Cardiovascular Flashcards
(243 cards)
<p>Define abdominal aortic aneurysm.</p>
<p>Abdominal aortic aneurysm (AAA) is a permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior (AP) diameter of that segment, given the patient's sex and body size.</p>
<p>Explain the aetiology/risk factors of an abdominal aortic aneurysm. Summarise the epidemiology of an abdominal aortic aneurysm.</p>
<p>Cigarette smoking<br></br>Hereditary/family history<br></br>Increased age<br></br>Male sex (prevalence)<br></br>Female sex (rupture)<br></br>Congenital/connective tissue disorders<br></br>Prevalence among men is 4 to 6 times higher than in women.</p>
<p>Recognise the presenting symptoms of an abdominal aortic aneurysm.</p>
<p>AAA is usually asymptomatic and is discovered incidentally. In the minority of patients who experience symptoms, abdominal, back, and groin pain are typical.</p>
<p>Recognise the signs of an abdominal aortic aneurysm on physical examination.</p>
<p>Pulsatile, expanding abdominal pulse. There may also rarely be a palpable pulsatile abdominal mass.</p>
<p>Identify appropriate investigations for an abdominal aortic aneurysm and interpret the results.</p>
<p>Abdominal USS</p>
<p>Define amyloidosis.</p>
<p>Any histological tissue specimen that binds the cotton wool dye, <strong>Congo red</strong>, and demonstrates <strong>green birefringence</strong> when viewed under polarised light is, by definition, an amyloid deposit. The patient with this deposit has amyloidosis. Deposits of amyloid may be localised in tissue or part of a systemic process. Progressive deposition of amyloid is disruptive to tissue and organ function and manifests its clinical sequelae by the dysfunction of those organs in which it deposits.</p>
<p>Explain the aetiology/risk factors of amyloidosis.</p>
<p>Monoclonal gammopathy of undetermined significance (MGUS)<br></br>Inflammatory polyarthropathy<br></br>Chronic infections<br></br>Inflammatory bowel disease<br></br>Familial periodic fever syndromes</p>
<p>Summarise the epidemiology of amyloidosis.</p>
<p>In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year, with around 60 new cases annually.</p>
<p>Recognise the presenting symptoms of amyloidosis. Recognise the signs of amyloidosis on physical examination.</p>
<p>Fatigue<br></br>Weight loss<br></br>Dyspnoea on exertion<br></br>Jugular venous distention<br></br>Lower extremity oedema</p>
<p>Identify appropriate investigations for amyloidosis and interpret the results.</p>
<p>Serum immunofixation - positive in 60% of patients with amyloidosis<br></br>Urine immunofixation - positive in 80% of patients with amyloidosis<br></br>Immunoglobulin free light chain assay - >95% sensitivity<br></br>Bone marrow biopsy - done on all patients with suspected amyloidosis</p>
<p>Define aortic dissection.</p>
<p>Aortic dissection describes the condition when a separation has occurred in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.</p>
<p>Explain the aetiology/risk factors of aortic dissection.</p>
<p>Aortic dissection results from an intimal tear that extends into the media of the aortic wall. Cystic medial degeneration predisposes to intimal disruption and is characterised by elastin, collagen, and smooth muscle breakdown in the lamina media. Bleeding from the vasa vasorum can also lead to this condition.</p>
<p><br></br><strong>Marfan</strong> and <strong>Ehlers-Danlos</strong> increases the risk of aortic dissection.</p>
<p>Summarise the epidemiology of aortic dissection.</p>
<p>The worldwide incidence of aortic dissection is 0.5 to 2.95 cases per 100,000 people annually.</p>
<p>Recognise the presenting symptoms of aortic dissection.</p>
<p>Acute severe chest pain<br></br>Interscapular and lower pain</p>
<p>Recognise the signs of aortic dissection on physical examination.</p>
<p>Left/right blood pressure differential<br></br>Pulse deficit<br></br>Diastolic murmur<br></br>Hypertension</p>
<p>Identify appropriate investigations for aortic dissection and interpret the results.</p>
<p>ECG<br></br>CXR<br></br>Cardiac enzymes<br></br>CT angiography<br></br>Renal function tests<br></br>Liver function tests<br></br>Lactate<br></br>FBC</p>
<p>Define aortic regurgitation.</p>
<p>Aortic regurgitation (AR) is the diastolic leakage of blood from the aorta into the left ventricle. It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root. It can remain asymptomatic for decades before patients present with irreversible myocardial damage.</p>
<p>Explain the aetiology/risk factors of aortic regurgitation.</p>
<p>AR can be caused by primary disease of the aortic valve leaflets or dilation of the aortic root. In developing countries, rheumatic heart disease (rheumatic fever during which the heart valves are damaged) is the most common cause, but congenital bicuspid aortic valve and aortic root dilation account for most of the cases in developed countries.</p>
<p>Summarise the epidemiology of aortic regurgitation.</p>
<p>AR is not as common as aortic stenosis and mitral regurgitation. One US study showed a prevalence of 13% in men and 8.5% in women with most being trace or mild; a prevalence of 15.6% was reported in African-Americans. Prevalence increases with age in both genders.</p>
<p>Recognise the presenting symptoms of aortic regurgitation.</p>
<p>Dyspnoea<br></br>Fatigue<br></br>Weakness<br></br>Orthopnoea<br></br>Paroxysmal nocturnal dyspnoea<br></br>Pallor</p>
<p>Recognise the signs of aortic regurgitation on physical examination.</p>
<p>Mottled extremities<br></br>Rapid and faint peripheral pulse<br></br>Jugular venous distension<br></br>Basal lung crepitations<br></br>Altered mental status<br></br>Urine output <30 mL/hour<br></br>Soft S1<br></br>Soft or absent A2<br></br><strong>Collapsing (water hammer or Corrigan's) pulse</strong><br></br>Cyanosis<br></br>Tachypnoea<br></br>Displaced, hyperdynamic apical impulse</p>
<p>Identify appropriate investigations for aortic regurgitation and interpret the results.</p>
<p>ECG<br></br>CXR<br></br>Echo<br></br>Colour flow Doppler<br></br>Pulsed wave Doppler<br></br>Continuous wave Doppler</p>
<p>Define aortic stenosis.</p>
<p>Aortic stenosis (AS) represents obstruction of blood flow across the aortic valve due to pathological narrowing. It is a progressive disease that presents after a long subclinical period with symptoms of decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure.<br></br>Can be due to aortic calcification.</p>
<p>Explain the aetiology/risk factors of aortic stenosis.</p>
<p>Age >60 years<br></br>Congenitally bicuspid aortic valve<br></br>Rheumatic heart disease<br></br>Chronic kidney disease</p>
Summarise the epidemiology of aortic stenosis.
AS is the most common valvular disease in the US and Europe and is the second most frequent cause for cardiac surgery. It is largely a disease of older people, and patients typically present in the seventh or eighth decade of life.
Recognise the presenting symptoms of aortic stenosis.
Dyspnoea
Chest pain
Syncope
Recognise the signs of aortic stenosis on physical examination.
Ejection systolic murmur
S2 diminished and single
Identify appropriate investigations for aortic stenosis and interpret the results.
Transthoracic echocardiogram (including Doppler)
ECG
Define arterial ulcers.
Arterial ulcers are caused by ischaemia to the leg. The ulcers are painful and more painful on elevation. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed.
Explain the aetiology/risk factors of arterial ulcers.
Smoking
Diabetes mellitus
Hypertension
Hyperlipidaemia
Strong family history of atherosclerotic disease
Male
Summarise the epidemiology of arterial ulcers.
Arterial ulcers are more common in males and people who have risk factors. They occur where the blood supply is the worst.
Recognise the presenting symptoms of arterial ulcers. Recognise the signs of arterial ulcers on physical examination.
Painful, especially on elevation
Deep, punched out, dry and often elliptical sore
Location: between toes, ball of foot, lateral malleolus and bony prominence
Cold, pale limbs
Poor capillary refill
Venous guttering
Absent or weak pulses
Atrophic skin changes
Identify appropriate investigations for arterial ulcers and interpret the results.
Investigate for signs of atherosclerotic disease:
BM
FBC
Fasting lipids
Urinalysis
Biopsy
Buerger’s test: Blanching of the foot on elevation to 15 degrees
Define atrial fibrillation.
Atrial fibrillation (AF) is a supraventricular tachyarrhythmia. It is characterised by uncoordinated atrial activity on the surface ECG, with fibrillatory waves of varying shapes, amplitudes, and timing associated with an irregularly irregular ventricular response when atrioventricular (AV) conduction is intact.
Explain the aetiology/risk factors of atrial fibrillation.
Coronary artery disease (CAD), hypertension, heart failure, valvular disease, diabetes, thyroid disorders, COPD and obstructive sleep apnoea, and advanced age are known risk factors for the development of new-onset AF.
Heavy alcohol intake can also increase the risk of atrial fibrillation.
Summarise the epidemiology of atrial fibrillation.
The incidence of AF increases progressively with age.
Incidence is higher in men but mortality is higher in women.
Recognise the presenting symptoms of atrial fibrillation.
SOB
Palpitations
Chest tightness
Recognise the signs of atrial fibrillation on physical examination.
Hypotension
Elevated jugular venous pressure
Added heart sounds
Identify appropriate investigations for atrial fibrillation and interpret the results.
ECG
Serum electrolytes
Cardiac biomarkers
Thyroid function tests
CXR
Transthoracic echocardiogram
Transoesophageal echocardiogram (TOE)
Generate a management plan for atrial fibrillation.
The 3 elements in the management of new-onset AF are:
Ventricular rate control
Restoration and maintenance of sinus rhythm
Prevention of thromboembolic events.
Identify the possible complications of atrial fibrillation and its management.
Acute stroke
MI
Congestive heart failure
Summarise the prognosis for patients with atrial fibrillation.
The prognosis depends on the onset, age and lifestyle of the patient.
Define atrial flutter.
Typical atrial flutter (anti-clockwise cavotricuspid isthmus-dependent atrial flutter) is a macro-reentrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm.
Explain the aetiology/risk factors of atrial flutter.
Increasing age
Valvular dysfunction
Atrial septal defects
Atrial dilation
Recent cardiac or thoracic procedures
Surgical or post-ablation scarring of atria
Heart failure
Hyperthyroidism
COPD
Asthma
Pneumonia
Summarise the epidemiology of atrial flutter.
The overall incidence has been reported as 88/100,000 person-years, with increasing rates with older age.
Recognise the presenting symptoms of atrial flutter. Recognise the signs of atrial flutter on physical examination.
Palpitations
Fatigue or lightheadedness
Jugular venous pulsations with rapid flutter waves
Chest pain
Dyspnoea
Syncope
Hypotension
Identify appropriate investigations for atrial flutter and interpret the results.
ECG: In the typical form, this entity is characterised electrocardiographically by flutter waves, which are a saw-tooth pattern of atrial activation, most prominent in leads II, III, aVF, and V1.
TFTs
Serum electrolytes
CXR
Generate a management plan for atrial flutter.
Synchronised cardioversion until stable.
Once stable:
1st line: Beta-blocker or CCB or amiodarone
Plus:
Anticoagulation
Treat co-existing acute disease process
Identify the possible complications of atrial flutter and its management.
Myocardial ischaemia
Acute stroke
Summarise the prognosis for patients with atrial flutter.
In approximately 60% of cases, atrial flutter occurs in the setting of an acute process. Once that process has been treated, sinus rhythm is usually restored and chronic therapy is not required.
Define cardiomyopathy.
Primary disease of the myocardium. Cardiomyopathy can be split into three different categories, dilated, hypertrophic and restrictive.
Explain the aetiology/risk factors of dilated cardiomyopathy.
Flabby heart of unknown cause.
- Alcohol
- Hypertension
- Viral infection
- Autoimmune
Explain the aetiology/risk factors of hypertrophic cardiomyopathy.
Obstruction of outflow tract from asymmetric septal hypertrophy.
- Inherited (autosomal dominant)
Explain the aetiology/risk factors of restrictive cardiomyopathy.
- Amyloidosis
- Haemochromatosis
- Sarcoidosis
- Scleroderma
Summarise the epidemiology of cardiomyopathy.
Dilated cardiomyopathy is the most common form and affects five in 100,000 adults and 0.57 in 100,000 children. It is the third leading cause of heart failure in the United States behind coronary artery disease (CAD) and hypertension.
Recognise the presenting symptoms of cardiomyopathy. Recognise the signs of cardiomyopathy on physical examination.
Angina
Dyspnoea
Syncope
Sudden death
Identify appropriate investigations for cardiomyopathy and interpret the results.
ECG
Echocardiogram.
MRI scan.
Heart rhythm monitor (24 or 48-hour ECG monitor)
Exercise tests
Family tree/genetic screening
Define constrictive pericarditis.
This is an inflammation of the pericardium.
Explain the aetiology/risk factors of constrictive pericarditis.
Acute pericarditis can be idiopathic or due to an underlying systemic condition (e.g. systemic lupus erythematosus).
Summarise the epidemiology of constrictive pericarditis.
Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men. It is the most common disease of the pericardium encountered in clinical practice.
Recognise the presenting symptoms of constrictive pericarditis.
Chest pain
Fever
Recognise the signs of constrictive pericarditis on physical examination.
Pericardial rub
Ankle oedema
Ascites
Identify appropriate investigations for constrictive pericarditis and interpret the results.
ECG
CXR
CRP
Serum troponin
Pericardial fluid/blood culture
ESR
Serum urea
FBC
Echocardiography
Define deep vein thrombosis (DVT).
A blood clot in the deep vein of the leg.
Explain the aetiology/risk factors of deep vein thrombosis (DVT).
Being immobile for long periods
The Pill (increases chance of blood clots)
Age
Trauma
Active cancer
Pregnancy
Clotting disorder
Smoking
Summarise the epidemiology of deep vein thrombosis (DVT).
Venous thromboembolism (VTE) is a relatively common medical problem with a yearly incidence of approximately 1 in every 1000 adults. About two thirds of these cases are DVT and one third progress to a PE.
Recognise the presenting symptoms of deep vein thrombosis (DVT). Recognise the signs of deep vein thrombosis (DVT) on physical examination.
Pain in leg
Asymmetric oedema
Prominent superficial vein
Identify appropriate investigations for deep vein thrombosis (DVT) and interpret the results.
Wells' score - Risk of DVT or PE
Quantitative D-dimer level - Tells you how much FDP (fibrin degradation product), doesn’t work for pregnancy or cancer as these can affect clotting.
Proximal duplex ultrasound
Whole-leg ultrasound
INR and activated partial thromboplastin time (aPTT)
Urea and creatinine
LFTs
FBC
Generate a management plan for deep vein thrombosis (DVT).
Heparin
Adjunct:
Stockings
Identify the possible complications of deep vein thrombosis (DVT) and its management.
The clot could travel to the lungs and cause a PE.
Summarise the prognosis for patients with deep vein thrombosis (DVT).
Patient should be fine as long as they start heparin. It depends on what caused the DVT (e.g. cancer).
Define gangrene.
Gangrene is a complication of necrosis characterised by the decay of body tissues. There are two major categories: infectious gangrene (wet gangrene) and ischaemic gangrene (dry gangrene).
Explain the aetiology/risk factors of gangrene.
Diabetes
Smoking
Atherosclerosis
Renal disease
Drug and alcohol abuse
Malignancy
Trauma or abdominal surgery
Contaminated wounds
Malnutrition
Hypercoagulable states
Prolonged use of tourniquets
Summarise the epidemiology of gangrene.
Gangrene occurs equally in men and women. Type I necrotising fasciitis occurs most commonly in patients with diabetes and patients with peripheral vascular disease. It is the most common form of necrotising fasciitis in the general population.
Recognise the presenting symptoms of gangrene. Recognise the signs of gangrene on physical examination.
Pain
Oedema
Skin discoloration
Crepitus (gas gangrene)
Diminished pedal pulses and ankle-brachial index (ischaemic gangrene)
Low-grade fever and chills (infectious gangrene)
Identify appropriate investigations for gangrene and interpret the results.
FBC
Comprehensive metabolic panel
Serum LDH
Coagulation panel
Blood cultures
Serum C-reactive protein
Plain x-rays
CT of affected site
MRI of affected site
Doppler ultrasonography
Define heart block.
Cardiac electric disorder characterised by delayed (or absent) conduction from the atria to the ventricles.
Explain the aetiology/risk factors of heart block.
Hypertension
Increased vagal tone
AV-nodal blocking agents
Chronic stable CAD
Acute coronary syndrome
CHF
Hypertension
Cardiomyopathy
Summarise the epidemiology of heart block.
The epidemiology of AV block is not well characterised.
Advanced AV block (usually type II second-degree and third-degree) is usually anatomically infranodal and is seen in advanced His-Purkinje disease.
Recognise the presenting symptoms of heart block.
Syncope
Bradycardia <40 bpm
Fatigue
Dyspnoea
Chest pain
Palpitations
Nausea/vomiting
Recognise the signs of heart block on physical examination.
High blood pressure
Sometimes low blood pressure
Identify appropriate investigations for heart block and interpret the results.
ECG
Serum troponin
Serum potassium
Serum calcium
Serum pH
Serum digitalis level
Generate a management plan for first degree or second degree Type I heart block.
Asymptomatic
1st line: Monitoring
Symptomatic
1st line: Discontinuation of AV-nodal blocking medications.
2nd line: Infrequently: PPM (permanent pacemaker) or cardiac resynchronisation therapy ± ICD placement.
Generate a management plan for second degree Type II or third degree heart block.
Asymptomatic or mildly to moderately symptomatic
1st line: Condition-specific management and discontinuation of AV node-blocking drugs.
2nd line: PPM or cardiac resynchronisation therapy ± ICD placement
Severely symptomatic
1st line: Condition-specific management, discontinuation of AV-nodal blocking drugs, and temporary (transcutaneous or transvenous) pacing.
2nd line: PPM or cardiac resynchronisation therapy ± ICD placement.
Identify the possible complications of heart block and its management.
In the short term, periprocedurally, the risks associated with pacemaker implantation are low: in the range of 2% to 3%. These include bleeding, infection, vascular trauma, pneumothorax, cardiac tamponade, lead dislodgement, and pocket haematoma development. The risk of MI, stroke, and death is <1%.
Long-term complications include pulse generator or lead malfunction and infection. The pulse generators run on batteries that average 7 to 10 years in longevity. Battery depletion requires replacing the pulse generator.
Over a lifetime, there is some risk of infection of the lead, which may require extraction, a complex procedure that should be performed at specialised centres.
Summarise the prognosis for patients with heart block.
The prognosis is related to the degree of AV block and the severity of associated symptoms. In certain conditions, such as sarcoid or amyloid heart disease or acute anterior MI, the underlying condition strongly determines prognosis.
Define hypercholesterolaemia.
Hypercholesterolaemia, an elevation of total cholesterol (TC) and/or low-density lipoprotein cholesterol (LDL-C) or non-high-density lipoprotein cholesterol (HDL-C).
Explain the aetiology/risk factors of hypercholesterolaemia.
Insulin resistance and type 2 diabetes mellitus
Excess body weight (body mass index >25 kg/m²)
Hypothyroidism
Cholestatic liver disease
Summarise the epidemiology of hypercholesterolaemia.
Approximately 28.5 million adults or nearly 12% of the adult population in the US have total cholesterol levels ≥6.2 mmol/L (≥240 mg/dL).
Recognise the presenting symptoms of hypercholesterolaemia. Recognise the signs of hypercholesterolaemia on physical examination.
Family history of early onset of coronary heart disease or dyslipidaemia in first-degree relatives
History of cardiovascular disease
Excess body weight (especially abdominal obesity)
Xanthelasmas
Corneal arcus
Identify appropriate investigations for hypercholesterolaemia and interpret the results.
Lipid profile
Serum thyroid-stimulating hormone (TSH)
Lipoprotein(a)
Generate a management plan for hypercholesterolaemia.
Statins
Lifestyle modifications
Can use ezetimibe or PCSK9 inhibitor
Identify the possible complications of hypercholesterolaemia and its management.
Ischaemic heart disease
Peripheral vascular disease (PVD)
Acute coronary syndrome
Stroke
Erectile dysfunction
Summarise the prognosis for patients with hypercholesterolaemia.
If the treatment plan includes detection and management of other factors that contribute to the development of coronary heart disease (CHD), such as hypertension, diabetes mellitus, and smoking, the overall prognosis of hypercholesterolaemia is improved.
Define hypertriglyceridemia.
Hypertriglyceridaemia is defined by the National Cholesterol Education Program Adult Treatment Panel III as fasting plasma triglyceride level ≥2.3 mmol/L (≥200 mg/dL).
Explain the aetiology/risk factors of hypertriglyceridemia.
Family history of hyperlipidaemia
Family history of diabetes
Overweight/obese patients
High-saturated-fat diet
High-carbohydrate diet
Insulin resistance
Liver disease
Hypothyroidism
Renal disease
Excessive alcohol consumption
HIV infection
Cystic fibrosis
Summarise the epidemiology of hypertriglyceridemia.
The 90th percentile for triglyceride levels has been historically noted to be approximately 2.8 mmol/L (250 mg/dL) in the US. Because hypertriglyceridemia is related to insulin resistance, its prevalence is expected to continue to increase in industrialised countries.
Recognise the presenting symptoms of hypertriglyceridemia. Recognise the signs of hypertriglyceridemia on physical examination.
Lipaemia retinalis
Eruptive xanthoma
Obesity/overweight
Diabetes
Coronary artery disease
Angina/claudication
Identify appropriate investigations for hypertriglyceridemia and interpret the results.
Fasting triglycerides
Generate a management plan for hypertriglyceridemia.
IV insulin + dextrose
Lifestyle modification
Identify the possible complications of hypertriglyceridemia and its management.
Coronary events
Acute pancreatitis
Summarise the prognosis for patients with hypertriglyceridemia.
The prognosis for patients with respect to coronary artery disease or acute pancreatitis is improved significantly with lowering of triglyceride levels to the recommended targets. This will require ongoing long-term therapy with monitoring of plasma lipids as well as side effects.
Define hypertension.
Resting blood pressure over 140/90 mmhg.
Explain the aetiology/risk factors of hypertension.
Blood pressure naturally increases as you grow older, however diastolic generally doesn’t change that much.
There are some important risk factors e.g. smoking, obesity, low activity, high cholesterol, poor diet etc.
Summarise the epidemiology of hypertension.
Worldwide, it is estimated that 1 billion people are hypertensive, accounting for an estimated 7.1 million deaths per year. It is becoming an increasingly common problem because of increased longevity and the prevalence of contributing factors such as obesity, physical inactivity, and unhealthy diet.
Recognise the presenting symptoms of hypertension.
Hypertension is generally asymptomatic.
Serious hypertension may present with signs such as headache, vision changes, SOB etc.
Recognise the signs of hypertension on physical examination.
A sustained resting blood pressure of 140/90 mmhg.
Retinopathy may also be present.
Identify appropriate investigations for hypertension and interpret the results.
ECG
Fasting metabolic panel with estimated GFR
Lipid panel
Urinalysis
Hb
Thyroid-stimulating hormone
These tests are to find the cause of the hypertension rather than to confirm the presence of hypertension.
Define infective endocarditis.
An infection of the endocardium or heart valves. Staphylococcus aureus followed by Streptococci of the viridans group and coagulase negative Staphylococci are the three most common organisms responsible for infective endocarditis.
Explain the aetiology/risk factors of infective endocarditis.
Poor dentition/gingivitis
Prior hx of infectious endocarditis
Presence of artificial prosthetic heart valves
Certain types of congenital heart disease
Post-heart transplant (patients who develop cardiac valvulopathy)
Summarise the epidemiology of infective endocarditis.
Men are affected 2.5 times more often than women, and there does not appear to be any difference among people of different ancestries.
Recognise the presenting symptoms of infective endocarditis.
Chest pain
SOB
Fever
Night sweats/fatigue/malaise
Recognise the signs of infective endocarditis on physical examination.
Janeway lesions
Osler nodes
Splinter haemorrhages
Identify appropriate investigations for infective endocarditis and interpret the results.
ECG
Echo
Serum chemistry panel with glucose
FBC
Urinalysis
Blood cultures
Generate a management plan for infective endocarditis.
Determine which antibiotics the bacteria is sensitive to and administer those antibiotics. Macrolides are usually popular (gentamicin etc.)
Surgery may be considered in severe cases.
Identify the possible complications of infective endocarditis and its management.
Congestive heart failure (CHF)
Systemic embolisation
Anterior mitral valve vegetation >10 mm
Valvular dehiscence, rupture, or fistula
Splenic abscess
Mycotic aneurysms
Summarise the prognosis for patients with infective endocarditis.
There are no comprehensive studies that have looked at overall prognosis in patients with IE. Congestive heart failure remains the single greatest predictor of prognosis in patients, regardless of the offending micro-organism. Surgery, if indicated, has been associated with a lower overall mortality; however, patients with definitive indications for surgery tend to be critically ill and carry a high intra-operative mortality rate.
Define mitral regurgitation.
Failure of the mitral valve which causes backwash of blood from the left ventricle into the left atrium.
Explain the aetiology/risk factors of mitral regurgitation.
Mitral valve prolapse
Hx of rheumatic heart disease
Infective endocarditis
Hx of cardiac trauma
Hx of MI
Hx of cvs disease
Hypertrophic cardiomyopathy
Anorectic/dopaminergic drugs
Summarise the epidemiology of mitral regurgitation.
Although the exact incidence and prevalence of MR is unknown it has been suggested that the prevalence probably exceeds 5,000,000 worldwide.
Recognise the presenting symptoms of mitral regurgitation.
SOB on exertion
Orthopnoea
Palpitations
Decreased exercise tolerance
Fatigue
Recognise the signs of mitral regurgitation on physical examination.
S3 sound
Lower extremity oedema
Diminished S1 sound
Identify appropriate investigations for mitral regurgitation and interpret the results.
ECG
Echocardiogram
Define mitral stenosis.
Narrowing of the mitral orifices which can be caused by rheumatic valvulitis producing fusion of the valve commissures and thickening of the valve leaflets.
Explain the aetiology/risk factors of mitral stenosis.
Streptococcal infection
Summarise the epidemiology of mitral stenosis.
Females are more likely to get mitral stenosis.
Most cases of mitral stenosis are caused by rheumatic fever. While rheumatic fever is now very rare in developed nations, it remains epidemic in much of the world.
Recognise the presenting symptoms of mitral stenosis. Recognise the signs of mitral stenosis on physical examination.
Loud S1
Irregularly irregular pulse
Malar flush
Hx of orthopnea
Dyspnoea
Identify appropriate investigations for mitral stenosis and interpret the results.
ECG
Echo
CXR
Define myocarditis.
Inflammation of the myocardium in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease. It is a clinical syndrome of non-ischaemic myocardial inflammation resulting from a heterogeneous group of infectious, immune, and non-immune diseases.
Explain the aetiology/risk factors of myocarditis.
Infection
HIV
Smallpox vaccine
Autoimmune disease
Peripartum and postnatal periods
Summarise the epidemiology of myocarditis.
Autopsy studies reveal myocarditis in 1% to 9% of routine postmortem examinations, and a prospective postmortem study of sudden cardiac death in young adults suggests myocarditis as the aetiology in approximately 10% of cases.
Recognise the presenting symptoms of myocarditis.
Chest pain
SOB
Fatigue
Palpitations
Recognise the signs of myocarditis on physical examination.
S3 gallop
Sinus tachycardia
Elevated neck veins
Identify appropriate investigations for myocarditis and interpret the results.
ECG
CXR
Troponin
Echo
CK
BNP
Define STEMI.
ST-elevation myocardial infarction (STEMI) is suspected when a patient presents with persistent ST-segment elevation in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history.
Explain the aetiology/risk factors of STEMI.
Smoking
Hypertension
Diabetes
Obesity
Metabolic syndrome
Physical inactivity
Dyslipidaemia
Renal insufficiency
Established coronary artery disease
Family history of premature coronary artery disease
Cocaine use
Male sex
Advanced age
Summarise the epidemiology of STEMI.
The overall prevalence of MI in the US is around 2.8% in adults aged 20 years or over. The estimated incidence is 550,000 new and 200,000 recurrent MIs annually.
Recognise the presenting symptoms of STEMI. Recognise the signs of STEMI on physical examination.
Chest pain
Dyspnoea
Pallor
Diaphoresis
Cardiogenic shock
Nausea and/or vomiting
Dizziness or light-headedness
Weakness
Tachycardia
Additional heart sounds
Identify appropriate investigations for STEMI and interpret the results.
ECG
Troponin
Electrolytes, urea, and creatinine
Serum lipids
CXR
Coronary angiogram
Generate a management plan for STEMI.
Aspirin
Adjunct:
GTN or morphine
Identify the possible complications of STEMI and its management.
Sinus bradycardia
Heart block
Recurrent chest pain
Acute mitral regurgitation
Ventricular septal defects (VSD)
Acute pericardial tamponade
Post-infarction pericarditis (Dressler's syndrome)
Congestive heart failure
Ventricular arrhythmias
Recurrent ischaemia and infarction
Summarise the prognosis for patients with STEMI.
About 15% of people who have an acute MI in the US will die of it, half within the first hour of symptoms. Prognosis for patients with STEMI varies depending on time to presentation after onset of chest pain and time to treatment after presentation.
Define NSTEMI.
Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischaemic event causing myocyte necrosis. The initial ECG may show ischaemic changes such as ST depressions, T-wave inversions, or transient ST elevations; however, it may also be normal or show non-specific changes.
Explain the aetiology/risk factors of NSTEMI.
Atherosclerosis
Diabetes
Smoking
Dyslipidaemia
Age >65 years
Hypertension
Obesity and metabolic syndrome phenotype
Physical inactivity
Cocaine use
Depression
Stent thrombosis or restenosis
Chronic kidney disease
Sleep apnoea
Summarise the epidemiology of NSTEMI.
Epidemiology data have shown that acute coronary syndrome (ACS) cases with ST-elevation myocardial infarction (STEMI) appear to be declining and that NSTEMI occurs more frequently than STEMI.
Recognise the presenting symptoms of NSTEMI. Recognise the signs of NSTEMI on physical examination.
Chest pain
Diaphoresis
Physical exertion
Shortness of breath
Weakness
Anxiety
Nausea
Vomiting
Abdominal pain
Hypertension
Identify appropriate investigations for NSTEMI and interpret the results.
ECG
Troponin
Glucose
U+Es
Creatinine
Cardiac angiogram
CXR
LFTs
CK
Generate a management plan for NSTEMI.
1st line: Antiplatelet therapy (aspirin + clopidogrel, ticagrelor or prasugrel)
Adjunct:
Oxygen
Glyceryl trinitrate ± morphine
Beta-blocker
Calcium-channel blocker
Identify the possible complications of NSTEMI and its management.
Cardiac arrhythmias
Congestive heart failure (CHF)
Cardiogenic shock
Ventricular rupture or aneurysm
Acute mitral regurgitation
Post-MI pericarditis (Dressler syndrome)
Venous thromboembolism (VTE)
Summarise the prognosis for patients with NSTEMI.
Patients who have experienced NSTEMI have a high risk of morbidity and death from a future event. The rate of sudden death in patients who have had a myocardial infarction (MI) is 4 to 6 times the rate in the general population.
Define pericarditis.
An inflammation of the pericardium. The acute form is defined as new-onset inflammation lasting <4-6 weeks. It can be either fibrinous (dry) or effusive with a purulent, serous, or haemorrhagic exudate.
Explain the aetiology/risk factors of pericarditis.
Having cardiac surgery or being on dialysis can also increase the risk of getting pericarditis. Viral or bacterial infections can also cause this.
Summarise the epidemiology of pericarditis.
Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men. It is the most common disease of the pericardium encountered in clinical practice. The true incidence and prevalence of the disease are unknown and there are a large number of undiagnosed cases.
Recognise the presenting symptoms of pericarditis.
Chest pain
Pericardial friction rub
Fever
Recognise the signs of pericarditis on physical examination.
Symptoms and signs of right-sided heart failure, including fatigue, ankle oedema, and, in severe cases, ascites.
Identify appropriate investigations for pericarditis and interpret the results.
ECG
Echocardiogram
CXR
Serum urea
FBC
Blood culture
Troponin
Generate a management plan for pericarditis.
Pericardiocentesis + systemic antibiotics
Non-steroidal anti-inflammatory drug (NSAID)
Proton-pump inhibitor
Exercise restriction
Second line treatment is a pericardiectomy.
Identify the possible complications of pericarditis and its management.
Pericardial effusion with or without cardiac tamponade
Chronic constrictive pericarditis
Summarise the prognosis for patients with pericarditis.
Prognosis generally depends on the underlying cause and disease severity. Features associated with a poor prognosis include:
Evidence of a large pericardial effusion (i.e., diastolic echo-free space >20 mm)
High fever (i.e., >38°C)
Sub-acute course (i.e., symptoms over several days without a clear-cut acute onset)
Failure to respond within 7 days to a non-steroidal anti-inflammatory drug (NSAID).
Define peripheral arterial disease.
Peripheral arterial disease (PAD) includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower-extremity arteries.
Explain the aetiology/risk factors of peripheral arterial disease.
Smoking
Diabetes
Hypertension
Hyperlipidaemia
Age >40 years
History of coronary artery disease/cerebrovascular disease
Low levels of exercise
Summarise the epidemiology of peripheral arterial disease.
The prevalence of PAD increases with age, beginning after 40 years of age. In the UK, one-fifth of people aged 65 to 75 years have evidence of PAD on clinical examination.
Recognise the presenting symptoms of peripheral arterial disease. Recognise the signs of peripheral arterial disease on physical examination.
Asymptomatic
Intermittent claudication
Thigh or buttock pain with walking that is relieved with rest
Diminished pulse
Identify appropriate investigations for peripheral arterial disease and interpret the results.
Ankle-brachial index
Doppler ultrasound
MRA
Dupplex scan
Angioplasty
Define pulmonary embolism.
Pulmonary embolism (PE) is a consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities. Approximately 51% of DVT will embolise to the pulmonary embolus which results in a PE.
Explain the aetiology/risk factors of pulmonary embolism.
Sitting for long periods of time without movement
Smoking
Increased age
Broken bones (fat embolus)
Clotting disorders which cause clots to form more easily.
Summarise the epidemiology of pulmonary embolism.
In the UK, 47,594 cases of PE were reported in the 1-year period between 2013 and 2014. Incidence increases with increased age.
Recognise the presenting symptoms of pulmonary embolism.
SOB
Chest pain
Cough
Recognise the signs of pulmonary embolism on physical examination.
Tachycardia
Tachypnoea
Swelling in leg
Haemoptysis
Identify appropriate investigations for pulmonary embolism and interpret the results.
Wells criteria/Geneva score
Multiple-detector computed tomographic pulmonary angiography (CTPA)
Ventilation-perfusion (V/Q) scan
Coagulation studies
Urea and creatinine
FBC
Pulmonary Embolism Rule-Out Criteria (PERC)
D-dimer test
Generate a management plan for pulmonary embolism.
- Respiratory support
- Intravenous fluids
- Vasoactive agents
- Anticoagulation
- Thrombolysis or embolectomy or catheter-directed therapy
Adjunct:
Venous filter
Identify the possible complications of pulmonary embolism and its management.
Acute bleeding during treatment
Pulmonary infarction
Cardiac arrest/death
Chronic thromboembolic pulmonary
Heparin-associated thrombocytopenia (HIT)
Recurrent venous thromboembolic event
Summarise the prognosis for patients with pulmonary embolism.
Patients in the high-risk category have a short-term mortality of 10.9%, while patients in the low-risk category have 30-day mortality of 1%.
Define pulmonary hypertension.
Idiopathic pulmonary arterial hypertension (IPAH) is a disease of the small pulmonary arteries characterised by vascular proliferation and remodelling. It results in a progressive increase in pulmonary vascular resistance (PVR) and, ultimately, right ventricular failure and death.
Explain the aetiology/risk factors of pulmonary hypertension.
Bone morphogenetic protein receptor type 2 (BMPR2) mutations
Appetite suppressants
Summarise the epidemiology of pulmonary hypertension.
While pulmonary artery hypertension remains a rare disease, it is being increasingly recognised, with an estimated prevalence of 15.0 cases per million adult inhabitants and incidence of 2.4 cases per million adult inhabitants per year.
Recognise the presenting symptoms of pulmonary hypertension.
SOB
Fatigue
Recognise the signs of pulmonary hypertension on physical examination.
Peripheral oedema
Cyanosis
Accentuated pulmonic component (P2) to the second heart sound
Tricuspid regurgitation murmur
Identify appropriate investigations for pulmonary hypertension and interpret the results.
CXR
ECG
Transthoracic Doppler
BNP
FBC
LFT
Define rheumatic fever.
Rheumatic fever is an autoimmune disease that may occur following group A streptococcal throat infection. It can affect multiple systems, including the joints, heart, brain, and skin. Only the effects on the heart can lead to permanent illness.
Explain the aetiology/risk factors for rheumatic fever.
Poverty
Overcrowded living quarters
Family history of rheumatic fever
D8/17 B cell antigen positivity
HLA association
Genetic susceptibility
Summarise the epidemiology of rheumatic fever.
Primary episodes of acute rheumatic fever occur mainly in children aged 5 to 14 years and are rare in people over 30 years old. More than 2.4 million children have rheumatic heart disease worldwide; 94% of these are in developing countries.
Recognise the presenting symptoms of rheumatic fever. Recognise the signs of rheumatic fever on physical examination.
Sore throat
Chest pain
Shortness of breath
Palpitations
Heart murmur
Pericardial rub
Signs of cardiac failure
Swollen joints
Restlessness, clumsiness
Emotional lability and personality changes
Jerky, uncoordinated choreiform movements
Identify appropriate investigations for rheumatic fever and interpret the results.
ESR
CRP
WBC count
Blood cultures
Electrocardiogram
CXR
Echocardiogram
Throat culture
Rapid antigen test for group A streptococci
Anti-streptococcal serology
Define supraventricular tachycardia.
Supraventricular tachycardia is characterised as a rapid regular rhythm arising from a discrete area within the atria. It occurs in a wide range of clinical conditions, including catecholamine excess, digoxin toxicity, paediatric congenital heart disease, and cardiomyopathy.
Explain the aetiology/risk factors of supraventricular tachycardia.
Supraventricular tachycardia has a variety of causes. It may occur in healthy people, although often there is underlying cardiac pathology. Associated conditions include cardiomyopathies, ischaemic heart disease, previous cardiac surgery, and hyperthyroidism.
Summarise the epidemiology of supraventricular tachycardia.
Focal atrial tachycardia is a relatively uncommon arrhythmia that occurs in all age groups and represents approximately 3% to 17% of the patients referred for supraventricular tachycardia ablation. There is no particular pattern in relation to sex or ancestry.
Recognise the presenting symptoms of supraventricular tachycardia.
Palpitations
Fatigue, weakness
SOB
Recognise the signs of supraventricular tachycardia on physical examination.
Rales
Oedema
Identify appropriate investigations for supraventricular tachycardia and interpret the results.
ECG
Digoxin level
Theophylline level
CXR
Electrolytes
Toxicology screen
Generate a management plan for supraventricular tachycardia.
- Beta-blocker or calcium-channel blocker
- Ibutilide or amiodarone
- Third-line pharmacotherapy or direct current (DC) cardioversion + cardiology consult
Identify the possible complications of supraventricular tachycardia and its management.
Congestive heart failure
Resistance to therapy
Cardiomyopathy
Summarise the prognosis for patients with supraventricular tachycardia.
Prognosis depends on the ability to control the arrhythmia. This is further influenced by the patient's age, underlying cause of the arrhythmia, tolerance of adverse effects of the chosen treatment, and comorbidities.
Define tricuspid regurgitation.
Tricuspid regurgitation (TR) occurs when blood flows backwards through the tricuspid valve. In the vast majority of patients, this occurs during systole, but severely elevated right ventricular filling pressure can be associated with diastolic TR.
Explain the aetiology/risk factors of tricuspid regurgitation.
Left-sided heart failure
Dilated tricuspid annulus
Rheumatic heart disease
Permanent pacemaker
Endocarditis
Carcinoid heart disease
Summarise the epidemiology of tricuspid regurgitation.
Some degree of valvular regurgitation is a quite common accidental finding in colour Doppler imaging. In fact, two-dimensional echocardiography has demonstrated that 50% to 60% of asymptomatic young adults exhibit mild tricuspid regurgitation.
Recognise the presenting symptoms of tricuspid regurgitation.
Fatigue and effort intolerance
Dyspnoea
Palpitations
Recognise the signs of tricuspid regurgitation on physical examination.
Jugular venous abnormality
Irregular heart rhythm
Parasternal systolic murmur
Increased systolic murmur on inspiration (Carvallo's sign)
Peripheral oedema
Identify appropriate investigations for tricuspid regurgitation and interpret the results.
ECG
Doppler USS
Echo
LFTs
Serum urea and creatinine
FBC
Define varicose veins.
Varicose veins are subcutaneous, permanently dilated veins 3 mm or more in diameter when measured in a standing position.
Explain the aetiology/risk factors of varicose veins.
Increasing numbers of births
DVT
Occupation with prolonged standing
Obesity
Summarise the epidemiology of varicose veins.
Prevalence estimates vary based on population, selection criteria, disease definition, and imaging techniques. Generally, prevalence rates are higher in industrialised countries and in more developed regions.
Recognise the presenting symptoms of varicose veins.
Dilated tortuous veins
Leg fatigue or aching with prolonged standing
Leg cramps
Restless legs
Recognise the signs of varicose veins on physical examination.
Haemosiderin deposition
Corona phlebectatica
Identify appropriate investigations for varicose veins and interpret the results.
Duplex ultrasound
Generate a management plan for varicose veins.
Patients should also be counselled on lifestyle modifications including weight loss, leg elevation, and exercise. Use of compression stockings can also help the physician and patient to determine whether symptoms are truly related to varicosities.
Identify the possible complications of varicose veins and its management.
Chronic venous insufficiency
Haemorrhage
Venous ulceration
Lipodermatosclerosis
Haemosiderin deposition
Summarise the prognosis for patients with varicose veins.
Although there are small variations in overall efficacy depending on the type of intervention, generally resolution of symptoms occurs in >95% of patients. However, patients need to be counselled that new varicosities will very likely occur with time.
Define vasovagal syncope.
Vasovagal syncope occurs when you faint because your body overreacts to certain triggers, such as the sight of blood or extreme emotional distress. It may also be called neurocardiogenic syncope. The vasovagal syncope trigger causes your heart rate and blood pressure to drop suddenly.
Explain the aetiology/risk factors of vasovagal syncope.
Prior syncope
Prior history of arrhythmias, myocardial infarction, heart failure, or cardiomyopathy
Severe aortic stenosis
Prolonged standing
Emotional stress (especially in a warm, crowded environment)
Dehydration/hypovolaemia
Preceding episode of nausea and/or vomiting
Prior syncope
Prior history of arrhythmias, myocardial infarction, heart failure, or cardiomyopathy
Severe aortic stenosis
Prolonged standing
Emotional stress (especially in a warm, crowded environment)
Dehydration/hypovolaemia
Preceding episode of nausea and/or vomiting
Summarise the epidemiology of vasovagal syncope.
Prevalence of syncope varies in the population:
15% of children (<18 years)
25% of a military population aged 17 to 26 years
16% and 19%, respectively, in men and women aged 40 to 59 years
Up to 23% in a nursing home population aged >70 years.
Recognise the presenting symptoms of vasovagal syncope.
Nausea
Lightheadedness
Pallor
Diaphoresis
Diminished vision or hearing
Fatigue after episode
Recognise the signs of vasovagal syncope on physical examination.
Palpitations
Bradycardia
Identify appropriate investigations for vasovagal syncope and interpret the results.
12-lead ECG
Serum haemoglobin
Plasma blood glucose
Serum beta-human chorionic gonadotropin - rules out syncope caused by the effects of pregnancy
Cardiac enzymes
D-dimer level - rules out pulmonary embolism
Serum cortisol
Urea or serum creatinine
Define venous ulcers.
Venous ulcers are caused by venous stasis in the leg and thus less painful when elevated and drained of blood. Only 30% of venous ulcers are painful.
Explain the aetiology/risk factors of venous ulcers.
Varicose veins
Immobility
Malnourished (reduced healing)
Patients with recurrent DVT
Pelvic mass (compressing iliac veins)
Arteriovenous malformations
Major joint replacement
Summarise the epidemiology of venous ulcers.
Venous ulcers commonly present in older people who have varicose veins are quite immobile.
Recognise the presenting symptoms of venous ulcers. Recognise the signs of venous ulcers on physical examination.
Location: where venous pressure is highest (e.g. medial malleolus)
Shallow, wet, irregular borders that look white and fragile
Oedema
Extravasation
Death of erythrocytes (atrophie blanche)
Superficial varicose veins
Identify appropriate investigations for venous ulcers and interpret the results.
Investigate for signs of atherosclerotic disease:
BM
FBC
Fasting lipids
Urinalysis
Venous duplex ultrasound
Ankle-brachial pressure index
Biopsy
Generate a management plan for venous ulcers.
Adequate nutrition
Lifestyle modification
Leg elevation
Compression bandages
Graduated class I or II elastic stockings
Varicose vein surgery
Identify the possible complications of venous ulcers and its management.
Risk of infection
Blood loss
Summarise the prognosis for patients with venous ulcers.
With management, 80% of venous ulcers will heal within 6 months.
Define ventricular fibrillation.
Ventricular fibrillation is a heart rhythm problem that occurs when the heart beats with rapid, erratic electrical impulses. This causes pumping chambers in your heart (the ventricles) to quiver uselessly, instead of pumping blood.
Explain the aetiology/risk factors of ventricular fibrillation.
A previous episode of ventricular fibrillation
A previous heart attack
Congenital heart disease
Cardiomyopathy
Injuries that cause damage to the heart muscle, such as electrocution
Use of illegal drugs, such as cocaine or methamphetamine
Significant electrolyte abnormalities, such as with potassium or magnesium
Summarise the epidemiology of ventricular fibrillation.
Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3–9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40.
Recognise the presenting symptoms of ventricular fibrillation. Recognise the signs of ventricular fibrillation on physical examination.
Chest pain
Rapid heartbeat (tachycardia)
Dizziness
Nausea
Shortness of breath
Loss of consciousness
Identify appropriate investigations for ventricular fibrillation and interpret the results.
ECG
CXR
CT Angiogram
FBC
Serum potassium
Serum magnesium
Generate a management plan for ventricular fibrillation.
Beta blockers
Permanent pacemaker
In acute ventricular fibrillation (VF), drugs (eg, vasopressin, epinephrine, amiodarone) are used after three defibrillation attempts are performed to restore normal rhythm.
Identify the possible complications of ventricular fibrillation and its management.
Ventricular fibrillation is the most frequent cause of sudden cardiac death. The condition's rapid, erratic heartbeats cause the heart to abruptly stop pumping blood to the body. The longer the body is deprived of blood, the greater the risk of damage to your brain and other organs. Death can occur within minutes.
The condition must be treated immediately with defibrillation, which delivers an electrical shock to the heart and restores normal heart rhythm.
Summarise the prognosis for patients with ventricular fibrillation.
The rate of long-term complications and death is directly related to the speed with which you receive defibrillation.
Define ventricular tachycardia.
In ventricular tachycardia (V-tach or VT), abnormal electrical signals in the ventricles cause the heart to beat faster than normal, usually 100 or more beats per minute, out of sync with the upper chambers.
Explain the aetiology/risk factors of ventricular tachycardia.
Lack of oxygen to the heart due to tissue damage from heart disease
Abnormal electrical pathways in the heart present at birth (congenital heart conditions, including long QT syndrome)
Cardiomyopathy
Medication side effects
An inflammatory disease affecting skin or other tissues (sarcoidosis)
Abuse of recreational drugs, such as cocaine
Imbalance of electrolytes, mineral-related substances necessary for conducting electrical impulses
Summarise the epidemiology of ventricular tachycardia.
The prevalence of VT was 16% in men and 15% in women with CAD, 9% in men and 8% in women with hypertension, valvular disease, or cardiomyopathy without CAD, and 3% in men and 2% in women with no cardiovascular disease.
Recognise the presenting symptoms of ventricular tachycardia. Recognise the signs of ventricular tachycardia on physical examination.
Dizziness
Shortness of breath
Lightheadedness
Palpitations
Angina
Seizures
Sustained or more serious episodes of ventricular tachycardia may cause:
Loss of consciousness or fainting
Cardiac arrest (sudden death)
Identify appropriate investigations for ventricular tachycardia and interpret the results.
ECG
Electrolytes
Troponin I
CK-MB
Investigations to consider
Transthoracic echocardiogram
Generate a management plan for ventricular tachycardia.
- Antiarrhythmic medications + treatment of reversible cause (if present)
- Synchronised cardioversion ± antiarrhythmic medications
Identify the possible complications of ventricular tachycardia and its management.
Complications of ventricular tachycardia vary in severity depending on such factors as the rate, and duration of a rapid heart rate, the frequency with which it happens, and the existence of other heart conditions. Possible complications include:
- Inability of the heart to pump enough blood (heart failure)
- Frequent fainting spells or unconsciousness
- Sudden death caused by cardiac arrest
Summarise the prognosis for patients with ventricular tachycardia.
Idiopathic VT generally carries a favourable prognosis. In most patients, idiopathic VT is not a progressive condition.
Define Wolff-Parkinson-White syndrome.
Wolff-Parkinson-White occurs when one or more strands of myocardial fibres capable of conducting electrical impulses (known as accessory pathways or bypass tracts) connect the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus.
Explain the aetiology/risk factors of Wolff-Parkinson-White syndrome.
Ebstein's anomaly
Hypertrophic cardiomyopathy
Mitral valve prolapse
Atrial septal defect
Ventricular septal defect
Transposition of great vessels
Coarctation of aorta
Dextrocardia
Coronary sinus diverticula
Right and left atrial aneurysms
Cardiac rhabdomyomas
Marfan's syndrome
Friedreich's ataxia
Family history
Summarise the epidemiology of Wolff-Parkinson-White syndrome.
The prevalence of WPW-pattern ECG in the general population is 0.1% to 0.3%. The yearly incidence is 0.004% to 0.1% (50% of these are asymptomatic).
Recognise the presenting symptoms of Wolff-Parkinson-White syndrome. Recognise the signs of Wolff-Parkinson-White syndrome on physical examination.
Palpitations
Dizziness
Shortness of breath
Chest pain
Atrial fibrillation
Atrial flutter
Congenital cardiac abnormalities
Identify appropriate investigations for Wolff-Parkinson-White syndrome and interpret the results.
ECG: Slurred PQ (delta waves)
Echocardiogram
Treadmill exercise test
Electrophysiology study
