Cardiology Flashcards
1
Q
What is the definition of, and epidemiology of an AAA?
A
An Abdominal Aortic Aneurysm (AAA) is a permanent dilation of the abdominal aorta with a diameter >1.5 times the expected diameter for that segment given the patient’s sex and body size. The prevalence of AAAs in men ranges from 1.3% in 45-55 yr olds, to 12.5% in 75-84 year olds (increases with age).
2
Q
What is the aetiology and [pathophysiology] of an AAA?
A
Typically, the aneurysm is around 3cm (as normal abdominal aortic diameter is 2cm) 90% of AAAs happen below the renal arteries as there is less collagen around the segment, making it weaker. The aetiology if aortic aneurysms are multifactorial, including atherosclerosis and altered tissue metalloproteinases which diminishes the integrity of the abdominal wall.
3
Q
What are the risk factors for an AAA?
A
Risk factors include: • Cigarette smoking • Hereditary/family history • Increasing age • Male sex (prevalence) • Female sex (rupture)
4
Q
What are the clinical features of an AAA?
A
Tend to be asymptomatic and picked up only on screening. It is therefore important to know the risk factors. On examination a pulsatile mass may only be felt in slim patients with an AAA >5cm (therefore not a good screening tool).
Ruptured AAA:
• Abdominal, back or groin pain (do not dismiss as renal colic)
• Hypotension
• Pulsatile mass
5
Q
How can an AAA be investigated?
A
An abdominal ultrasound is the first test to do, which can show vessel diameter.
Blood tests can show increased CRP/ESR with leukocytosis and positive blood cultures in infective AAA.
CT, MRI and aortography can also be used in investigation.
6
Q
What is the definition and epidemiology of an Aortic Dissection?
A
An aortic dissection is where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen. It is most common in males between the ages of 40 and 60.
7
Q
What is the aetiology of an Aortic Dissection?
A
The aetiology of an aortic dissection causes degenerative changes in the smooth muscle of the aortic media. Causes and predisposing factors are:
• Hypertension
• Aortic atherosclerosis
• Connective tissue disease (e.g. SLE, Marfan’s, Ehlers-Danlos)
• Congenital cardiac abnormalities
• Aortitis (e.g. Takayasu’s aortitis, tertitary syphilis)
• Iatrogenic (e.g. during angiography or angioplasty)
• Trauma
• Crack cocaine
8
Q
What are the symptoms of an Aortic Dissection?
A
Patients commonly present with an acute severe central ‘tearing’ chest pain that may radiate to the back (or may mimic an MI). Interscapular pain is a feature of descending aorta dissection.
Up to 20% of patients present with syncope and no pain.
An aortic dissection can also lead to occlusion of the aorta and its branches:
• Carotid obstruction - hemiparesis, dysphasia, blackout.
• Coronary artery obstruction - chest pain (angina or MI)
• Subclavian obstruction - ataxia or loss of consciousness.
• Coeliac obstruction - severe abdominal pain.
• Renal artery obstruction - anuria, renal failure.
9
Q
What are the examination features of an Aortic Dissection?
A
- May find a murmur in the back below the left scapula, descending to the abdomen.
- Blood pressure differential between the two arms, as well as a widened pulse pressure
- A pulse differential or deficit between the two legs
- Signs of aortic insufficiency such as collapsing pulse, and early diastolic murmur.
Hypotension is a sign of cardiac tamponade.
There may also be signs of Marfan’s or Ehlers-Danlos syndrome such as tall stature, arachnodactyly, pectus excavatum, hypermobile joints, and narrow face.
10
Q
What are the complications of an Aortic Dissection?
A
Complications: Aortic rupture is often fatal. Cardiac tamponade is also very dangerous, and occurs when blood leaks into the pericardium.
Other complications include pulmonary oedema, MI, syncope, and cerebrovascular, renal, mesenteric or spinal ischaemia.
11
Q
How can an Aortic Dissection be investigated?
A
An ECG is an important first-line test to look for evidence of myocardial ischaemia, and is often normal. ST depression may occur in acute aortic dissection (inferior MI), but ST elevation is rare.
A CXR is used to exclude pulmonary causes of pain. A widened mediastinum or a localised bulge points to an aortic dissection.
Bloods:
• FBC can show anaemia or is normal
• Cross-match 10 units of blood (in case of surgery)
• Cardiac enzymes are usually negative unless an MI is caused by the dissection. • U&Es to look for renal function.
A CT of the thorax can be used to visualise the false lumen of dissection. A trans-oesophageal echocardiography is a highly specific way to confirm diagnosis.
12
Q
Define cardiac arrest
A
Cardiac arrest is the acute cessation of cardiac function.
13
Q
What are the most common causes of cardiac arrest?
A
Most cases of cardiac arrest occur secondary to structural heart disease:
• Coronary artery disease (up to 70%): both ACS and stable CAD
• Heart failure
• Cardiomyopathy particularly hypertrophic and arrythmogenic right ventricular sub-types.
14
Q
What are the classically reversible causes of cardiac arrest?
A
Hypoxia
Hypothermia
Hypovolemia
Hypo- or hyperkalaemia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins and other metabolic disorders
15
Q
What are the clinical features of a Cardiac Arrest?
A
(History obtained from patient’s relatives) Patients may have a family history of sudden cardiac arrest. They may have a history of pulmonary disease, chest pain, palpitations or syncope.
Patient may have had symptoms of main risk factors such as:
• Coronary artery disease
• Left ventricular dysfunction
• Hypertrophic cardiomyopathy (due to disordered myofibrils and scaring)
• Arrythmogenic right ventricular dysplasia
• Long QT syndrome
• Acute medical or surgical emergency (4 H’s and 4T’s)
Patients suffering from cardiac arrest rarely have symptoms prior to arrest, and lose consciousness 10-15 seconds after cerebral hypoxia. Patients can sometimes take gasps (agonal breathing) unconsciously, but often stop breathing all together.
On examination: Patient is unconscious, not breathing and has absent carotid pulses.
16
Q
How can Cardiac Arrest be investigated?
A
Cardiac monitor is important as classification of the rhythm directs management. There are four main non-perfusing rhythm abnormalities that occur in cardiac arrest:
• Pulseless Ventricular Tachycardia (shockable)
• Ventricular Fibrillation (shockable)
• Pulseless Electrical Activity (PEA): organised electrical activity on the ECG with no demonstrable pulse or blood pressure.
• Asystole: absence of any electrical or mechanical cardiac activity.
Bloods: ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose.
17
Q
What are the complications of Cardiac Arrest?
A
Irreversible hypoxic brain damage, death.
18
Q
What is the management of Cardiac Arrest?
A
DR (Danger, Response) : Ensure there is no danger at the arrest scene, summon help as soon as possible. Check if patient is unconscious
ABC:
• Ensure airway is clear with jaw thrust and chin lift.
• Assess breathing by looking, listening and feeling If not breathing, give 2 breaths immediately
• Assess circulation at carotid pulse for 10s.
Basic Life Support (includes ABC) if carotid pulse is not felt:
- Give 30 chest compressions at a rate of 100 /min.
a. Compressions at lower sternum at least depth of 5cm. Allow sufficient recoil of the chest after each compression. Sub-optimal compression greatly reduces the chance of survival. - Give two breaths using mouth-to-mouth or bag-mask.
- Continue cycles, proceed to advanced life support as soon as possible.
Advanced Life Support:
- Attach cardiac monitor and defibrillator.
- Assess the rhythm.
a. If shockable, defibrillate once. Resume CPR immediately for 2 minutes, re-assess rhythm before shock. Continue CPR and shock cycle until return of spontaneous circulation. Administer adrenaline every 3-5 minutes, and consider amioderone.
If un-shockable, start CPR and administer adrenaline every 3-5 minutes. Re-assess rhythm after two minutes of CPR, and return to step 2.
19
Q
What is the prognosis of cardiac arrest?
A
Resuscitation is less successful in the arrests that occur outside hospital. Duration of inadequate effective cardiac output is associated with poor prognosis.
20
Q
What is the definition and epidemiology of Aortic Regurgitation?
A
Aortic Regurgitation is the reflux of blood from the aorta into the left ventricle during diastole. AR is also called aortic insufficiency. Chronic AR often begins in the late 50s, documented most frequently in patients >80 years old.
21
Q
What is the aetiology of Aortic Regurgitation?
A
Causes are either due to:
• Aortic root dilation which pulls the leaflets apart. This can be secondary to:
○ Systemic hypertension
○ Aortic distention
○ Aortitis (due to syphilis, or Tayakasu’s aortitis)
• Aortic valve abnormalities or damage. This can be secondary to a biscuspid valve, rheumatic fever, infective endocarditis, or trauma.
Acute causes are: infective endocarditis, ascending aorta dissection and chest trauma.
22
Q
What are the symptoms of Aortic Regurgitation?
A
Chronic AR can be asymptomatic initially, but later progress to symptoms of heart failure such as exertional dyspnoea, orthopnoea, fatigue and occasionally angina.
In acute AR, the left ventricle is of normal size and unable to compensate, leading to shortness of breath and pulmonary oedema due to backwards transmission of pressure through the pulmonary system.
Sudden cardiovascular collapse can be a symptom of acute AR. Patient may also have symptoms of aetiology such as chest or back pain due to aortic dissection.
23
Q
What are the examination features of Aortic Regurgitation?
A
An early diastolic murmur can be heard best with the patient lent forward with breath on expiration and with the stethoscope on the lower left sternal edge. The absence of a diastolic murmur significantly reduces the chances of AR.
You may also hear an Austin Flint mid-diastolic murmur .
A collapsing ‘water-hammer’ pulse and a wide pulse pressure is also a common feature. A displaced apical pulse is also common.
Uncommon signs are those due to a hyperdynamic pulse producing visible pulsations.
24
Q
How is Aortic Regurgitation investigated?
A
An echocardiography and Doppler is diagnostic as can visualise the regurgitant jet.
An ECG may show signs of left ventricular hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6 and left-axis deviation).
A CXR can show cardiomegaly and dilation of the ascending aorta. Signs of pulmonary oedema can also be seen with left heart failure.
A cardiac catheterisation with angiography can also be done.
25
What is the definition and epidemiology of Aortic Stenosis?
Aortic stenosis is the narrowing of the left ventricular outflow at the level of the aortic valve. It affects 3% of over 75-year-olds, and men more than women. However, those with bicuspid valves may present earlier (as young adults).
26
What is the aetiology of Aortic Stenosis?
Causes include:
1. Stenosis due to rheumatic heart disease (commonest worldwide)
2. Calcification of a congenital bicuspid aortic valve
3. Calcification/degeneration of a tricuspid valve in the elderly.
27
What are the clinical features of Aortic Stenosis?
May be asymptomatic initially. Symptoms are due to insufficient oxygen delivery to tissues, common ones include:
• Dyspnoea on exertion
• Angina
• Syncope or dizziness on exercise.
On examination:
• Ejection systolic murmur (crescendo-decrescendo pattern) radiating to the carotids. S2 may be diminished or softened.
• BP: narrow pulse pressure
• Pulse: slow rising
• Palpation: trill in the aortic area (if severe)
28
How is Aortic Stenosis investigated?
A transthoracic echocardiogram is the best test for the initial diagnosis and subsequent evaluation of AS. The sensitivity and specificity of the test are high. It shows increased aortic pressure gradient.
An ECG can show left ventricular hypertrophy and absent Q waves, AV block, hemiblock, or bundle branch block.
A CXR can show post-stenotic enlargement of the ascending aortic valve area and calcification of the aortic valve.
Cardiac angiography allows differentiation from other causes of angina, and to assess for concomitant coronary artery disease (50% of patients with severe aortic stenosis have significant coronary artery disease).
29
What is the definition and epidemiology of Atrial Fibrillation?
Atrial fibrillation is an atrial tachyarrhythmia characterised by an irregularly irregular heart rhythm and indiscernible P waves on an ECG. It is the most common atrial tachyarrhythmia seen in 1% of the entire population, and is commonly seen in the elderly. Prevalence increases with age. Male predominance.
30
What are the subtypes of Atrial Fibrillation?
Often subdivided into:
• Paroxysmal - Self-resolving episode of less than 7 days
• Persistent - Non self-resolving episode of more than 7 days
• Permanent - AF for more than 1 year.
31
What is the aetiology of Atrial Fibrillation?
There may be no identifiable cause. Secondary causes lead to abnormal electrical pathways that result in AF. These include:
• Systemic causes: Thyrotoxicosis, hypertension, pneumonia and alcohol.
• Heart: Mitral valve disease, ischaemic heart disease, rheumatic heart disease, cardiomyopathy, pericarditis, suck sinus syndrome, atrial myxoma.
• Lung: Bronchial carcinoma, pulmonary embolism.
32
What are the clinical features of Atrial Fibrillation?
Often patients are asymptomatic. Some patients experience palpitations, dyspnoea on exertion, and syncope/light-headedness.
On examination: Patient has irregularly irregular pulse, with or without pulse deficit. Look for thyroid disease and valvular heart disease.
33
How is Atrial Fibrillation investigated?
ECG: Uneven baseline (fibrillation) with absent P waves, irregular QRS complexes. If there is a saw-tooth baseline, consider if there is atrial flutter.
Bloods:
• Cardiac enzymes to rule out ischaemic causes of symptoms
• TFTs to identify underlying cause
• U&E used to assess for co-morbid conditions, as well as helpful in choosing anti-rhythmic agents.
Electrocardiogram to assess structural causes e.g. mitral valve disease, left atrial dilation or ventricular dysfunction.
CXR can show signs of pneumonia.
34
What is the GENERAL (just strategy) management outlines for Atrial Fibrillation?
If haemodynamically unstable, then use DC cardioversion immediately.
The AFFIRM and RACE trial have shown similar outcomes (in both mortality benefit and stroke risk) with either rate or rhythm control. As a general rule of thumb:
• Asymptomatic or mildly symptomatic patients above the age of 65, consider rate control.
• Symptomatic patients under 65, or concomitant heart failure, consider rhythm control.
Symptomatic patients given heparin before cardioverted.
Assess stroke risk and anticoaugulate if needed.
35
How do you elicit rate control in an patient with atrial fibrillation?
In symptomatic patients:
Rate control is indicated as first-line option unless there is a reversible cause, or if AF is secondary to heart failure, or if new-onset AF.
1. Beta-blockers (esmolol, atenolol, propranlol, metoprolol) or calcium-channel blockers (diltiazem or verapamil). (Unless patient has heart failure, in which case use digoxin)
2. Add Digoxin if need to, or if patient has heart failure.
36
How do you assess and manage stroke risk in a patient with Atrial Fibrillation?
Assess stroke risk with CHA2DS2-VASc score.
• No anticoagulation for patient with a CHA2DS2-VASc score of 0-1 and has not got heart failure.
• Anticoagulate patients with a score of ≥2 and/or with heart failure.
○ Once sinus rhythm is restored, add warfarin to heparin. In select patients warfarin may be replaced by direct oral anticoagulants such as dabigatran (direct thrombin inhibitor), or rivaroxaban or apixaban (direct factor Xa inhibitor).
37
What is the definition and epidemiology of Atrial Flutter?
Atrial flutter is an atrial tachyarrhythmia which is characterised by a regular, rapid atrial rate. It is less common than atrial fibrillation and the prevalence ratio in males to females is 5:2. Incidence increases with age.
38
What is the aetiology of Atrial Flutter?
Common causes include (all cause macro re-entrant circuit):
1. Right atrial dilatation - due to pulmonary embolus, mitral and/or tricuspid pathologies, congestive heart failure.
2. Ischaemic heart disease
3. Idiopathic - no underlying hear disease
4. Normal variant - tall males
5. Patients with a history of endurance sports (causing atrial enlargement).
Other causes include drugs, metabolic disturbances, and iatrogenic (catheter ablation, cardiac surgery).
39
What are the clinical features of Atrial Flutter?
Patients commonly present with breathlessness and palpitations. Syncope and severe dyspnoea (at very rapid rates), can also present with chest pain.
40
How can Atrial Flutter be investigated?
ECG shows narrow-complex tachycardia with characteristic regular sawtooth pattern of flutter waves.
Classically has an atrial rate of 300bmp and a ventricular rate of 150bmp. Has fixed conduction ratio (2:1, 3:1, etc.).
Sometimes the ECG does not show flutter waves, as they are buryed by the QRS complexes. Only tend to show flutter waves on injection of adenosine?? In general, a narrow complex tachycardia that has a division of 300bmp e.g 150 bmp or 200bmp is likely to be atrial flitter.
41
How is Atrial Flutter managed?
Managed similar to AF, however achieving rate control is more difficult.
Radiofrequency ablation is highly recommended in patients with chronic atrial flutter as therapy can induce high rates of remission (90%).
42
Define cardiomyopathy, and what are the three main types?
Cardiomyopathy is disease of the myocardium (heart muscle).
There are several types with the majority of causes being idiopathic for each type. The three main types of cardiomyopathy and non-idiopathic causes include:
* Dilated cardiomyopathy (heart is dilated and has impaired function) - post-viral myocarditits, alcohol, drugs, familial (25% of idiopathic causes), thyrotoxicosis, haemochromatosis, peripartum.
* Hypertrophic cardiomyopathy - up to 50% are genetic.
* Restrictive cardiomyopathy - amyloidosis, sarcoidosis, haemochromatosis.
43
What are the clinical features of dilated cardiomyopathy?
* Patients present with symptoms of heart failure, dyspnoea, chest discomfort, paliptations, and syncope.
* Patient may also have arrythmias, thromboembolisms, and a family history of sudden death.
* On examination, they may have a raised JVP, displaced apex beat, functional mitral and tricuspid regurgitations and a third heart sound (made by blood hitting thin wall).
44
What are the clinical features of hypertrophic cardiomyopathy?
* Patients are usually asymptomatic.
* May also complain of syncope, angina, arrhythmias, and have a family history of sudden cardiac death.
* On examination may have a jerky carotid pulse, double apex beat, and an ejection systolic murmur.
45
What are the clinical features of restrictive cardiomyopathy?
* Patients present dyspnoea, fatigue, arrhythmias, and ankle or abdominal swelling.
* On examination, patients have an increased JVP, palpable apex beat, third heart sound, ascites, ankle oedema and hepatomegaly.
46
How is cardiomyopathy investigated?
CXR may show cardiomegaly and signs of heart failure.
ECG may show non-specific ST changes, conduction defects and arrhythmias for all types.
• In hypertrophic cardiomyopathy, may also note left axis deviation, and signs of left ventricular hypertrophy. Q waves in inferior and lateral leads.
• In restrictive cardiomyopathy ECG shows low-voltage complexes.
Echocardiography may show:
• Dilated: dilated ventricles with global hypokinesia.
• Hypertrophic: Ventricular hypertrophy
• Restrictive: non-dilated non-hypertrophic ventricles. Atrial enlargement, preserved systolic function, diastolic dysfunction, granular or 'sparkling' appearance of myocardium in amyloidosis.
Cardiac cathertisation and endocardial biopsy may be helpful.
47
What is the definition and epidemiology of cardiac failure?
Cardiac failure is the inability of the cardiac output to meet the body's demands despite normal venous pressures. Heart failure is common, affecting 10% of > 65-year-olds.
48
How can cardiac failure be classified by function?
Low output causes of heart failure can be divided into systolic (low ejection fraction) or diastolic heart failure (preserved ejection fraction, but reduced ventricular filling).
High output heart failure is due to increased demand from the body. This is usually rare, and sometimes seen in thyrotoxicosis, beriberi, severe anaemia, pregnancy, and AV malformation.
49
What are the common causes of heart failure (classified anatomically)?
Alternatively, they can be divided anatomically:
* Left heart failure: Commonly caused by ischaemic heart disease, hypertension, valvular disease and cardiomyopathy.
* Right heart failure: Commonly secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease (cor pulmonale/pulmonary heart disease), chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade.
* Biventricular failure: Caused by arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug toxicity.
50
[What are the mechanical and neurohumoral adaptation of cardiac failure/]
Mechanical adaptations:
• Frank-Starling Law states that as myocardial contractility declines, stroke volume reduces as a consequence. This results in an increased end diastolic volume due to incomplete emptying, and this increases stroke volume in the following contraction. Eventually, this process results in ventricular remodelling, increased wall stress and reduced cardiac output as this mechanism fails.
Neurohumoral adaptations:
• Activation of the sympathetic nervous system. As cardiac output declines, there is early activation of the SNS. This causes tachycardia, increased sodium and fluid reabsorption by the kidneys and increased peripheral vascular resistance.
• Activation of the renin-angiotensin-aldosterone system (RAAS). In heart failure, activation of the RAAS is a late compensatory mechanism. This is mediated primarily by angiotensin II, and causes increased preload and afterload. As the heart tries to cope with this increased workload, further activation of the RAAS leads to a vicious cycle of fluid overload and worsening wall stress.
51
What are the clinical features of Chronic Left-sided Heart Failure?
Left-sided heart failure: As blood is not adequately pushed out from the left ventricle, blood gets backed up to the lungs via the pulmonary veins. This is called pulmonary congestion. Symptoms are primarily due to this pulmonary oedema (fluid inside the lungs), but also can be due to a pulmonary effusion. These symptoms include:
• Dyspnoea due to the pulmonary oedema causing impaired gas exchange.
• Orthopnoea - as lying down allows blood from legs and abdomen to return to the heart leading to more fluid in lungs.
• Paroxysmal nocturnal dyspnoea
• Nocturnal cough and chest discomfort
• Fatigue.
On examination: Note tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles (due to pulmonary oedema), third heart sound (due to rapid ventricular filling), and a pan-systolic murmur (functional mitral regurgitation).
52
What are the clinical features of Right-sided Heart Failure?
```
Right-sided heart failure is usually a result of left-sided heart failure, and so symptoms of LVF are commonly also present: In right-sided heart failure, blood backs up to the rest of the systemic venous circulation. Symptoms include:
• Swollen ankles
• Fatigue
• Increased weight (due to oedema)
• Decreased exercise tolerance
```
On examination: Note increased JVP, hepatosplenomegaly, ascites, ankle/sacral pitting oedema and signs of functional tricuspid regurgitation.
53
What are the clinical features of ACUTE Left-sided Heart Failure?
Acute LVF is characterised by dyspnoea, wheeze, cough and pink frothy sputum. On examination, patient would have tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans, gallop rhythm, wheeze and fine crackles throughout lung.
54
How can Cardiac Failure be investigated?
Bloods:
• FBC, U&Es, LFTs, CRP, glucose, lipids and TFTs are roitinely performed.
• In acute: ABG, troponin, BNP (brain natriuretic peptide) - high BNP suggests cardiac failure, low plasma BNP rules out cardiac failure.
CXR is used to exclude other causes of dyspnoea and support a diagnosis of heart failure. CXR appearance includes:
• A: Alveolar Oedema
• B: Kerley B lines (sign of interstitial oedema)
• C: Cardiomegaly
• D: Diversion of upper lobes, resulting in prominent upper lobe vessels secondary to increased pulmonary pressures.
• E: Pleural Effusion.
ECG may show ischaemic changes, arrhythmia, left ventricular hypertrophy or may be normal.
Echocardiogram can be used to assess ventricular contraction.
Swan-Ganz catheter allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures.
55
What are the non-pharmacologic/surgical treatments for Cardiac Failure?
```
Lifestyle modifications are necessary. Notably:
• Salt and fluid retention
• Weight reduction
• Smoking cessation
• Alcohol reduction
• Low intensity aerobic exercise.
```
56
What are the pharmacological treatments for Cardiac Failure?
First-line:
• ACE-inhibitors such as Ramipril, Captopril, decrease mortality and morbidity associated with heart failure.
○ Angiotensin-II receptor blockers such as Valsartan should replace ACEi if not well tolerated.
• Beta-blockers such as Bisoprolol and Carvediol also improve mortality and morbidity and should be prescribed with ACEi.
• Diuretics should also be prescribed to patients with previous evidence of fluid retention. First line are loop diuretics (e.g. frusemide), then thiazide-like diuretics (e.g. metolazone).
Second-line:
• Aldosterone antagonists such as spironolactone should be prescribed to patients with moderate-severe LVF (but also beneficial to people with mild LVF). Improves mortality. Monitor K+ as can cause hyperkalaemia.
• Vasodilators such as hydralazine may be added to patients (particularly in Afro-Caribbeans) with persistent symptoms.
• Digoxin is a positive inotrope. Decreases hospitalisation, but not mortality.
57
What are the device therapy and Surgical management options for Cardiac Failure?
Cardiac resynchronisation therapy (CRT) is used for conduction defects that lead to poorly coordinated contraction of ventricles. With CRT, both ventricles are simultaneously activated with an electrical impulse to allow synchronous contraction. Indicated in patients with severe symptoms, LVEF <35%, and broad QRS complexes. Improves mortality.
Left Ventricular Assist Device (LVAD) is used as a bridge to transplantation. Blood flows out from the LV to the LVAD pump and is pumped back into the aorta to be distributed throughout the body.
Cardiac transplantation is an option for especially young patients with refractory end-stage disease. Most commonly done in patients with CAD or dilated cardiomyopathy. Not generally performed in patients with pulmonary vascular resistance.
58
What is the prognosis of Heart Failure?
Poor prognosis. 30-40% die within first year of diagnosis. Mortality then falls to 10% a year.
59
What is the definition and epidemiology of DVT?
A DVT is the development of a blood clot in a major deep vein of the leg, thigh, pelvis or abdomen, which may result in impaired venous flow and consequent leg swelling and pain. A DVT is a venous thromboembolism (another type of venous thromboembolism is a PE). Venous thromboemboli are relatively common, with an incidence rate of 1 in 1000 a year. 2/3 of these are DVTs and 1/3 are PEs. Incidence goes up exponentially with age.
60
What are the risk factors for DVT?
The three factors that lead to blood clots are known collectively as Virchow's Triad, and includes:
• Vessel wall injury
• Venous stasis
• Activation of clotting system
Thus, many patients who develop DVTs have an abnormal clotting system (factor V Leiden, cancer, genetics). There is a clear association between DVT and the following:
• Active malignancy
• Recent major surgery, especially orthopaedic procedures
• Recent hospitalisation (within 90 days of discharge)
• Recent trauma
• Medical illness.
61
What are the clinical features of DVT?
The patient may be asymptomatic, but commonly present with an asymmetrically swollen (oedema) leg. Patient may also have pain along the deep venous system.
On examination: Leg is swollen, red, and may have engorged superficial veins. The affected calf is warmer.
Patients may also present with signs/symptoms of a pulmonary embolism (sudden onset dyspnoea, haemoptysis, pleuritic chest pain).
62
What are the complications of DVT?
* Pulmonary embolism (high likelihood)
* Acute bleeding during treatment involving anticoagulants (medium likelihood)
* Post-Phlebitic Syndrome (/PTS) is a long-term complication of DVT.
63
How is DVT investigated?
It is very difficult to differentiate a DVT from other causes of acutely swollen leg.
A Well's Score should be used if a DVT is at all suspected.
A score of ≤1 should prompt a D-dimer test as this test has a high negative predicted value. If D-dimer is low, this makes DVT unlikely. If normal or high, perform an ultrasound test.
A score of ≥2 (meaning likely) should prompt an ultrasound test (Venous Duplex Ultrasound) which assess venous flow by Doppler and vein compression. It has a high sensitivity and specificity.
64
What is the treatment of DVT?
Anticoagulation therapy is required for at least 3 months (some patients may require longer) for everyone with above-the-knee (proximal) DVT. Generally anticoagulation with dabigatran (direct thrombin inhibitor), rivaroxaban (inhibits factor Xa), apixaban (also inhibits Xa) is recommended over warfarin. Warfarin is recommended over LMWH (low molecular-weight heparin), however LMWH is used in patients with active cancer, hepatic impairment, obese and pregnant patients.
Patients with below-the-knee (distal DVT) may be observed with serial imaging if asymptomatic. Then can be escalated to anti-coagulation.
Early physical activity is recommended in patients.
Gradient stockings are useful for many patients with acute or chronic symptoms of DVT, but not recommended for certain groups of patients.
65
Define heartblock
Heart block is the impairment of the atrioventricular (AV) node impulse conduction, as represented by the interval between P wave and QRS complex. The majority of pacemakers implanted annually are for heart block.
66
What are the different types of heartblock?
There are several types of heart block:
• First-degree heart block is when there is a prolonged PR interval (>0.2s) on ECG.
• Second-degree heart block is when there is intermittent failure of AV conduction resulting in occasional dropped beats. These can be further classified by:
○ Mobitz Type 1 (Wenckebach) - Progressive prolongation of PR interval until a beat is dropped.
○ Mobitz Type 2 - An AV conduction deficit resulting in intermittent drop beats without changes in PR interval.
• Third-degree (complete) heart block - Complete dissociation between P waves and QRS complexes - atria and ventricles beat independently of one another.
67
What is the aetiology of hearblock?
* MI or Ischaemic heart disease (most common cause)
* Infection (e.g. rheumatic fever, infective endocarditis)
* Drugs (e.g. digoxin, beta-blockers, Ca-channel antagonists)
* Metabolic - hyperkalaemia, cholestatic jaundice, hypothermia
* Infiltration of conductive system - sarcoidosis, cardiac neoplasms, amyloidosis
Degeneration of the conductive system.
68
What are the clinical features of 1st degree heartblock?
Asymptomatic. Also normal on examination (with signs of cause).
69
What are the clinical features of Wenkebach's heartblock?
Also usually asymptomatic. Also normal on examination (with signs of cause).
70
What are the clinical features of Mobitz T2 heartblock?
* Dizziness and syncope
* May present with haemodynamic instability and sudden cardiac death in some cases.
* Serious because caused by dangerous pathology and likely to develop into third degree heart block.
71
What are the clinical features of 3rd degree heartblock?
* Symptoms of low cardiac output - dizziness, dyspnoea, fatigue.
* Stokes-Adams attack - episodes of syncope characterised by a sudden unexpected collapse, accompanied by a transient loss of consciousness (less than a minute). Patients are often described to have a death-like pallor with immediate flushing on awakening.
* Patient may also complain of palpitations
* On examination: slow large volume pulse, JVP may show cannon waves. Other signs of low cardiac output such as hypotension and heart failure.
72
What are the complications of heartblock?
Asystole. Cardiac arrest. Heart failure. Complications of any pacemaker inserted.
73
How is heartblock investigated?
ECG:
First Degree AV Block:
PR interval is greater than 0.20s, however the P wave to QRS complex is still 1:1. The rate can vary, and rhythm is usually regular. The QRS complex is within normal limits or may have a bundle branch block.
Mobitz Type 1/Wenckebach:
Progressive delay of conduction at the AV node (progressive prolongation of PR interval), until the conduction is completely blocked (QRS dropped), then the cycle begins again.
Mobitz Type 2 AV block:
2-4 P-waves are needed before conduction to start a QRS complex (2-4:1).
• Ventricular rate is less than atrial rate
• Atrial and ventricular rhythm is irregular
Third Degree AV Block:
This is when P waves and QRS complexes are completely dissociated, and so the ventricles beat independently.
CXR may show cardiac enlargement, or pulmonary oedema (signs of heart failure).
Bloods: TFTs, digoxin level, cardiac enzymes, troponin.
Echocardiogram may show wall motion abnormalities, aortic valve disease and vegetations.
74
How is heartblock managed?
Treatment not required for asymptomatic heart block (Type 1 and Wenkebach).
Acute block is treated with I.V atropine (and consider temporary external pacemaker).
Chronic block is treated with permanent pacemaker.
75
Define hypetension (and the two stages).
Blood Pressure and cardiovascular disease risk have a continuous relationship, so it is not possible to precisely define hypertension. However, a useful clinical definition is: a systolic BP >140mmHg and/or diastolic BP >85mmHg measured on three separate occasions. Very common, affecting 10-20% of adults in the Western world. Prevalence increases with age.
Stage 1 hypertension = 140/90mmHg or higher. Stage 2 hypertension = 160/100mmHg or high.
76
What is the aetiology of hypertension?
95% of cases are essential (idiopathic) hypertension.
Common secondary causes include:
• Renal disease such as diabetic nephropathy, renovascular disease, glomerulonephritis, vasculitides, chronic pyelonephritis, polycystic kidneys.
• Endocrine disease notably Conn's and Cushing's syndromes, glucocorticoid remediable hypertension, pheochromocytoma, acromegaly, hyperparathyroidism.
• Other conditions such as aortic coarctation, drugs (sympathomimetics, corticosteroids, oral contraceptive pill), pre-eclampsia.
77
What are strong risk factors for hypertension?
* Obesity
* Aerobic exercise <3x a week
* Moderate/high alcohol intake
* Metabolic syndrome
* Diabetes mellitus
* Black ancestry
* Age >60 years
* Family history of hypertension
78
What are the clinical features of hypertension?
Often asymptomatic. May have symptoms of complications such as retinopathy (common), heart failure etc. Also may have symptoms of the cause if secondary hypertension.
On examination: There may be a loud second heart sound, fourth heart sound. Examine for signs of causes, e.g. radio-femoral delay (aortic coarctation), renal artery bruit. Examine for end-organ damage, e.g. fundoscopy for retinopathy.
79
How is hypertension investigated?
In the clinic, measure blood pressure in both arms. If raised, instruct on Ambulatory BP monitoring (BP measured throughout the day) to reduce white coat hypertension effect.
Also take bloods (U&Es to look for endocrine and renal causes), urine dipstick (blood and protein). ECG may show signs of left ventricular hypertrophy.
Other tests are especially relevant in patients who are <35.
80
What is the treatment strategy for hypertension?
Assess and modify all other cardiovascular risk factors. This includes cessation of smoking, losing weight, decrease alcohol consumption and reduce dietary Na+.
Treatment threshold:
• Patients under age of 80 with stage 1 hypertension who have target organ damage, cardiovascular or renal disease, or diabetes.
• Patients with stage 2 hypertension.
81
How is hypertension managed pharmacologically?
Step 1
• If under the age of 55: give ACE inhibitors such as captopril or enalapril. Or give angiotensin receptor blockers (ARBs), such as losartan.
• If over the age of 55, or black: start with CCB (Calcium Channel Blockers) such as amlodipine. Or give thiazide diuretics (such as hydrochlorothiazide).
Step 2
Combination treatment: ACEi/ARB + CCB.
Step 3
Triple combination: ACEi/ARB + CCB + Thiazide diuretic
Step 4
Triple combination + Consider further diuretic therapy e.g. sprionolactone. If diuretic therapy is not tolerated: alpha- or beta-blocker.
82
What is the definition and epidemiology of Infective Endocarditis?
Infective endocarditis is the infection of the inner-layer (endocardium) of the heart. Not very common, only affecting 4000 patients a year, about half are over the age of 60.
83
What bacteria most commonly cause infective endocarditis?
```
Viridans group streptococci (most common)
Streptococcus aureus (common in IV drug users)
```
84
What are the important risk factors for infective endocarditis?
Prosthetic heart valves
Congenital heart defects
Rheumatic heart disease
I.V Drug use
85
What are the symptoms of infective endocarditis?
Any patient presenting with fever and a new cardiac murmur should make you consider infective endocarditis.
Patients commonly present with fevers/chills as well as non-specific symptoms such as night sweats, weight loss/anorexia, malaise, fatigue, and myalgia.
General weakness is also a common symptom. However, if asymmetric, suspect systemic emboli. Shortness of breath (dyspnoea on exertion, orthopnoea, paroxysmal nocturnal dyspnoea are all symptoms of congestive heart failure.
Parts of the vegetation can break off, and become septic emboli, which can lodge in places, leading to other symptoms and signs:
• Arthralgia can represent a constitutional symptom, or can be due to septic emboli to the affected joint.
• Headache can also be a general symptom, or can be due to septic emboli.
• Signs of meningitis due to septic emboli
86
What are the examination features of infective endocarditis?
Patient can have developed a new cardiac murmur due to turbulent blood flow.
Splinter haemorrhages and janeway lesions are due to deposits of septic emboli in the hand.
Osler's nodes occur when antigen-antibody complexes deposit in the fingers and toes. In the eyes, these deposits can lead to Roth spots, and in the kidneys can cause glomerulonephritis.
87
Define Ischaemic Heart Disease
IHD refers to a group of conditions where an imbalance between myocardial oxygen demand and oxygen supply results in tissue hypoxia. This may progress to an infarction (see Acute Coronary Syndrome - which can be further divided into unstable angina, STEMI and NSTEMI).
88
Define stable angina
Stable angina results from fixed narrowing of the coronary arteries normally resulting in a fixed threshold for symptoms, which are typically associated with one or more of: exertion, emotion, eating, cold weather, and occasionally recumbence.
89
What is the epidemiology and risk factors of stable angina?
It is not uncommon. Prevalence is 28 per 100,000 in men, and 21 per 100, 000 in women. Male predominance.
Risk factors include: diabetes mellitus, hypertension, hyperlipidaemia, smoking and south Asian ethnicity.
90
What are the clinical features of Stable Angina?
Angina usually presents with 3 features:
1. Chest pressure/pain (rarely actually described as pain, instread a 'heaviness, squeezing, or smothering) lasting several minutes.
2. Provoked by exercise or emotional stress.
3. Relieved by rest or GTN.
When all three of these features are present, we call this typical angina. When only 2 are present, it is called atypical angina.
Patient can also uncommonly have jaw pain, arm pain, nausea/vomiting, dyspnoea, fatigue etc.
On examination:
Features are relatively non-specific, and many have normal examination. May have signs of risk factors such as xanthelasma and retinopathy.
91
How is Stable Angina investigated?
First perform an ECG. The result is often normal. However, an ECG taken during an episode of chest pain may demonstrate ST-segment depression suggestive of ischaemia.
Bloods are important:
• FBCs and LFTs (for baseline LFT before introduction of statin therapy).
• U&Es, glucose (diabetes is an important risk factor), cholesterol and triglycerides (lipid profile is important in risk assessment).
• Troponin? (Not in book or on BMJ best practise).
NICE Guidelines for 'assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin' is based on stratifying patients by likelihood of coronary artery disease:
1. CT calcium scoring should be done for patients with a mild risk of coronary disease. This may prompt a CT coronary angiography, or if calcium score is >400, an invasive angiography.
2. If risk is moderate (30-60%), then perform non-invasive functional testing such as myocardial perfusion testing or stress echocardiography.
3. If risk is high (61-90%) perform coronary angiography or functional testing (e.g. stress testing).
4. If risk is very high (>90%) then proceed straight to management. Further diagnostic testing is unnecessary.
92
How is stable angina managed?
Management
A GTN spray or sublingual administration should be prescribed for immediate symptom relief.
The primary treatment is explanation and lifestyle treatment to minimise cardiac risk factors.
• Explain the conditions and factors which precipitate angina pain
• Control BP, hyperlipidaemia and diabetes (cardiac risk factors)
• Provide advice on smoking, exercise, weight loss and a low-fat diet
• All patients should receive aspirin (75 mg/day) unless contraindicated.
Long-term pharmacological therapy includes:
• Glyceryl trinitrate (GTN) spray to be used when necessary. Repeat in 5 minutes of the pain persists Call an ambulance if the pain continues 5 minutes after a second dose.
• Beta-blockers such as atenolol or calcium channel blockers such as amlodipine should be used as first-line treatments.
○ If symptoms are not controlled, switch the initial drug or use both in combination.
• Statins such as simvastatin should be prescribed for lipid control.
Patients who continue with unacceptable angina despite guideline directed therapy may considered for revascularisation (PCI or CABG ). They must also have at least 1 significant coronary artery stenosis (>70%), which are amenable to revascularisation.
• Most single vessel disease can be managed with angioplasty (PCI)
• Left main stem disease, 3-vessel disease, and those with reduced ejection fraction may benefit from CABG
93
Define ACS
ACS encompasses a group of conditions in which acute myocardial ischaemia occurs secondary to a sudden disruption in coronary blood supply to the heart. This ranges from the progression of tissue ischaemia (unstable angina) to the development of infarction and necrosis (non-ST or ST elevation myocardial infarction). Clinically, these conditions are classified according to changes in the ECG and biochemical markers of myocardial necrosis.
94
What are the risk factors for ACS?
```
Risk factors can be divided into modifiable and non-modifiable risk factors:
• Modifiable risk factors:
○ Diabetes mellitus
○ Hypertension
○ Cigarette smoking
○ Dyslipidaemia
○ Obesity
○ Sedentary lifestyle and physical inactivity
```
• Non-modifiable risk factors:
○ Age (average age is 66 for males, and 70 for females).
○ Male sex
○ Ethnicity: South Asians are at higher risk
○ Family history of coronary heart disease
○ Previous MI.
95
What are the clinical features of ACS?
Patients present with sudden onset severe chest pain. This can be left-sided or central crushing retrosternal chest pain. The pain may radiate to the jaw, neck or arm (usually the left). Unlike stable angina, the pain of ASC typically:
• Commences at rest
• Is new in onset and severe
• Crescendo or worsening in nature.
Only 20% of ACS patients have a history of angina.
Other important features include dyspnoea, diaphoresis (sweating), nausea/vomiting, fatigue and angor animi (sense of impending doom).
On examination: Patients may present with Levine's sign (a clenched fist on the chest), pallor, diaphoresis and anxiety, low-grade pyrexia, and occasionally a fourth heart sound.
96
How is ACS managed?
The purpose is to elicit evidence of myocardial damage, and to exclude other conditions that mimic ACS.
An ECG should be the first test ordered.
• STEMI shows as ST-elevation, but only lasts hours. T wave inversion lasts days, but pathological Q waves last days to months.
• NSTEMI or UA, are seen by ST-depression, T-wave inversion (TWI is normal in aVR, III and V2), or may be normal.
Bloods:
• FBC, U&Es, glucose (diabetes), lipid profile (dyslipidaemia), LFTs.
• Serial cardiac troponins (highly specific for myocardial damage). Cardiac troponins are elevated as early as 2 hours, and peak around 12-18 hours.
○ CK-MB (Creatine Kinase) is not specific for myocardial damage, but because disappear after 48h, can be useful in diagnosing reinfarction (10% of cases).
A CXR is performed to exclude other causes of chest pain and dyspnoea, such as an Aortic Dissection.
Coronary angiography is the gold standard for assessing coronary artery disease. It is performed in medium- to high-risk individuals with UA/NSTEMI, all patients with STEMI (everyone with ACS and with positive troponin) and concominantly with reperfusion therapy.
97
What is the immediate management of ACS?
Use the mnemonic MONACA:
• Morphine - IV for pain, anxiety or pulmonary oedema.
• Oxygen
• Nitrates - sublingual GTN provides symptomatic relief
• Aspirin - 300mg is the most important early intervention in ACS.
• Continuous cardiac monitoring as pulseless VT and VF are common in ACS.
• Antiplatelet agents - clopidogrel/ticagrelor/prasugrel lower mortality.
Blood glucose control improves survival in diabetics or those with higher glucose levels. It is also important to perform an early risk stratification so that those at high risk may benefit from early revascularisation.
98
How is STEMI managed?
MONACA +
PCI is the mainstay management of STEMI. While undergoing PCI, bivalirudin (direct thrombin inhibitor) with aspirin and clopidogrel is recommended.
Thrombolysis (fibrinolysis) is only performed in STEMI patients unable to receive pPCI within 120 minutes of diagnosis, or where it is contraindicated.
+ Post-acute management of lifestyle, pharmacological and rehabilitation programmes.
99
How is NSTEMI/UA managed?
MONACA +
The mainstay treatment for NSTEMI or Unstable Angina is symptomatic relief, antiplatelet therapy and anticoagulation to halt the progression of the unstable plaque.
Reperfusion therapy is only indicated in select cases where this is not enough.
• Most single vessel disease can be managed with angioplasty (PCI)
• Left main stem disease, 3-vessel disease, and those with reduced ejection fraction may benefit from CABG
+ Post-acute management of lifestyle, pharmacological and rehabilitation programmes.
100
What is the post-acute management of ACS?
Lifestyle modification as for stable angina: manage cardiovascular risk factors and promote dietary and activity modification.
Long-term pharmacological therapy includes:
• Long-term aspirin 75mg once daily with antiplatelet 75mg once daily (clopidogrel/ ticagrelor /prasugrel).
• ACEi such as perindopril / enalapril / ramipril should be started early when haemodynamically stable - optimally on first day of hospital.
• Beta-blockers such as atenolol improve long-term survival and provide symptomatic relief of angina.
• Statins such as simvastatin should be prescribed for lipid control. It reduces all cause mortality and vascular events including MI.
• Nitrates: sublingual GTN is indicated for symptomatic relief of post-ACS angina pectoris
A structured cardiac rehabilitation programme is beneficial in that it improves survival, and is recommended in all patients following ACS.
101
What are the complications of ACS?
At risk of MI and other vascular diseases e.g. stroke, peripheral vascular disease.
Early complications of MI are death, cardiogenic shock, heart failure, ventricular arrhythmias, heart block, pericarditis, myocardial rupture and thromboembolism.
Late complications of MI are ventricular wall rupture, valvular regurgitation, ventricular aneurysm, cardiac tamponade, Dressler's syndrome, and chronic heart failure.
102
What is the definition and epidemiology of Mitral Regurgitation?
Mitral regurgitation refers to backflow of blood from the left ventricle to the left atrium as a result of a leaky mitral valve. Not uncommon, thought to affect over 5 million people worldwide.
103
What is the aetiology of Mitral Regurgitation?
• Any aberrations to the mitral valve apparatus.
```
• Acute mitral regurgitation
○ Papillary muscle infarction
○ Ruptured chordae tendineae
○ Acute rheumatic fever
○ Infective endocarditis
○ Trauma
```
• Chronic mitral regurgitation
○ Mitral valve prolapse (most common cause in developed countries)
○ Rheumatic heart disease (common in developing countries)
○ Mitral valve calcification
○ Connective tissue disorders such as Ehlers-Danlos syndrome or Marfan's syndrome
• Secondary mitral regurgitation - this is where there is left ventricular remodelling which distorts the valvular apparatus. Usually caused by coronary heart disease (ischaemic mitral regurgitation).
104
What are the symptoms of Mitral Regurgitation?
Acute mitral regurgitation presents as an emergency. Patients experience sudden onset severe dyspnoea, and rapidly progressive pulmonary oedema. Hypotension and cardiogenic shock (inadequate perfusion of tissue to meet demands).
Chronic mitral regurgitation can be asymptomatic if mild. Symptoms occur when left heart failure develop in severe mitral regurgitation. These are not pathognomonic of MR, but are common and include dyspnoea on exertion and fatigue.
• Chronic MR can also cause atrial fibrillation, which is felt as palpitations.
Patients with mitral valve prolapse are can be asymptomatic, but can also have atypical chest pain.
105
What are the examination features of Mitral Regurgitation?
* Patient may have atrial fibrillation felt as irregularly irregular pulse.
* Laterally displaced apex beat and thrusting.
* Pansystolic murmur loudest at the apex, radiating to the axilla (and may be palpable as a thrill).
* Patients with a mitral valve prolapse also have a mid-systolic click. The click moves towards the first heart sound on standing, and moves away on lying down.
106
How can Mitral Regurgitation be investigated?
1. First-line is a transthoracic echocardiogram with Doppler. Regurgitant blood flow is diagnostic. Can also determine left and right ventricular function and pulmonary artery pressures.
2. An ECG can also be helpful. AF is common. Can also show P-mitrale (bifid P waves) due to left atrial enlargement.
3. CXR may show cardiomegaly due to enlarged left atrium and ventricle. May also have signs of congestive heart failure. In acute mitral regurgitation, heart size is usually normal but shows pulmonary oedema.
107
What is the definition and epidemiology of Mitral Stenosis?
Mitral stenosis is the narrowing of the mitral valve that occurs a result of fusion of the leaflet commissures. Its incidence is declining in the develop world (because rheumatic fever incidence is declining).
108
What is the aetiology of Mitral Stenosis?
The most common cause is rheumatic heart disease (95%). Rarer causes are congenital mitral stenosis, SLE, rheumatoid arthritis, endocarditis and atrial myxoma (rare cardiac tumour).
109
What are the symptoms of Mitral stenosis?
May be asymptomatic or present with symptoms that mimic heart failure:
• Fatigue
• Dyspnoea on exertion or lying down (orthopnoea).
Can also present with palpitations due to strong association with AF (47%).
Rarer symptoms include cough, haemoptysis, and hoarseness caused by compression of the left laryngeal nerve by an enlarged left atrium.
Can also present with cor pulmonale (right heart failure due to pulmonary hypertension) causing abdominal pain (hepatosplenomegaly) and peripheral oedema.
110
What are the examination features of Mitral Stenosis?
* May have a malar flush (looks like SLE malar rash).
* Pulse may be thready (low volume) and/or irregularly irregular.
* Apex beat is undisplaced and tapping. Parasternal heave.
* On auscultation, there is a loud first heart sound with opening snap. Also a mid diastolic murmur which is accentuated when the patient leans to their left. The severity of the stenosis is directly related to the duration of the murmur because of the longer time required for the left atrium to empty.
* Evidence of pulmonary oedema on lung auscultation if decompensated.
111
How can Mitral Stenosis be investigated?
An ECG can show AF commonly (47% of cases). It can also show left atrial enlargement and right ventricular hypertrophy.
An echocardiography (trans-thoracic) is the definitive test to confirm the diagnosis of mitral stenosis and to see the severity of disease. Transoesophageal gives better valve visualisation and can help with detecting a thrombus.
A CXR may show left atrial enlargement.
Cardiac catheterisation can be used to calculate valve areas.
112
What is the definition and epidemiology of Pericarditis?
Pericarditis is the inflammation of the pericardium (the double-membrane sac that contains the heart). Acute pericarditis is more common in adults and in men. It may account for 5% of emergency department visits for chest pain.
It can be acute (lasting <4-6 weeks), and either:
• Fibrinous (dry)
• Effusive (with a purulent, serous, or haemorrhagic exudate)
It can also be constrictive pericarditis, which can be a medium to late complication of pericarditis.
113
What is the aetiology of Pericarditis?
Inflammation can be due to:
• Idiopathic
• Infective agents (Coxsackie virus A9 or B1-4, Echo 8, mumps, EBV, cytomegalovirus, varicella, rubella, HIV, Parvo-19)
• Connective tissue disease (e.g. rheumatoid arthritis, sarcoid, SLE, scleroderma)
• Post myocardial-infarction
• Malignancies of surrounding tissue
• Metabolic: myxoedema, uraemia.
114
What are the clinical features of Pericarditis?
Chest pain is the most common symptom. Pain is sharp, stabbing, pleuritic (as this moves the pericardium) and severe as pericardium is well innervated by the phrenic nerve.
• Pain is worse on coughing, deep inspiration and lying flat.
• Almost all patients report pain is relieved by sitting forward.
• Generally constant, not related to exertion and poorly responsive to nitrates.
On Examination:
Patient is uncommonly feverish. More commonly, you can auscultate a pericardial rub (heard as a high-pitched or squeaky sound, heard best at the left sternal edge).
Complications:
Patient may also present with signs of:
• Cardiac tamponade: Raised JVP, reduced BP and muffled heart sounds (Beck's triad). Tachycardia, pulsus paradoxus (reduced systolic BP by >10mmHg on inspiration).
• Constrictive pericarditis (raised JVP with inspiration, pulsus paradoxus, hepatosplenomegaly, ascites, oedema, pericardial knock and AF)
115
How can Pericarditis be investigated?
An ECG is the most useful test and should be ordered for all patients. ECG shows concave-up ST elevation and PR segment depression.
Echocardiogram is indicated especially when cardiac tamponade is suspected, it can show a pericardial effusion.
Bloods:
• FBC shows leukocytosis.
• Serum troponin may be raised if there is myocardial involvement.
• ESR and CRP are often raised
• Blood culture if suspected bacterial cause
• ANA, rheumatoid factor
• Viral serology
CXR is usually normal. May have globular heart shadow if large pleural effusion. Pericardial calcification can be seen in constrictive pericarditis.
116
How is Pericarditis managed?
If presents with cardiac tamponade, treatment is a pericardiocentesis.
If not, treat the cause, NSAIDs for pain relief and to treat fever.
If reccurrent, treat with low-dose steroids or immunosuppressants.
If patient has constrictive pericarditis, then perform a pericardiectomy (surgical removal of the pericardium).
117
What is the prognosis of Pericarditis?
Good prognosis if viral cause (settles in 2 weeks). Poorer prognosis of malignant causes.
118
What is the definition and epidemiology of Peripheral Vascular Disease?
Peripheral vascular disease includes a range of arterial symptoms that are caused by atherosclerotic obstruction of the lower-extremity arteries. The prevalence of PVD increases with age.
119
What is the aetiology and classification of Peripheral Vascular Disease?
PVD is most commonly caused by atherosclerosis. Rarer causes of claudication are aortic coarctation, arterial fibrodysplasia, arterial tumour, arterial dissection, arterial embolism, thrombosis, vasospasm, and trauma.
There are four general stages of severity, based on severity of blood flow reduction:
1. Asymptomatic
2. Intermittent Claudication (Chronic Limb Ischaemia involves this and asymptomatic stage)
3. Ischaemic Rest Pain (also called Critical Limb Ischaemia)
4. Ulceration or Gangrene (also Critical Limb Ischaemia).
120
What are the risk factors for Peripheral Vascular Disease?
```
Risk factors are the same (mostly) as any atherosclerotic disease:
• Smoking
• Diabetes
• Hyperlipidaemia
• Hyperhomocysteinaemia
• Low levels of exercise
• History of coronary artery disease or cerebrovascular disease
• Age >40
```
121
What are the symptoms of Peripheral Vascular Disease?
Most patients are asymptomatic (2/3) and diagnosis is prompted on risk factors.
Intermittent claudication (basically angina of the leg) is a muscle pain (ache, numbness, cramp) that occurs during exercise, typically in the calf muscle. Can happen anywhere in leg, as well as thigh or buttock, and is relieved during rest. Most patients are able to localise the pain to one leg.
Patients may also present with erectile dysfunction, an early sign of PVD.
Symptoms of critical limb ischaemia include paraesthesia in the foot or toes, pain at rest, and at night (helped by hanging food off bed).
Non-healing wound/ulceration and gangrene are late stages of Critical Limb Ischaemia, and are uncommon.
122
What are the examination features of Peripheral Vascular Disease?
* Diminished pulse or even absent pulse in lower extremity
* Pallor when elevated, and following rubor when gravity pulls down blood. Doing this is called Buerger's test.
* Signs of limb ischemia include: pale extremity, loss of hair over the dorsum of the foot, thickened toenails, shiny/scaly skin, and nerve loss.
* Ulcers at sites of pressure and distal extremities.
123
How can Peripheral Vascular Disease be investigated?
Bloods:
• U&Es to assess renal function
• Lipids, glucose to look at presence of cardiovascular risk factors.
Ultrasound: ankle-brachial pressure index (ABPI). This is when an ultrasound Doppler determines the ratio between the systolic blood pressure of the ankle and the brachial artery. A ratio of <0.9 is suggestive of PVD. The lower the value, the greater the extent of atherosclerosis and thus disease.
A duplex ultrasound can be used to confirm diagnosis, and assess the extent degree of stenosis.
CT or MR angiography can also be used.
124
What is the definition, epidemiology and aetiology of AVNRT?
AVNRT is a type of paroxysmal supraventricular tachycardia caused by an aberrant circuit within the AV node. It is the most common cause of paroxysmal supraventricular tachycardia, and affects females more than men.
Mainly idiopathic aetiology, occurring most commonly in structurally normal hearts.
125
What are the clinical features of AVNRT?
Patients can present with sudden onset rapid palpitations, dizziness, breathlessness and syncope occasionally occurs.
126
What are the ECG features of AVNRT?
* The QRS complexes are regular as the re-entrant loop is regular.
* Narrow-complex as the ventricular conduction (Bundle of His and Purkinje Fibres) are functioning normally.
* P waves may not be visible as they are buried in the QRS complexes.
127
How is AVNRT managed?
Some AVNRT can be terminated with vagal manoeuvres such as the Valsalva manoeuvre or carotid sinus massage.
I.V adenosine or rate-limiting calcium channel blockers may be used in vagal manoeuvres fail.
In emergencies, when patients present with haemodynamic compromise, DC Cardioversion is advised.
Catheter ablation of re-entrant circuit is indicated in patients with recurrent episodes; associated with a <1% chance of heart block.
128
What is the definition and aetiology of AVRT?
AVRT refers to a form of paroxysmal supraventricular tachycardia caused by an anatomically defined re-entrant circuit involving one or more accessory pathways.
The most common type of AVRT is Wolff-Parkinson White Syndrome (where an accessory pathway connects the ventricles to the atria). The accessory pathway is formed by tissue called the Bundle of Kent.
Most are congenital or can be associated with hypertrophic cardiomyopathy and Epstein's anomaly.
129
What are the clinical features of AVRT?
Palpitations
Chest pain
Syncope
130
What are the ECG features of AVRT?
* Short PR interval (<0.2 sec)
* Delta wave (slurring of the QRS upstroke)
* Broad QRS (>0.12s)
131
How is AVRT managed?
In the acute setting, vagal manoeuvres. I.V adenosine and procainamide or rarely DC cardioversion.
Catheter ablation of the accessory pathway is the definitive therapy.
132
What is the definition and epidemiology of Varicose Veins?
Varicose veins refer to irreversibly tortuous (full of twists and turns) and dilated superficial veins. It is very common, up to one third of the population has varicose veins. Incidence is similar between males and females, but females are more likely to present. Incidence increases with age.
133
What is the aetiology of Varicose Veins?
Primary varicose veins (95%) has an unknown cause. Some individuals have inheritably weak vein walls. There is a strong familial component.
Secondary varicose veins (5%) are caused by obstruction to venous flow. This can be due to intravascular (DVT) or extravascular (trauma, or compression) obstruction, or valvular damage (secondary to DVT).
134
What are the risk factors for Varicose Veins?
* Pregnancy
* Obesity
* Prolonged standing and sitting
* Family history
* Female sex
* DVT
135
What are the clinical features of Varicose Veins?
Patients usually complain of cosmetic concerns. They may also experience itching, discomfort and heaviness in the legs.
Patients can also complain of pain, oedema, night cramps and restless legs.
Symptoms can be exacerbated by prolonged standing, pregnancy, menstruation, HRT or oral pill.
```
On Examination:
Signs of chronic venous insufficiency include:
• Eczema
• Telangiectasia
• Ulcers
• Atrophie blanche (white skin surrounding a healing ulcer)
• Lipodermatosclerosis
• Haemosiderin staining
```
136
How can varicose veins be investigated?
A duplex ultrasound can be used to confirm reversed flow and this diagnosis.
137
How are varicose veins managed? What is the prognosis?
If secondary: treat the cause
Lifestyle modification may prevent progression and complications. This includes weight loss, regular exercise and avoiding exacerbating factors.
Compression stockings are offered for all patients with proven varicose veins.
Interventional treatment includes:
1. Radiofrequency ablation or endovenous laser treatment
2. USS-guided foam sclerotherapy
3. Surgery
If left untreated, varicose veins tend to grow larger and patients may develop chronic venous insufficiency.
Recurrence rate is high.
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What is a leg ulcer?
A leg ulcer is defined as the loss of skin below the knee on the leg or foot, which takes more than two weeks to heal. They can be arterial, venous or neuropathic.
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What are the risk factors for venous ulcers?
* Varicose veins
* Previous DVT
* Phlebitis in affected leg
* Previous fracture, trauma or surgery
* Family history
* Symptoms of venous insufficiency: leg pain, heavy legs, aching, itching, swelling, skin breakdown, pigmentation and eczema.
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What are the clinical features of a venous ulcer?
They happen between the mid-calf and just below the malleolus. There is often peripheral oedema.
They are larger but shallower than other ulcers. They can ooze venous blood when handled. There may be varicose veins and varicose eczema. Hyperpigmentation is due to heamosiderin deposition in the skin.
There may also be atrophie blanche (smooth, ivory-white plaques surrounded by hyperpigmentation).
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What are the clinical features of arterial ulcers?
These are often more distal and on the dorsum of the foot.
Initially they have irregular edges but this may become more clearly defined. The ulcer base contains greyish, granulation tissue. Handling, such as debriding these ulcers, produces little or no blood.
Nocturnal pain is typical. It is worse when supine and is relieved by dangling the legs out of bed.
There are often features of chronic ischemia, such as hairlessness, pale skin, absent pulses, nail dystrophy and wasting of calf muscles.
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What are the clinical features of neuropathic ulcers?
They have a punched-out appearance with deep sinus. These are often under calluses or over pressure points such as the plantar aspect of the first or fifth metatarsophalangeal joint.
They are often surrounded by chronic inflammatory tissue. Probing or debriding may lead to brisk bleeding. They are usually painless and the surrounding area will show diminished or absent sensation.
