause symptoms else where in the body e.g. stroke
Janeway lesions (emboli deposition)
Osler’s Nodes
```
88
How should suspected infective endocarditis be investigated?
Echocardiogram
ECG
Blood cultures
Routine bloods
89
What is the modified Duke criteria for endocarditis?
```
Infective endocarditis can be diagnosed with
• pathological criteria positive, or
• 2 major criteria, or
• 1 major and 3 minor criteria, or
• 5 minor criteria
```
90
What criteria are used in the modified duke criteria for diagnosing infective endocarditis?
Pathological criteria
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Major criteria
Positive blood cultures
Two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
• Persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
• Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
• Positive molecular assays for specific gene targets
Evidence of endocardial involvement
• Positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
• New valvular regurgitation
Minor criteria
• Predisposing heart condition or intravenous drug use
• Microbiological evidence does not meet major criteria
• Fever > 38ºC
• Vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
• Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
91
How is infective endocarditis managed?
Blind native valve – amoxicillin and consider gentamicin
Blind penicillin allergic, MRSA or severe sepsis, vancomycin, and low-dose gentamicin
Blind prosthetic valve – vancomycin and low-dose gentamicin
Staphylococci native valve – flucloxacillin (vancomycin and rifampicin if penicillin allergic or MRSA)
Staphylococci prosthetic valve – flucloxacillin, rifampicin and low dose gentamicin (if penicillin allergic or MRSA vancomycin, rifampicin, and low-dose gentamicin)
```
Sensitive streptococci (Viridans) – benzylpenicillin (vancomycin and low dose gentamicin if penicillin allergic)
Less sensitive streptococci – Benzylpenicillin and low dose gentamicin (vancomycin and low dose gentamicin if penicillin allergic.
```
92
When is surgery indicated for infective endocarditis?
Indications for surgery
• Severe valvular incompetence
• Aortic abscess (indicated by lengthening PR interval)
• Infection resistant to antibiotics/fungal infections
• Cardiac failure refractory to standard medical treatment
• Recurrent emboli after antibiotic therapy
93
What is aortic stenosis?
Definition – stiffening of the aortic heart valve, most common valve disorder.
94
What causes aortic stenosis?
Congenital e.g. bicuspid aortic valve, William’s syndrome (supravalvular aortic stenosis)
Rheumatic Disease
Degenerative and calcification
Hypertrophic obstructive cardiomyopathy
95
What are the clinical features of aortic stenosis?
```
LV hypertrophy
LV dysfunction
Heart failure
Syncope
Angina
Dyspnoea
Narrowing pulse pressure
Slow rising pulse
```
96
What are the features of the murmur heard in aortic stenosis?
Ejection Systolic murmur and soft S2 heart sound. Heard best in the aortic area (right 2nd intercostal space). To differentiate from pulmonary stenosis AS will be louder on expiration whilst PD on inspiration – remember LEft and RIght. This murmur radiates to the carotids and decreased following the Valsalva manoeuvre
97
How should aortic stenosis be investigated?
```
Echocardiogram - severity of stenosis is according to aortic valve area, velocity of blood through the valve and left ventricle ejection fraction.
Exercise testing
Stress Echocardiogram
Trans-oesophageal echocardiogram
Cardiac MRI scan
BNP
Coronary angiogram
```
98
How can aortic stenosis be managed?
Good dental care
Medical treatment of Heart failure
TAVI – less traumatic surgery but does not last as long and prevents progression
AVR – open heart surgery and is more long term
99
What is aortic regurgitation?
Definition – Leaking of blood from the aorta into the left ventricle through the aortic valve
100
What can cause aortic regurgitation?
```
Primary causes (due to aortic valve)
Endocarditis, bicuspid aortic valve, rheumatic disease, and connective tissue diseases such as rheumatoid arthritis and systemic lupus erythematous.
```
```
Secondary causes (due to aortic root disease)
Aortic dissection, ankylosing spondylitis, hypertension, syphilis and Marfan’s/Ehlers-Danlos
```
101
What are the clinical features of aortic regurgitation?
```
LV hypertrophy
Palpitations
Angina
Dyspnoea
Colpasing pulse
Wide pulse pressure
Quincke’s sign (nailbed pulsation that are red and blanching)
De musset’s sign (head bobbing)
Mueller’s sign (pulsation of the uvula)
```
102
What are the features of the murmur heard in aortic regurgitation?
Early diastolic murmur heard in the aortic region and heard loudest when patient sits forwards and expires.
103
How should aortic regurgitation be investigated?
```
Echocardiogram
TOE
CT aortogram
Cardiac MRI
BNP
Coronary Angiogram
```
104
How is aortic regurgitation managed?
Treat Heart failure
Check for connective tissues disease and screen 1st degree relatives if positive
Aortic Valve Repair
105
What is mitral stenosis?
Definition – stiffening of the Mitral valve preventing proper filling of the left ventricle.
106
What age does mitral stenosis most commonly occur in is it more common in males or females?
Usually becomes symptomatic in 30s and 40s and is more common in females due to rheumatic fever being more common in females.
107
What causes mitral stenosis?
Rheumatic disease is the most common cause
| Infective endocarditis and mitral annular calcification
108
What are the clinical features of mitral stenosis?
```
Left atrial dilation
Pulmonary venous hypertension
Right heart failure
Can cause Atrial fibrillation.
Palpitations
Dyspnoea
Haemoptysis (rupture of bronchial vessel secondary to pulmonary venous hypertension)
Malar flush
```
109
What are the features of the murmur heard in mitral stenosis?
Mid-late diastolic murmur heard over mitral area which radiates to the axilla (listen with diaphragm here). Will be loudest on expiration.
110
How should mitral stenosis be investigated?
ECG looking for AF
Chest X-ray looking for LA enlargement and pulmonary congestion
Echocardiogram
111
How is mitral stenosis managed?
Medical management of Heart failure
| Surgery for MVR
112
What is mitral regurgitation/insufficiency?
leaking of the mitral valve so that blood flows from the left ventricle to the atria. Second most common valvular heart disease and affects men and women equally and about 2% of the population in total. Common in healthy individuals to a trivial degree, not requiring treatment.
113
What are the risk factors for mitral regurgitation?
```
Female sex
Lower BMI
Age
Renal dysfunction
Previous MI
Prior mitral stenosis or valve prolapse
Collagen disorders
```
114
What causes mitral regurgitation?
```
Infective endocarditis
Acute MI (damages papillary muscles)
Malfunction of prosthetic heart valve
Mitral valves prolapse
Rheumatic disease
Congenital
```
115
What are the clinical features of mitral regurgitation?
```
Pulmonary hypertension
Cardiomegaly
Left ventricle hypertension.
Palpitations
Dyspnoea
Heart failure
Thrusting apex beat
Atrial fibrillation
```
116
What are the features of the murmur heard in mitral regurgitation?
Pansystolic murmur heard best in the mitral area (apex) which radiates to the axilla. If mid to late systole then more likely to be mitral valve prolapse.
117
How should suspected mitral regurgitation be investigated?
ECG showing broad P wave
Chest X-ray looking at left atrial enlargement and pulmonary congestion
Echocardiogram and TOE
BNP
118
How is mitral regurgitation managed?
Medical management of Heart failure and mitral valve repair or replacement.
119
What is pericarditis?
Definition – Inflammation of the pericardium
120
What causes pericarditis?
Idiopathic
Secondary to
• Post-MI due to oedema and inflammation (Dressler’s syndrome)
• Virus – EBV, Coxsackie, CMV, adenovirus, mumps, varicella, or HIV
• Bacteria – TB (most common worldwide), Lyme disease, rheumatic fever,
• Malignancy
• Autoimmune – SLE and vasculitis
• Drugs – penicillin’s and chemotherapy
• Metabolic – uraemia, hypothyroidism, and anorexia nervosa
• Trauma
121
What are the clinical features of pericarditis?
```
Generalised chest pain that is worse in inspiration or lying flat and relieved on sitting forwards. This radiates to the inferior border of the scapula. May be pleuritic
Non-productive cough
Dyspnoea
Flu like symptoms
Pericardial rub (3rd heart sound)
Tachycardia and Tachypnoea
```
122
What ECG changes are seen in pericarditis?
ECG changes
• Global saddle shaped ST elevation
• PR depression (most specific)
123
How should suspected pericarditis be investigated?
ECG
TOE to check for effusion
Troponin and BNP (may be raised)
124
How is pericarditis managed?
```
NSAIDs
Gastric protection for 1-2 weeks
Colchicine for 3 months to prevent recurrence
Rest until symptoms resolve
Treat cause
Consider steroids to reduce inflammation
```
125
What is constrictive pericarditis?
Fibrotic and thickened pericardium that restricts the hearts ability to pump It occurs after any cause of pericarditis but most commonly after a TB pericarditis.
126
What are the clinical features of constrictive pericarditis?
Dyspnoea
Right heart failure (JVP, ascites, oedema, hepatomegaly)
JVP shows prominent X and Y descent
Pericardial knock (loud S3)
Kussmaul’s sign (paradoxical rise in JVP during inspiration)
CXR shows pericardial calcification
127
What is cardiac tamponade?
A pericardial effusion that raises intrapericardial pressure enough to limit ventricular filling This is a medical emergency.
128
What are the clinical features of cardiac tamponade?
Beck’s triad – hypotension, raised JVP and muffled heart sounds
Dyspnoea
Tachycardia
Absent Y descent on JVP (due to limited right ventricular filling)
Pulsus paradox – abnormally large drop in BP during inspiration
ECG – electrical alternans (alternating amplitude of QRS complex between beats)
Rarely Kussmaul’s sign
Echocardiogram will show an echo free zone around the heart greater than 1cm and diastolic collapse of the right side of the heart.
129
How should cardiac tamponade be managed?
Urgent pericardiocentesis and expert guidance/help.
130
What are the absolute contraindications to fibrinolytic therapy for ACS?
```
Absolute contraindications to fibrinolytic therapy
• Previous haemorrhagic stroke
• Other stroke or CVA within past 6 months
• CNS damage or neoplasm
• Active internal bleeding
• Aortic dissection
• Recent major surgery or trauma
• Known bleeding disorder
```
131
If someone requires both an antiplatelet for ACS management and an anticoagulant for something else (PE or VTE), how should this be managed?
1. Secondary prevention of stable cardiovascular disease – if also indication for anticoagulant then give anticoagulant monotherapy and stop the antiplatelet
2. ACS/PPI – give triple therapy for 4-6 weeks then dual therapy (one antiplatelet and one anticoagulant) for 12 months
3. VTE – calculate HAS-BLED score, if intermediate or high risk consider stopping antiplatelet.
132
What is Arrhythmogenic right ventricular cardiomyopathy?
Form of inherited CVD and is regarded as the second most common cause of sudden cardiac death in the young. Autosomal dominant but with variable expression, ventricular myocardium is replaced by fatty fibrofatty tissue.
133
What are the clinical features of arrhythmogenic right ventricular cardiomyopathy?
Palpitations, syncope, and sudden cardiac death. ECG abnormalities in V1-3 typically with T wave inversion, epsilon wave (terminal notch in QRS complex. Echo changes may be seen but MRI is better.
134
How is arrhythmogenic right ventricular cardiomyopathy managed?
Sotalol most widely used drug, catheter ablation to prevent ventricular tachycardia and ICD
135
What is Brugada syndrome?
A form of inherited CVD which can present with sudden cardiac death. Inherited in an autosomal dominant and is more common in Asians. Many variants exist but a large number are due to mutations in a myocardial sodium ion channel protein.
136
What are the clinical features of brugada syndrome?
Convex ST segment elevation in V1-3 followed by a negative T wave, partial RBBB. ECG changes become more apparent after the administration of flecainide or ajmaline and this is the investigation of choice.
137
How is brugada syndrome managed?
Implantable cardioverter-defibrillator
138
What is amiodarone and how does it work?
Class II antiarrhythmic agent that works by blocking potassium channels and so inhibiting repolarisation and so prolongs the actions potential. It also has some class I effects by blocking sodium channels.
139
How should amiodarone be administered?
Administration and safety – Amiodarone has a very long half-life (20-100 days) so requires loading doses and can cause thrombophlebitis so must be given via central veins.
140
What are the adverse effects of amiodarone?
```
Thyroid dysfunction (in both directions)
Corneal deposits
Pulmonary fibrosis/pneumonitis
Liver fibrosis/hepatitis
Peripheral neuropathy, and myopathy
Photosensitivity
Bradycardia
Lengthens QT interval
p450 inhibitor.
```
141
How should amiodarone be monitored?
TFT, LFT, U&E and CXR prior to treatment and then TFT, LFT every 6 months
142
What is adenosine and how does it work?
Causes transient block of the AV node working on Adenosine A1 receptors in the AV node. Adenosine has a very short half life of 8-10 seconds so must be administered via a high calibre cannula. Its effect is enhanced by dipyridamole (antiplatelet agents and blocked by theophylline.
143
What are the adverse effects of adenosine?
Chest pain
Bronchospasm (avoid in asthmatics)
Transient flushing
Can enhance conduction via accessory pathways causing increased ventricular rate i.e. in WPW syndrome
144
What is an aortic dissection?
Tear in the tunica intima of the wall of the aorta.
145
What are the risk factors for aortic dissection?
```
Hypertension (most important)
Trauma
Bicuspid aortic valve
Collage disease
Turner’s and Noonan’s syndrome
Pregnancy
Syphilis
```
146
What are the clinical features of an aortic dissection?
Chest pain – severe and radiates through to the back in a tearing feeling
Aortic regurgitation
Hypertension
Angina due to involvement of coronary arteries
Paraplegia due to involvement of spinal arteries
Limb ischaemia due to distal aorta
Non specific ECG changes (minority have ST elevation in inferior leads)
147
What are the two classifications of aortic dissections?
Stanford
Type A – ascending aorta – 2/3 of cases
Type B – descending aorta distal to left subclavian origin – 1/3 of cases
DeBakey
Type 1 – originates in ascending and propagates to at least aortic arch and beyond
Type 2 – originates in and is confined to ascending aorta
Type 3 – originates in descending aorta rarely extend proximally but does distally
148
How should someone with suspected aortic dissection be investigated?
ECG
CXR
Routine bloods including U&Es, LFTs, Lactate, FBC, troponin and crossmatch, G&S
CT angiography
149
How are the two types of aortic dissection managed?
Type A – Surgical but BP controlled to a target of 100-120 systolic whilst waiting
Type B – conservative management, bed rest and reduce blood pressure with IV labetalol to prevent progression
150
What complications can occur from aortic dissection?
Backwards tear – aortic incompetence/regurgitation and inferior MI due to right coronary
Forwards tear – unequal arm pulses and BP, stroke, and renal failure
151
What is long QT syndrome?
Inherited condition associated with delayed repolarisation of the ventricles. It can lead to VT and torsade’s to points. Can be exacerbated or caused by drugs and physiological disturbances.
152
What are the upper limits for the QT interval in males and females?
Normal QT interval
Males – less than 0.43s
Females – Less than 0.45s
153
What are the classical clinical features of long QT syndrome?
Syncope – exertional, emotional, auditory stimuli, at night or at rest
Sudden cardiac death
Palpitations
154
What are the causes or exacerbations of long QT syndrome?
Congenital
• Jervell-Lange-Nielsen syndrome (also deaf and is caused by an abnormal potassium channel)
• Romano-Ward syndrome (No deafness
```
Drugs
• Amiodarone, sotalol and class 1a antiarrhythmic drugs
• TCAs, SSRIs (citalopram)
• Methadone
• Chloroquine
• Terfenadine (antihistamine)
• Erythromycin
• Haloperidol
• Ondansetron
```
```
Physiological disturbances
• Electrolytes – calcium, potassium, and magnesium
• Acute MI
• Myocarditis
• Hypothermia
• Subarachnoid haemorrhage
```
155
How should long QT syndrome be managed?
```
Avoid drugs which prolong QT
Magnesium sulphate if Torsade’s de points
Beta blockers (not sotalol)
Implantable cardioverter defibrillators
```
156
What is myocarditis?
This describes inflammation of the myocardium and typically occurs in younger patients presenting with chest pain.
157
What causes myocarditis?
```
Viral – coxsackie B and HIV
Bacteria – diphtheria and clostridia
Spirochaetes – Lyme’s disease
Protozoa (chagas disease and toxoplasmosis)
Autoimmune
Doxorubicin
```
158
What are the clinical features and investigation results in myocarditis?
Clinical Features
Acute chest pain
Dyspnoea
Arrhythmias
Investigations
Routine bloods, BNP, and trop (raised inflammatory markers, BNP and trop)
ECG – tachycardia, arrhythmias and ST/T wave changes including ST elevation and T inversion
159
How is myocarditis managed?
Treat underlying cause
| Supportive care in heart failure or arrhythmias
160
What is takotsubo cardiomyopathy?
Takotsubo cardiomyopathy is a type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium. It may be triggered by stress. Takotsubo is a Japanese word that describes an octopus trap. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap).
161
What are the clinical features of Takotsubo cardiomyopathy?
Chest pain
Features of heart failure
ECG: ST-elevation
Normal coronary angiogram
162
How is Takotsubo cardiomyopathy managed?
Supportive
| Prognosis – the majority of patients improve with supportive treatment
163
Are there any driving restrictions on people with Hypertension?
Can drive as long as treatment does not cause unacceptable side effects
Group 2 driving then disqualification if BP consistently > 180 systolic or diastolic > 100mmHg
164
What are the 5 different types of Myocardial Infarction?
1. Type 1 – spontaneous MI
2. Type 2 – MI secondary to ischaemic imbalance – infarction due to hypoxia not caused by coronary artery disease e.g. anaemia, respiratory failure, hypotension etc.
3. Type 3 – MI resulting in sudden death without biomarkers
4. Type 4 – relating to PCI or stent thrombosis
5. Type 5 – relating to CABG
165
What is hypercholesterolaemia?
Raised levels of cholesterol in a fasting lipid sample, aim should be < 5mmol/L.
166
How can we classify hypercholesterolaemia?
1. Common primary hyperlipidaemia – accounts for 70% and involves LDL only
2. Familial primary hyperlipidaemia – many genotypes and phenotypes
3. Secondary hyperlipidaemia – e.g. Cushing’s, hypothyroidism, nephrotic syndrome and cholestasis causing raised LDL
4. Mixed hyperlipidaemia – results in raised LDL and TGL and occurs due to T2DM, metabolic syndrome, alcohol abuse and chronic renal failure
167
What features may you see suggestive of hyperchoelsterolaemia?
Xanthomata
Paler xanthoma – remnant of hyperlipidaemia
Eruptive xanthoma – multiple red/yellow vesicles on extensor surfaces
Tendon xanthoma, tuberous xanthoma and xanthelasma
Cardiovascular disease
168
Who should be investigated for hypercholesterolaemia and how is this done?
Fasting lipid profile (note non-HDL-cholesterol is the most important risk factors)
Who to screen
Those at risk of hyperlipidaemia – family history of hyperlipidaemia, corneal arcus at < 50yrs, xanthomata or xanthelasmata
Those at risk of CVD – known CVD, family history of CVD < 60yrs, DM either type, hypertension, smoker, raised BMI, low socioeconomic background or asian background
169
How is hypercholesterolaemia managed?
Encourage lifestyle changes including Mediterranean diet and regular exercise in all patients as well as discussing drug treatment
Statins
Niacin
Ezetimibe
170
How do statins work?
Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
171
What are the adverse effects of statins?
* Myopathy, which is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
* Liver impairment, treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
172
What monitoring requirements are required when and after starting statins?
Baseline non fasting Lipid profile
Baseline LFTs then again at 3 months and 12 months
Baseline Renal function
Baseline HbA1c
Baseline Creatinine kinase if persistent generalised muscle pain (do not start if persistently > 5 x normal)
TSH if dyslipidaemia is present
173
What are the contraindications for statins?
Macrolides (e.g. erythromycin, clarithromycin), stop until course complete
Pregnancy
174
Who should stains be started in?
* In all stablished cardiovascular disease including stroke and peripheral vascular disease
* Anyone with a 10-year cardiovascular risk >= 10%
* Patients with T1DM for more than 10yrs OR aged >40 OR have established nephropathy
175
When should statins be taken?
Statins should be taken at night as this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins. Note doses differ if for primary over secondary prevention.
176
What is niacin?
Nicotinic acid (niacin) is used in the treatment of patients with hyperlipidaemia, although its use is limited by side-effects. As well as lowering cholesterol and triglyceride concentrations it also raises HDL levels.
177
What are the adverse affects of niacin?
Adverse effects
• Flushing: mediated by prostaglandins
• Impaired glucose tolerance
• Myositis
178
What is Ezetimibe?
Cholesterol absorption inhibitor – can be used in statin intolerance or in combination with statins to achieve target reduction
