Cardiovascular Flashcards
Define abdominal aortic aneurysm.
A permanent pathological dilation of the aorta with diameter >1.5 times the expected anteroposterior (AP) diameter of that segment, given the patient’s sex and body size - e.g. 3cm+
Explain the aetiology / risk factors of an abdominal aortic aneurysm.
Cause - degeneration of the elastic lamellae and smooth muscleloss. also genetic component.
Risk factors:
- Cigarette smoking
- Hereditary / family history
- Increased age
- Male sex (prevalence)
Summarise the epidemiology of an abdominal aortic aneurysm.
3% of those 50+ years .
M:F 3:1
Less common in diabetes
Recognize the presenting symptoms of an abdominal aortic aneurysm.
- Abdominal, back or groin pain
- Presence of risk factors- cigarette smoking, family history, increased age, male sex
Recognize the signs of an abdominal aortic aneurysm on physical examination.
- Palpable pulsatile abdominal mass
- Abdominal, back or groin pain
- Hypotension
Identify appropriate investigations for an abdominal aortic aneurysm and interpret the results.
- Abdominal ultrasound
- Bloods - ESR, CRP, FBC, blood cultures
- CT angiography
Define amyloidosis.
Heterogenous group of diseases characterized by extracellular deposition of amyloid fibrils.
Can be systemic or localised - e.g. pancreatic islets of Langerhans, cerebral cortex, cerebral blood vessels, bones and joints
Pancreatic Islets of Langerhans - T2DM
Cerebral Cortex - Alzheimer’s
Cerebral Blood Vessels - amyloid angiopathy
Bones & Joints - long-term dialysis caused by B2 microglobulin
Explain the aetiology / risk factors of amyloidosis.
Amyloid fibrils are polymers comprising low-molecular-weight subunit proteins.
Amyloid fibril subunits are derived from proteins that undergo conformational changes to adopt anti-parallel B-pleated sheet configuration.
Amyloid fibril subunits associated with GAGs and serum amyloid P-component (SAP), and their sdeposition progressively disrupts the structure and function of nromal tissue.
Classification:
- AA - serum amyloid A protein - e.g. Chronic inflammatory (RA, seronegative arthritides, Crohn’s, familial Mediterranean fever), chronic infections (TB, bronchiectasis, osteomyelitis), malignancy (Hodgkin’s disease, renal cancer)
- AL - monoclonal immunoglobulin light chains fibril protein - e.g. subtle monoclonal plasma cell dyscrasias, multiple myeloma, Waldenstrom’s macroglobulinaemia, B-cell lymphoma
- ATTR (familiar amyloid polyneuropath) - genetic-variant transthyretin - autosomal dominantly transmitted muttaions in the gene for transthyretin (TTR), variable penetrance
Risk factors:
- Monoclonal gammopathy of undetermined significance (MGUS)
- Inflammatory polyarthropathy
- Chronic infections
- IBD
Summarise the epidemiology of amyloidosis.
AA = 1-5% incidence among patients with chronic inflammatory disease
AL = estimated annual incidence of about 3,000 cases in US, 300-600 cases in UK
Hereditary - 5% of patients with systemic amyloidosis
Recognise the presenting symptoms of amyloidosis.
Renal
- Proteinuria
- Nephrotic syndrome
- Renal failure
Cardiac
- Restrictive cardiomyopathy
- Heart failure
- Arrythmia
- Angina - due to accumulation of amyloid in coronary arteries
GI
- Macroglossia - characteristic of AL
- Hepatomegaly
- Splenomegaly
- Gut dysmotility
- Malabsorption
- Bleeding
Neurological
- Sensory and motor neuropathy
- Autonomic neuropathy - symptoms of bowel or bladder dysfunction, postural hypotension
- Carpal tunnel syndrome
Skin
- Waxy skin
- Easy brusing
- Purpura around the eyes - characteristic of AL
- Plaques
- Nodules
Joints
- Painful asymmetrical large joint
- Shoulder pad sign - enlargement of the anterior shoulder
Haematological
- Bleeding diathesis - factor X deficiency due to binding on amyloid fibrils primarily in the liver and spleen and reduce synthesis of coagulation factors in patients with advanced liver disease
Recognise the signs of amyloidosis on physical examination.
Renal
- Proteinuria
- Nephrotic syndrome
- Renal failure
Cardiac
- Restrictive cardiomyopathy
- Heart failure
- Arrythmia
- Angina - due to accumulation of amyloid in coronary arteries
GI
- Macroglossia - characteristic of AL
- Hepatomegaly
- Splenomegaly
- Gut dysmotility
- Malabsorption
- Bleeding
Neurological
- Sensory and motor neuropathy
- Autonomic neuropathy - symptoms of bowel or bladder dysfunction, postural hypotension
- Carpal tunnel syndrome
Skin
- Waxy skin
- Easy brusing
- Purpura around the eyes - characteristic of AL
- Plaques
- Nodules
Joints
- Painful asymmetrical large joint
- Shoulder pad sign - enlargement of the anterior shoulder
Haematological
- Bleeding diathesis - factor X deficiency due to binding on amyloid fibrils primarily in the liver and spleen and reduce synthesis of coagulation factors in patients with advanced liver disease
Identify appropriate investigations for amyloidosis and interpret the results.
- Tissue biopsy - congo red stain, immunohistochemistry (diagnose amyloidosis, identify amyloid fibril protein)
- Urine (proteinuria, free immunoglobi light chains in AL)
- Blood (CRP, ESR, RF, Ig levels, serum protein electrophoresis, LFTs, U&E, SAA levels)
- 123I-SAP Scan - radiolabeled SAP localizes to the deposits enabling quantitative imaging of amyloidotic organs throughout the body
Define aortic dissection.
A condition where a tear in the aortic intima allows blood to surge into the aortic ball, causing a split between the inner and outer tunica media, and creating a false lumen.
Type A Stanford = ascending aorta tear
Type B Standford = descending aorta tear distal to the left subclavian artery
Explain the aetiology / risk factors of aortic dissection.
Degenerative changes in the smooth muscle of the aortic media are the predisposing event.
Risk factors:
- Hypertenison
- Aortic atherosclerosis
- Connective tissue disease - e.g. SLE, Marfan’s, Ehlers-Danlos
- Congenital cardiac abnormalities - e.g. aortic coarctation
- Aortitis - e.g. Takayasu’s aortitis, tertiary syphilis
- Iatrogenic - e.g. during angiography, angioplasty
- Trauma
- Crack cocaine
Summarise the epidemiology of aortic dissection.
Female betwene 40-60 years
Recognise the presenting symptoms of aortic dissection.
- Sudden central ‘tearing’ pain
- Radiates to back - mimics MI
(Can lead to occlusion of the aorta and its branches)
Carotid obstruction = hemiparesis, dysphasia, blackout
Coronary artery obstruction = chest pain, angia, MI
Subclavian obstruction = ataxia, loss of conscioussness
Anterior spinal artery = paraplegia
Coeliac obstruction = severe abdominal pain (ischaemic bowel)
Renal artery obstruction - anuria, renal failure
Recognise the signs of aortic dissection on physical examination .
Murmur on the back below the left scapula, descending to the abdomen.
BP - hypertension (discrepancy between arms of >20mmHg), wide pulse pressure, if hypotensive = ?tamponade - check pulsus paradoxus
Aortia insufficiency - collapsing pulse, early diastolic murmer over aortic area, unequal arm pulses
Palpable abdominal mass?
Identify appropriate investigations for aortic dissetcion and interpret the results.
- Bloods
- CXR
- ECG
- CT-Thorax
- Echocardiography
- Cardiac catheterization and aortography
Bloods
- FBC
- Cross match 10-units of blood
- U&E - renal function
- Clotting
CXR
- Widened mediastinum
- Localized bulge in aortic arch
ECG
- Often nromal
- Signs of left ventricular hypertrophy or inferior MI if dissection compromises the ostia of the right coronary artery
CT-Thorax
- False lumen of dissection can be visualized
Echocardiography
- Transoesophageal highly specific
Define aortic regurgitation.
Reflux of blood from the aorta into the left ventricle during diastole. (also called aortic insuffiency)
Explain the aetiology / risk factors of aortic regurgitation.
- Reflux of the blood into the left ventricle during diastole
- Increase end-diastolic volume
- Incrwase stroke volume
- Low end-diastolic pressure in aorta
- Collapsing pulse & wide pulse pressure
- Acute AR - LV cannot adapt to rapid increase in end-diastolic volume caused by regurgitant blood
1) Aortic Valve Leaflet Abnormalities or Damage
- Bicuspid aortic valve
- Infective endocarditis
- Rheumatic fever
- Trauma
2) Aortic Root / Ascending Aorta Dilation
- Systemic hypertension
- Aortic dissection
- Aortitis - e.g. syphilis, Takayasu’s arteritis
- Arthritides - e.g. RA, seronegative athritides
- Marfan’s Syndrome
- Pseudoxanthoma elasticum
- Ehlers-Danlos Syndrome
- Oestogenesis imperfecta
Risk Factors:
- Bicuspid aortic valve
- Rheumatic fever
- Endocarditis
- Marfan’s Syndrome
- Connective tissue disease
Summarise the epidemiology of aortic regurgitation.
Chronic = late 50s
Documented most frequently in patients >80 years
Recognise the presenting symptoms of aortic regurgitation.
Chronic AR - initially asymptomatic, later symptoms of heart failure = e.g. exertional dyspnoea, orthopnoea, fatigue, angina
Severe acute AR - sudden cardiovascular collapse
Symptoms related to aetiology - e.g. chest or back pain in patients with aortic dissection
Recognise the signs of aortic regurgitation on physical examination.
- Collapsing water-hammer pulse
- Wide pulse pressure
- Thrusting and heavy (volume-loaded) displaced apex beat
- Early distolic murmer at lower left sternal edge - better when sitting forward and expiration
- Ejection systolic murmer heard due to high flow across valve
- AUSTIN-FLINT mid-diastolic murmer - over the apex from turbulent reflex hitting anterior cusp of mitral valvae and causing mitral stenosis
Rare signs:
- Quincke’s sign - visable pulsations on the nail-bed
- de Musset’s sign - head nodding in time with the pulse
- Becker’s sign - visible pulsations of the pupils and retinal arteries
- Muller’s sign - visible pulsation of the uvula
- Corrigan’s sign - visible pulsations in the neck
- Traube’s sign - pistol shot (systolic and diastolic sounds) heard on auscultation of the femoral arteries
- Duroziez’s sign - a systolic and diastolic bruit heard on partial compression of the femoral artery with a stethoscope
- Rosenbach’s sign - systolic pulsations of the liver
- Gerhard’s sign - systolic pulsations of the spleen
- Hill’s sign - popliteal cuff systolic pressure exceeding brachial pressure by >60mmHg
Identfiy appropriate investigations for aortic regurgitation and interpret the results.
- CXR
- ECG
- Echocardiogram
- Cardiac catheterisation with angiography
CXR
- Cardiomegaly
- Dilation of the ascending aorta
- Signs of pulmonary oedema may be seen with left heart failure
ECG
- Left ventricular hypertrophy
- Deep S waves in V1-2
- Tall R wave in V5-6
- Inverted T waves in I, AVL, V5-6
- Left-axis deviation
Echocardiogram
- 2D echo and M-mode - shows underlying cause (e.g. aortic root dilation, bicuspid aortic valve) or effects of AR (left ventricular dilation, dysfunction and fluttering of anterior mitral valve leaflet)
- Doppler echocardiography for detecting AR and assessing severity
- Periodic follow-up echocardiogram for serial meaurements of LV size and function
Cardiac Catheterization with Angiography
- If there is uncertainty about the functional state of the ventricle or the presence of coronary artery disease
Define aortic stenosis.
Narrowing of the left ventricular outflow at the level of the aortic valve.
Explain the aetiology / risk factors of aortic stenosis.
1) Stenosis secondary to rheumatic heart diseas
2) Calcification of a congenital bicuspid aortic valve
3) Calcification and degeneration of a tricuspid aortic valve in the elderly
Risk factors:
- Age 60+years
- Congenitally bicuspid aortic valve
- Rheumatic heart disease
- Chronic kidney disease
Summarise the epidemiology of aortic stenosis.
Prevalence in 3% of 75 year olds
F>M
Bicuspid aortic valve - may present earlier
Recognise the presenting syjmptoms of aortic stenosis.
- Initially asymptomatic
- Angina - due to increased oxygen demand of the hypertrophied ventricles
- Syncope or dizziness on exercise
- Symptoms of heart failure - e.g. dyspnoea
Recognise the signs of aortic stenosis on physical examination.
- BP - narrow pulse pressure
- Pulse - slow rising
- Palpation - thrill in the aortic area, forceful sustained thrusting undisplaced apex beat
- Auscultation - harsh ejection systolic murmer at aortic area, radiates to carotid artery and apex, 2nd heart sound softened or absent, ejection click due to bicuspid valve
Distinguish from Aortic Sclerosis and Hypertorphic Obstructive Cardiomyopathy (HOCM).
Aortic sclerosis - senile degernation with no left ventricular outflow tract obstruction (normal pulse character, no thrill, ejection systolic murmur radiates faintly, S2 heart sound normal)
Identify appropriate investigations for aortic stenosis and interpret the results.
- ECG
- CXR
- Echocardigram
- Cardiac angiography
ECG
- Signs of left ventricular hypertrophy, LBBB
- Deep S wave in V1-2
- Tall R wave in V5-6
- Inverted T waves in I, AVL, V5-6
- Left axis deviation
CXR
- Post-stenotic enlargement of the ascending aorta
- Calcification of aortic valve
Echocardiogram
- Visualises structual changes of the valves and level of stenosis - valvar, supravalvar, subvalvar
- Estimation of the aortic valve area and pressure gradient across valev in systole and left ventricular function assessed
Cardiac Angiography
- Allows differentiation from other causes of angina
- Assessment for concomitant coronary artery disease - 50% of patients
Define arterial ulcers.
A localised area of damage and breakdown of skin due to inadequate aterial blood supply.
Usually seen on the feet of patients with severe artheromatous narrowing of the arteries supplying the legs.
[ischaemic ulcer]
Explain the aetiology / risk factors of arterial ulcers.
Risk Factors:
- Coronary heart disease
- History of stroke or TIA
- Diabetes mellitus
- Peripheral aterial disease - e.g. intermittent claudication
- Obesity
- Immobility
Cause: Lack of blood flow to the capillary beds of the lower extremities.
Summarise the epidemiology of arterial ulcers.
22% of leg ulcers
Prevalence increases with age and obesity
Recognise the presenting symptjoms of arterial ulcers.
- DISTAL - at the dosrum of the foot or between the toes over body prominences
- Punched out appearance
- Elliptical with clearly defined edges - sharp demarcation
- Grey, granulation tissue
- Night Pain - hallmark of arterial ulcers - e.g. at night, when legs are elevated, supine, relieved by dangling leg off the end of the bed
Recognise the signs of arterial ulcers on physical examination.
- Night Pain
- Punched-out appearance
- Hairlessness
- Pale, cold skin
- Absent pulses
- Wasting of calf muscles
- Dry necrotic base
Identfiy appropriate investigations for arterial ulcers and interpret the results.
- Duplex ultrasonography of lower limbs - assess patency of arteries, potential for revascularisation or bypass surgery
- ABPI - <0.8
- Percutaneous angiography
- ECG
- Fasting serum lipids, fasting glucose, HbA1C
- FBC - anaemia can worsen the ischaemia
Define atrial fibrillation / flutter.
Characterized by rapid, chaotic and ineffective atrial electrical conduction.
Permanent, persistent, paroxysmal.
Atrial flutter - characterized by atrial rate of 300/min, ventricular rate 150/min (2:1 heart block as the AV node conducts every second beat = saw tooth baseline
Can be reversed by vagal maneouvres, IV adenosine (with cardiac monitoring) or chemical cardioversion.
Explain the aetiology / risk factors of atrial fibrillation / flutter.
May be no identifiable cause (lone AF)
Secondary causes lead to abnormal atrial electircal pathways.
Systemic
- Thyrotoxicosis
- Hypertension
- Pneumonia
- Alcohol
Heart
- Mitral valve disease
- Ischaemic heart disease
- Rheumatic heart disease
- Cardiomyopathy
- Pericarditis
- Sick sinus syndrome
- Atrial myxoma
Lung
- Bronchial carcinoma
- Pulmonary embolism
Risk Factors (Chornic):
- Hypertension
- CAD
- CHF
- Advancing age
Risk Factors (Acute):
- Increasing age
- DM
- Hypertension
- CHF
Summarise the epidemiology of atrial fibrillation / flutter.
Very common in the elderly - 5% of those >65 years
May be paroxysmal
Recognise the presenting symptoms of atrial fibrillation / flutter.
- Asymptomatic
- Palpitations
- Syncope
- Symptoms of the cause of AF
Recognise the signs of atrial fibrillation / flutter on physical examination.
- Irregularly irregular pulse
- Difference in apical beat and radial pulse
- Look for thyroid disease
- Look for valvular heart disease
Identify appropriate investigations for arterial fibrillation / flutter and interpret the results.
- ECG
- Blood
- Echocardiogram
ECG
- Uneven baseline (fibrillations)
- Absent P waves
- Irregular QRS complexes
- Saw-tooth baseline
- Consider atrial flutter
Bloods
- Cardiac enzymes
- TFT
- Lipid profile
- U&E
- Mg2+
- Ca2+
NB: Risk of digoxin toxicity increased with hypokalaemia, hypomagnesaemia or hypercalcaemia
Echocardiogram
- ?Mitral valve disease
- ?Left atrial dilation
- ?Left ventricular dysfunction
- ?Structural abnormalities
Generate a management plan for arterial fibrillation / flutter.
- Treat reversible causes - e.g. thyrotoxicosis, chest infection
1) Rhythm Control
- AF > 48 from onset, anticoagulate (3-4 weeks) before attempting cardioversion
- DC cardioversion - synchronized DCshock (2x100J, 1x200J)
- Chemical cardioversion - flecainide (contraindicated if IHD) or amiodarone
- Prophylaxis against AF - sotalol, amiodarone, flecainide (pill in pocket strategy?)
2) Rate Control
- Chronic AF - ventricular rate control with digoxin, verapamil and B-blockers (90/min rate aim)
3) Stroke Risk Stratification
- Low risk - with aspirin
- High risk - with anticoagulation with warfarin
Risk Factors:
- Previous TBE
- Age 75 years+
- Hypertension
- Diabetes
- Vascular disease
- Valve disease
- Heart Failure
- Impaired Left Ventricular Function
Identify the possible complications of arterial fibrillation / flutter and its management.
- TBE - 4% per year, increased risk with left atrial enlargement or left ventricular dysfunction
- Worsens existing heart failure
Summarise the prognosis for patients with arterial fibrillation / flutter.
Chronic AF in a diseasedheart does not usually return to sinus rhythm.
Define cardiac arrest.
Acute cessation of cardiac function.
Explain the aetiology / risk factors of cardiac arrest.
4 H’s:
- Hypoxia
- Hypothermia
- Hypovolaemia
- Hypo or hyperkalaemia
4 T’s:
- Tamponade
- Tension pneumothorax
- Thromboembolism (TBE)
- Toxins (drugs, therapeutic agents, sepsis)
Recognise the presenting symptoms of cardiac arrest.
Management precedes or is concurrent to history (e.g. from witnesses)
Recognise the signs of cardiac arrest on physical examination.
- Unconscious
- Not breathing
- Absent carotid pulses
Identfiy apporpriate investigations for cardiac arrest and interpret the results.
1) Cardiac monitor - classifcation of rhythm directs management
2) Bloods - ABG, U&E, FBC, cross-match,clotting, toxicology screen, glucose
Generate a management plan for cardiac arrest.
Safety
- Approprach with caution
- Cause of arrest may still pose a threat
- Defibrillators and oxygen = hazards
- Help summoned as soon as possible
BLS
- If arrest is witnessed and monitored, consider giving a precordial thump if no defibrillators avaliable
- Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift
- Assess breathing by look, listen and feel
- If not breathing, give 2 effective breaths immediately
- Assess circulation at carotid pulse for 10s
- If absent, give 30 chest compressions at a rate of 100/min
- Continue cycles of 30 compressions for every two breaths
- Proceed to advanced life support as soon as possible
ALS
- Attach cardiac monitor and defibrillator
- Assess rhthym
A) If pulseless ventricular tachycardia or ventricularfibrillation (SHOCKABLE)
- Defibrillate once - 150-360J biphasic, 360J monophasic
- Resume CPR immediately for 2 mins and then return to 2
- Administer adrenaline (1mg IV) after 2nd defibrillation and again every 3-5 mins
- If SHOCKABLE persists, administer amiodarone 300mg IV bolus or lidocaine
B) If pulseless electrical activity (PEA) or asystole:
- CPR for 2 minutes then return to 2
- Administer adrenaline 1mg IV every 3-5 minutes
- Atropine (3mg IV) if asystole or PEA with rate <60/min
C) During CPR
- Check electrodes, paddle positions and contacts
- Secure the airway - e.g. attempt ET intubation, high-flow oxygen
- Once airway secure, give continuous compresisons and breaths
- Consider Mg, HCO3, external pacing
- Stop CPR and check pulse only if change in rhythm or signs of life
Treatment of Reversible Causes:
- Hypothermia - warm slowly
- Hypo/hyperkalaemia - correction of electrolytes
- Hypovolaemia - IV colloids, crystalloids or blood products
- Tamponade - pericardiocentesis under xiphisterum up and leftwards
- Tension pneumothorax - needle into second intercostal space, mid-clavicular line
Identify the possible complications of cardiac arrest and its management.
- Irreversible hypoxic brain damage
- Death
Summarise the prognosis for patients with cardiac arrest.
- Less successful outside hospital
- Duration of inadequate effective cardiac output is associated with poor prognosis
Define cardiac failure (acute and chronic).
Inability of the cardiac output to meet the body’s demands despite normal venous pressures.
Explain the aetiology /risk factors of cardiac failure (acute and chronic).
LOW CARDIAC OUTPUT
- Left heart failure - ischaemic heart disease, hypertesion, cardiomyopathy aortic valve disease, mitral regurgitation
- Right heart failure - secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade
- Biventricular failure - arrhythmia, cardiomyopathy (dilated or restirctive), myocarditis, drug toxicity
HIGH DEMAND
- Anaemia
- Berberi
- Pregnancy
- Paget’s disease
- Hyperthyroidism
- Arteriovenous malformation
Summarise the epidemiology of cardiac failure (acute and chronic).
10% of 65 year olds
Recognise the presenting symptoms of cardiac failure (acute and chronic).
Left - caused by pulmonary congestion
- Dyspnoea
- Orthopnea
- Paroxysmal nocturnal dyspnoea
- Fatigue
Acute LVF
- Dyspnoea
- Wheeze
- Cough
- Pink frothy sputum
Right
- Swollen ankles
- Fatigue
- Increased weight - due to oedema
- Reduced exercise tolerace
- Anorexia
- Nausea
NB: New York Heart Association Classification
- No dyspnoea
- Dyspnoea or ordinary activities
- Dyspnoea on less than ordinary activities
- Dyspnoea at rest
Recognise the signs of cardiac failure (acute and chronic) on physical examination.
Left
- Tachycardia
- Tachypnoea
- Displaced apex beat
- Bilateral basal crackles
- 3rd heart sound - gallop rhythm, rapid ventricular filling
- Pansystolic murmuer - functional mitral regurgitation
Acute Left
- Tachyhypnoea
- Cyanosis
- Tachycardia
- Peripheral shutdown
- Pulsus alternans
- Gallop rhythm
- Wheeze cardiac asthma
- Fine crackles throughout the lung
Right
- High JVP
- Hepatomegaly
- Ascites
- Ankle/sacral pitting
- Oedema
- Signs of functional tricuspid regurgitation
Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results.
- Bloods
- CXR
- ECF
- Echocardiogram
- Swan-Ganz Catheter
Bloods
- FBC
- U&E
- LFTs
- CRP
- Glucose
- Lipids
- TFTs
- Acute LVF - ABG, troponin, brain natriuretic peptide (BNP)
- High plasma BNP suggests cardiac failure
CXR (Acute LVF)
- Cardiomegaly - heart >50% of thoracic width
- Prominent upper lobe vessels
- Pleural effusion
- Intestitial oedema - Kerley B lines
- Perihilar shadowing - bat’s wings
- Fluid in fissures
ECG
- May be normal
- Ischaemic changes
- Arrhthmia
- Left ventricular hypertrophy
Echocardiogram
- LVEF <40% = systolic dysfunction
- Diastolic dysfunction - reduced compliance leading to a restrictive filling defect
Swan-Ganz Catheter
- Allows measurements of right atrial, right ventricular, pulonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Generate a management plan for cardiac failure (acute and chronic) and its management.
Acute LVF
- Cardiogenic shock - severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine), manage in ITU
- Pulmonary oedema - sit up patient, 60-10% oxygen, CPAP.
- Monitor BP, respiatory rate, sats, urine output, ECG
- Treat the cause - e.g. MI, arrythmia
Also consider: diamorphine (venodilator and axiolytic), GTN infusion (reduce preload) IV furosemide if fluid overloaded (venodilator and diuretic)
Chronic LVF
- Treat the cause - e.g. hypertension
- Treat exacerbating factors - e.g. anaemia
- ACE inhibitors - e.g. enalapril, perindopril, ramipril
- B-Blockers - e.g. bisprolol, carvidolol
- Loop diuretics - e.g. furosemide - and dietary salt restritcion to correct fluid overload
- Aldosterone Antagonists - e.g. spironolactone, eplerenone
- Angiotensin Receptor Blokcers - e.g. candesartan
- Hydralazine and Nitrate
- Digoxin
- N-3 Polyunsaturated Fatty Acids
- Cardiac Resynchroniszation Therapy (CRT)
- Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction - e.g. NSAIDs, non-dihydropyridine calcium channel blockers - e.g. diltiazem and verapamil.
Identify the possible complications of cardiac failure (acute and chronic) and its management.
- Respiratory failure
- Cardiogenic shock
- Death
Summarise the prognosis for patients with cardiac failure (acute and chronic).
50% of patients with severe heart failure die within 2 years.
Outline the mechanism of action of ACE-Inhibitors in heart failure patients.
- Inhibit intracardiac renin-angiotensin system that may contribute to myocardial hypertrophy and remodelling
- Slow progression of heart failure and improves survival
- Additive benefits of ACE inhibitors and beta-blockers
Outline the mechanism of action of Beta-Blockers in heart failure patients.
- Block the effects of chronically activated sympathetic system
- Slows progresion of heart failure and improves survival
- Additive benefits of ACE inhibitors + Beta-blockers
Outline the mechanism of action of Aldosterone Antagonists in heart failure patients.
- Improve survival in patients with NYHA class II/IV symptoms and on standard therapy
- Monitor K+ - may cause hyperkalaemia
- Used to assist with management of diuretic induced hypokalaemia
Outline the mechanism of action of Angiotensin Receptor Blockers in heart failure patients.
- May be added in pateints with persistent symptoms despite ACE inhibitors and B-blockers
- Monitor K+ - may cause hyperkalaemia
Outline the mechanism of action of Hydralazine and Nitrates in heart failure patients.
- May be added in patients (Afro-Carribeans) with persistent symptomsdespite therapy with ACE inhibitor and beta-blocker
Outline the mechanism of action of Digoxin in heart failure patients.
- Positive ionotrope
- Reduced hospitalisation
- Does not improve survival
Outline the mechanism of action of N-3 Polyunsaturated Fatty Acids in heart failure patients.
- Provide small beneficial advantage in terms of mortality
Outline the mechanism of action of CRT in heart failure patients.
- Biventricular pacing
- Improves symptoms and survival in patients with LVEF<35%, cardiac dyssynchrony (QRS>120msec) and moderate to severe symptoms despite optimal medical therapy
- Most patients who meet these criteria are also candidates for implanatable cardiac defibrillator (ICD) and recieve combined device
Define cardiomyopathy.
Primary disease of the myocardium.
May be dilated, hypertrophic or restrictive.
Explain the aetiology /risk factors of cardiomyopathy.
Dilated - post-viral myocarditis, alcohol, drugs (doxorubicine, cocaine), familial (autosomal dominant), thyrotoxicosis, haemochromatosis, peripartum
Hypertrophic - genetic (autosomal dominant) mutations in beta-myosin, troponin T or alpha-tropomyosin
Restrictive - amyloidosis, sarcoidosis, haemachromatosis.
Summarise the epidemiology of cardiomyopathy.
0.05-0.20% prevalence - dilated and hypertrophic
Restrictive cardiomyopaty is very rare
Recognise the presenting symptoms of cardiomyopathy.
Dilated:
- Symptoms of heart failure
- Arrythmias
- Thromboembolism
- Family history of sudden death
Hypertrophic:
- Usually none
- Syncope
- Angina
- Arrythmias
- Family history of sudden death
Restrictive:
- Dyspnoea
- Fatigue
- Arrythmia
- Ankle or abdominal swelling
- Enquire about family history of sudden death
Recognise the signs of cardiomyopathy on physical examination.
Dilated:
- Raised JVP
- Displaced apex beat
- Functional mitral and tricuspid regurgitations
- 3rd heart sound
Hypertrophic
- Jerky carotid pulse
- Double apex beat
- Ejection systolic murmur
Restrictive
- Raised JVP
- Kussmaul’s sign - further raised JVP on inspiration
- Palpable apex beat
- 3rd heart sound
- Ascites
- Ankle oedema
- Hepatomegaly
Identify appropriate investigations for cardiomyopathy and interpret the results.
- CXR - show cardiomegaly, heart failure signs
- ECG
- Echocardiography
- Cardiac catheterization - measure pressures
- Endomyocardial biopsy - restrictive cardiomyopathy
- Pedigree or Genetic Analysis - rare
ECG:
- All types –> non-specific ST changes, conduction defects, arrythmias
- Hypertrophic –> left axis deviation, signs of left ventricular hypertrophy (aortic stenosis), Q waves in inferior and lateral leads
- Restrictive - low voltage complexes
Echocardiography:
- Dilated –> dilated ventricles with global hyookinesia
- Hypertrophic –> ventricular hypertrophy (disproportionate septal involvement)
- Restritcive –> non-dilated non-hypertrophied ventricles, atrial enlargement, preserved systolic function, diastolic dysfunction, gradular or sparkling appearance of myocardium in amyloidosis
Define constrictive percarditis.
The heart is incased in a rigid pericardium.
Explain the aetiology / risk factors of constrictive pericarditis.
Unknown. (UK)
TB or after any pericarditis (elsewhere).
Risk Factors:
- 1% = idiopathic and viral pericarditis
- 2-5% = autoimmune, immunemediated and neoplastic aetiology
- 20-30% = bacterial aetiology (e.g. TB, purulent percarditis).
Summarise the epidemiology of constrictive pericarditis.
- 76 cases per 1000 person-years after acute idiopathic or viral pericarditis.
- 7 cases per 1000 person-years for acute tuberculous pericarditis.
- 7 cases per 1000 person-years for purulent pericarditis.
Recognise the presenting symptoms of constrictive pericarditis.
- Difficulty breathing that develops slowly and becomes worse
- Fatigue
- Swollen abdomen
- Chronic, severe swelling in legs and ankles
- Weakness
- Low grade fever
- Chest pain
Recognise the signs of constrictive pericarditis on physical examination.
- Raised JVP
- Kussmaul’s sign - raised JVP paradoxically with inspiration
- Soft, diffuse apex beat
- Quiet heart signs
- S3
- Diastolic percardial knock
- Hepatosplenomegaly
- Ascites
- Oedema
Identfiy appropriate investigations forconstrictive pericarditis and interpret the results.
- CXR - small heart + pericardial calcification
- CT/MRI - distinguish from restrictive cardiomyopathy
- Echocardiography
- Cardiac catheterisation
Define coronary angiography and PCI.
Coronary angiography - a procedure that uses contrast dye, usually containing iodine, and X-rays to detect blockages in the coronary arteries that are caused by plaque buildup.
PCI = Percutaneous Coronary Intervention (Coronary Angioplasty) - a non-surgical procedure that improves blood flow to your heart, requiring cardiac catheterisation.
Cardiac Catheterisation - the insertion of a catheter tube and injection of contrast dye (usually iodine-based) into your coronary arteries
Summarise the indications for coronary angiography and PCI.
Coronary angiography:
- Symptoms of coronary artery disease - e.g. angina
- Pain in your chest, jaw, neck or arm
- New or increasing chest pain (unstable angina)
- Unexplained congestive heart failure
- Acute myocardial infarction with mechanical complications requiring cardiac surgery
PCI:
- Acute ST-elevated myocardial infarction (STEMI)
- Non-ST-elevated acute coronary syndrome (NSTE-ACS)
- Unstable angina
- Stable angina
- Anginal equivalent - e.g. dyspnea, arrythmia, dizziness, cyncope
- High risk stress test findings
Identify the possible complications of coronary angiography and PCI.
Coronary Angiography:
- Heart attack
- Stroke
- Injury to catheterized artery
- Arrhythmias
- Allergic reactions to the dye or medications used during the procedure
- Kidney damage
- Excessive bleeding
- Infection
PCI:
- Bleeding
- Haematoma
- Pseudoaneurysm at access site
- Heart attack
- Stroke
Identify appropriate investigations for cardiomyopathy and interpret the results.
- CXR - show cardiomegaly, heart failure signs
- ECG
- Echocardiography
- Cardiac catheterization - measure pressures
- Endomyocardial biopsy - restrictive cardiomyopathy
- Pedigree or Genetic Analysis - rare
ECG:
- All types –> non-specific ST changes, conduction defects, arrythmias
- Hypertrophic –> left axis deviation, signs of left ventricular hypertrophy (aortic stenosis), Q waves in inferior and lateral leads
- Restrictive - low voltage complexes
Echocardiography:
- Dilated –> dilated ventricles with global hyookinesia
- Hypertrophic –> ventricular hypertrophy (disproportionate septal involvement)
- Restritcive –> non-dilated non-hypertrophied ventricles, atrial enlargement, preserved systolic function, diastolic dysfunction, gradular or sparkling appearance of myocardium in amyloidosis
Define constrictive percarditis.
The heart is incased in a rigid pericardium.
Explain the aetiology / risk factors of constrictive pericarditis.
Unknown. (UK)
TB or after any pericarditis (elsewhere).
Risk Factors:
- 1% = idiopathic and viral pericarditis
- 2-5% = autoimmune, immunemediated and neoplastic aetiology
- 20-30% = bacterial aetiology (e.g. TB, purulent percarditis).
Summarise the epidemiology of constrictive pericarditis.
- 76 cases per 1000 person-years after acute idiopathic or viral pericarditis.
- 7 cases per 1000 person-years for acute tuberculous pericarditis.
- 7 cases per 1000 person-years for purulent pericarditis.
Recognise the presenting symptoms of constrictive pericarditis.
- Difficulty breathing that develops slowly and becomes worse
- Fatigue
- Swollen abdomen
- Chronic, severe swelling in legs and ankles
- Weakness
- Low grade fever
- Chest pain
Identify the possible complications of DC cardioversion.
[Direct Current Cardioversion]
- Dislodged blood clots
- Abnormal heart rhythm dollowing the procedure
- Skin burns
- Ventricular fibrillation due to general anaesthetia or lack of synchronisation between DC shock and QRS
- Thromboembolus - insufficient anticoagulant therapy
- Non-sustained ventricular tachycardia
- Atrial arrhthmia
- Heart block
- Bradycardia
- Transient left bundle branch block
- Myocardial necrosis
- Myocardial dysfunction
- Transient hypotension
- Pulmonary oedema
- Pain at application site
Define coronary artery bypass graft (CABG).
A healthy artery or vein from the body is grafted to the blocked coronary artery. The grafted artery or vein bypasses the blocked portion of the coronary artery, creating a new passage for oxygen-rich blood to be routed around the blockage to the heart muscle.
Summarise the indications for a coornary artery bypass graft (CABG).
- Triple coronary vessel disease
- Left main stem coronary artery disease
- Two coronary vessel disease with a proximal left anterior descending artery lesion
Identify the possible complications of a coronary artery bypass graft (CABG).
- Stroke
- Neurocognitie dysfunction
- Intraoperative myocardial infarction
- Temporary conduction abnormalities
- Arrhythmias - e.g. atrial fibrillation
- Pericardial effusion / tamponade
- Haemorrhage
- Mediastinitis
- Steral wound infection
- Renal dysfunction
- Death
Define DC cardioversion.
[Direct Current Cardioversion]
A procedure to convert an abnormal heart rhythm to a normal heart rhythm.
Atrial fibrillation - most common arrhythmia
Aim to completely depolarize the heart using a direct current.
Summarise the indications for DC cardioversion.
[Direct Current Cardioversion]
To restore sinus rhythm if Ventricular Fibrillation / Ventricular Tachycardia, Atrial Fibrillation, Flutter, Supraventricular Tachycardias.
If other treatments have failured or there is haemodynamic compromise.
Emergency or electively.
Emergency = VF, VT
Electively = AF
Define deep vein thrombosis (DVT).
Formation of a thrombus within the deep veins - most comonly of the calf or thigh.
Generate a management plan for deep vein thrombosis (DVT).
Anticoagulation:
- Heparin - whilst awaiting therapeutic INR from warfarin anti-coag
- DVT below knee treated with anti-coagulation for 3 months
- DVT above knee treated with anticoagulation for 6 months
- Recurrent DVT - long term warfarin
- If active anticoagulation is contraindicated and/or high risk of embolisation - place IVC filter by IVR to prevent embolus in lungs
Prevention:
- Use of graduated compression stockings
- Mobilisation if possible
- At-risk groups should have prophylactic heparin - e.g. low-molecular weight heparin if no contraindications
Identify the possible complications of deep vein thrombosis (DVT) and its management.
Of the disease:
- PE
- Damage to vein valves
- Chornic venous insufficiency of the lower limb (pro-thrombotic syndrome)
- Venous infarction - phlegmasia cerulea dolens
Of the treatment:
- Heparin-induced thrombocytopaenia
- Bleeding
Summarise the prognosis for patients with deep vein thrombosis (DVT).
Depends on extent of DVT, below-knee DVTs lower risk of embolus.
More proximal DVTs have higher risk of propagation and embolisation, which if large, may be fatal.
Recognise the signs of deep vein thrombosis (DVT) on physical examination.
- Examine for swelling
- Examine for calf tenderness
- Severe leg oedema and cyanosis (phlegmasia cerulea dolens) is rare
- Respiratory examination for signs of a PE
Use Wells Clinical Prediction Score
Identify appropriate investigations for deep vein thrombosis (DVT).
- Doppler ultrasound
- Bloods
- ECG, CXR, ABG - if PE?
Doppler US
- Gold standard
- Good sensitivity for femoral veins
- Less sensitive for calf veins
Bloods
- D-dimers = fibrinogen degradation products - sensitive but non-specific and only useful as a negative predictor in low-risk patinets
- Thrombophilia screen, prior to starting anticoagulation - if recurrent episodes
- FBC - platelet count prior to starting heparin
- U&E
- Clotting
Generate a management plan for deep vein thrombosis (DVT).
Anticoagulation:
- Heparin - whilst awaiting therapeutic INR from warfarin anti-coag
- DVT below knee treated with anti-coagulation for 3 months
- DVT above knee treated with anticoagulation for 6 months
- Recurrent DVT - long term warfarin
- If active anticoagulation is contraindicated and/or high risk of embolisation - place IVC filter by IVR to prevent embolus in lungs
Define dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
Elevation of one or more plasma lipid fractions.
Explain the aetiology / risk factors of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
LDL accummulates in the intima of systemic arteries.
Taken up by LDLR on macrophage = foam cell.
HDL is a shuttle in periphery for transport of cholesterol esters back to the liver –> cardioprotective
Primary - molecular genetic basis, some unknown
- Familial hypercholesterolaemia - reduced functional hepatic LDLR
- Familial hypertriglyceridaemia - unknown, autosomal dominant
- Hypertriglyceridaemia - lipoprotein lipase or apo-CII deficiency
- Familial combined hyperlipidaemia - unknown
- Remnant hyperlipidaemia - apo-E2 genotype inheritance, accumulation of LDL remnants
Secondary - subdivided depending on abnormality
- HIGH CHOLESTEROL - hypothyroidism, nephrotic syndrome, cholestatic liver disease, anorexia nervosa
- HIGH TRIGLYCERIDES - diabetes, drugs (e.g. B-blockers, thiazides, oestrogens), alcohol, obesty, chronic renal disease, hepatocellular disease
Summarise the epidemiology of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
50% of UK population have a cholesterol level high enough to be a risk for CHD.
Recognise the presenting symptoms of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
- Asymptomatic
- Symptoms of complications
Ask about other CVS risk factors:
- Diabetes
- Smoking
- Hypertension
- Family history
Recognise the signs of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) on physical examination.
Usually normal - examine for secondary causes.
Lipid deposits:
- Xanthelasmas - around eyes
- Corneal arcus
- Tendons xanthomas - e.g. extensor tendons of the hands, Achilles, patella
- Tuberous xanthomas on knees and elbows
- Xanthomas in palmar creases - in remnant hyperlipidaemia
- Eruptive xanthomas and lipidaemia retinalis (pale retinal vessels) - severe hypertriglyceridaemia
Signs of Complications:
- Reduced peripheral pulses
- Carotid bruits
- CVD risks
- High BP
Identify appropriate investigations for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and interpret the results.
- Bloods
- Cardiovascular Risk Assessment
Bloods
- Fasting lipid profile
- Exclude secondary causes - e.g. glucose, TFT, LFT, U&E
CVD Risk Assessment
- Algorithms
- E.g. Framingham risk equation, QRISK, ASSIGN
Generate a management plan for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
Treat secondary causes.
Advice
- Exercise
- Lose weight
- Control BP
- Control diabetes
- Low alcohol
- Dietary modification
Lipid-lowering Drugs
- Primary prevention - if multiple risk factors + no atherosclerosis + risk CHD >20% in 10 years
- Secondary prevention - if established atherosclerosis (e.g. CHD, CAD, AA)
- Target: total cholesterol <4mmol/L, LDL <2mmol/L
Drugs for HIGH Total Cholesterol or HIGH LDL:
- HMG-CoA Reductase Inhibitors - potently lowers mortality and CVS morbidity is demonstrated in numerous trials - high dose recommended as first line - e.g. 40mg simvastatin
- Ezetimibe - inhibits cholesterol absorption in gut, used if statin not tolerated or as adjunctive agent
Drugs for HIGH Triglycerides:
- Fibrates - stimulates lipoprotein lipase activity via specific transcription factors
- Fish oil - rich in omega-3 marine triglycerides, not recommended as can aggravate
Others:
- Anion-exchange resins - e.g. colestyramine, colestipol - binds bile acids and reduces reabsorption, increases hepatic cholesterol conversion to bile acids, increases LDLR on hepatocytes
- Nicotinic acid - reduced hepatic VLDL release, reduces TG, reduces cholesterol, increases HDL, bad side effectes (PG-mediated vasodilation, flushing, dizziness, palpitations), increases glucose and urate.
Identify the possible compications of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and its management.
- CAD
- MI
- PVD
- Stroke
- Hypertriglyceridaemia –> pancreatitis and retinal vein thrombosis
- Complications of treatment - statins –> myositis
Summarise the prognosis for patients with dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
Depends on early diagnosis, treatment of hyperlipidaemia and control of other CVS risk factors.
Lipid-lowering agents –> ?Reduce cerebrovascular accidents
Define gangrene.
Death of tissue from poor vascular supply.
2 main categories:
- Infectious gangrene - e.g. necrotising fasciitis, gas gangrene
- Ischaemia gangrene - e.g. arterial or venous obstruction
Explain the aetiology / risk factors of gangrene.
Due to:
- Ischaemia
- Infection
- Trauma
Risk factors:
- Diabetes
- Smoking
- Atherosclerosis
- Renal disease
- Drug and alcohol abuse
- Malignancy
- Trauma
- Abdominal surgery
- Contaminated wounds
- Malnutrition
- Hyper-coagulable states
- Prolonged use of tourniquets
- Community-acquired MRSA
Summarise the epidemiology of gangrene.
Fournier’s gangrene = 1.6 cases per 100,0000.
Incidence peaks and remains steady after 50 years, at 3.3 cases per 100,000.
Recognise the presenting symptoms of gangrene.
- Pain
- Swelling
- Fever
- Chills
Recognise the signs of gangrene on physical examination.
- Pain
- Oedema
- Swelling
- Skin discolouration
- Diminished pedal pulses and ankle-brachial index - e.g. ischaemic gangrene
- Low-grade fever - e.g. infectious gangrene
Identify appropriate investigations for gangrene and interpret the results.
- Bloods - FBC, serum LDH, coagulation panel, metabolic panel
- Surgical exploration and skin biopsy
- CT angiography
- Magnetic resonance angiography (MRA)
- CT chest and abdomen
Define heart block (1st, 2nd, 3rd degree).
Impairment of the AV node impulse conduction, as represented by the interval between P wave and QRS complex.
1st DEGREE:
- Prolonged conduction through AV node (prolonged PR interval)
2nd DEGREE:
MOBITZ TYPE I - progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node (cycle begins again - prolonged PR interval, longer and longer then skip).
MOBITZ TYPE II - intermittent or regular failure of conduction through AV node (ratio!)
3rd DEGREE:
- No relationship between atrial and ventricular contraction
- Failure of conduction through the AV node leads to a ventricular contraction generated by a focus of depolarisation within the ventricle (ventricular escape)
Explain the aetiology / risk factors of heart block (1st, 2nd, 3rd degree).
- MI or IHD
- Infection - e.g. rheumatic fever, infective endocarditis
- Drugs - e.g. digoxin, B-blockers, Ca2+ channel antagonists
- Metabolic - e.g. hyperkalaemia, cholestatic jaundice, hypothermia
- Infiltration of conducting system - e.g. sarcoidosis, cardiac neoplasms, amyloidosis
- Degeneration of the conducting system
Risk Factors:
- Age-related degenerative changes in the conduction system
- Increased vagal tone
- AV-nodal blocking agents
- Chronic stable coronary artery disease (CAD)
- Acute coronary syndrome
- CHF
- Hypertension
- Cardiomyopathy
- Left ventricular hypertrophy
- Recent cardiac surgery
- Acid-base or electrolyte disturbance
- Neuromuscular disorders
Summarise the epidemiology of heart block (1st, 2nd, 3rd degree).
250,000 pacemakers implanted annually for heart block
Recognise the presenting symptoms of heart block (1st, 2nd, 3rd degree).
1st DEGREE - asymptomatic
MOBITZ TYPE I - asymptomatic
MOBITZ TYPE II & 3rd DEGREE:
- Stokes-Adams attacks - syncope caused by ventricular asystole
- Dizziness
- Palpitations
- Chest pain
- Heart failure
Recognise the signs of heart block (1st, 2nd, 3rd degree) on physical examination.
Normal
Examine for signs of the cause
Complete Heart Block:
- Slow large volume pulse
- JVP may show cannon waves
MOBITZ TYPE II & 3rd DEGREE
- Reduced cardiac output - e.g. hypotension, heart failure
Identify appropriate investigations for heart block (1st, 2nd, 3rd degree) and interpret the results.
1) ECG (ambulatory Holter or 24h)
1st DEGREE
- Prolonged PR interval >0.02s
MOBITZ TYPE I
- Progressively prolonged PR interval
- Culminates in a P wave that is not followed by a QRS
- Pattern begins again
MOBITZ TYPE II
- Intermittently a P wave is not followed by a QRS
- Pattern begins again
- May be a ratio - e.g. 2:1 block
3rd DEGREE
- No relationship between P waves and QRS complexes
- If QRS initiated by focus in bundle of His, then QRS is narrow
- If QRS initiated distally, then QRS is wide and slow rate - 30bpm
2) CXR - cardiac enlargement, pulmonary oedema
3) Bloods - TFT, digoxin level, cardiac enzyme, troponin, potassium, calcium
4) Echocardiogram - wall motion abnormalities, aortic valve disease, vegetations
Generate a management plan for heart block (1st, 2nd, 3rd degree).
CHRONIC
- Permanent pacemaker insertion (PPM)
- If 3rd DEGREE , MOBITZ TYPE II, symptomatic MOBITZ TYPE I
ACUTE
- If associated with clinical deterioration
- IV atropine
- Temporary external pacemaker
Identify the possible complications of heart block (1st, 2nd, 3rd degree) and its management.
- Asystole
- Cardiac arrest
- Heart failure
- Complications of any pacemaker inserted
Summarise the prognosis for patients with heart block (1st, 2nd, 3rd degree).
MOBITZ TYPE II and 3rd DEGREE –> serious underlying cardiac disease
Define hypertension.
SBP > 140mmHg
DBP > 85mmHg
Measured on 3 separate occasions
Malignant hypertension - >200/130mmHg
Explain the aetiology / risk factors of hypertension.
Fibrotic intimal thickening of the arteries, reduplication of elastic lamina and smooth muscle hypertrophy.
Arteriolar wall layers replaced by pink hyaline material with luminal narrowing (hyaline arteriosclerosis).
Primary:
- Essential or idiopathic = 90% cases
Secondary:
- Renal - renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal disease
- Endocrine - DM, hyperthyroidism, Cushing’s, Conn’s, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly
- Cardiovascular - aortic coarctation, high intravascular volume
- Drugs - sympathomimetics, corticosteroids, oral contraceptive pill
- Pregnancy - pre-eclampsia
Risk factors:
- Obesity
- Aerobic exercise <3 times a week
- Moderate / high alcohol intake
- Metabolic syndrome
- DM
- Black ancestry
- Age > 60 years
- Family history of hypertension or coronary artery disease
- Sleep apnoea
Summarise the epidemiology of hypertension.
10-20% of adults in Western world.
Recognise the presenting symptoms of hypertension.
- Asymptomatic
- Symptoms of complications
- Symptoms of the cause
Accelerated or Malignant Hypertension
- Scotomas (visual field loss)
- Blurred vision
- Headache
- Seizures
- Nausea
- Vomiting
- Acute heart failure
Recognise the signs of hypertension on physical examination.
- Measure on 2-3 different occasions before diagnosing hypertension and record lowest reading
- Loud 2nd heart sound, 4th heart sound
- Examine for causes - e.g. radiofemoral delay (aortic coarctaction), renal artery bruit (renal artery stenosis)
- Examine for end-organ damage - e.g. fundoscopy for retinopathy
Keith-Wagner Classification of Retinopathy:
(I) - Silver wiring
(II) - + arteriovenous nipping
(III) - + flame haemorrhages and cotton wool exudates
(IV) - + papilloedema
Identify appropriate investigations for hypertension and interpret the results.
1) Bloods
2) Urine dipstick
3) ECG
4) Ambulatory BP monitoring
5) Others
Bloods
- U&E
- Glucose
- Lipids
Urine Dipstick
- Blood
- Protein
ECG
- Left ventricular hypertrophy - deep S waves in V1-2, tall R wave in V5-6, inverted T waves in I, AVL, V5-6, left axis devation
- Ischaemia
Ambulatory BP Monitoring
- White coat hypertension
- Allows monitoring of treatment response
- Assesses preservation of nocturnal dip
Others
- Patients <35 years old
- Suspected secondary cases
Generate a management plan for hypertension (including hypertensive emergencies).
Assessment and modification of CVD risk factors.
Conservative
- Stop smoking
- Lose weight
- Reduced alcohol
- Reduced dietary sodium
Investigate for Secondary Causes
- Young patients
- Malignant hypertension
- Poor response to treatment
Medical - if SBP >160mmHg, DBP >100mmHg
- Thiazide diuretics - 1st line if 55 years+, black patients (e.g. bendrofluamethiazide)
- ACE Inhibitors (e.g. ramipril) or Angiotensin-II Antagonists (e.g. losartan) - 1st line <55 years, diabetics, HF, left ventricle dysfunction
- Ca2+ channel Antagonists - 1st line for >60 years, black patients (e.g. amlodipine)
- B-blockers - not preferred, younger patients, avoid combination with thiazides to avoid diabetes, increased risk of HF (e.g. atenolol)
- alpha-blockers - 4th line, patients with prostatism
Target BP:
- Non-diabetic - <140/85 mmHg
- Diabetic (no proteinuria) - <130/80mmHg
- Diabetic (proteinuria) - <125/75mmHg
Severe Hypertension (DBP >140mmHg) - atenolol (B-blocker) or nifedipine
Acute Malignant Hypertension - IV B-blocker, labetolol or hydralazine sodium nitroprusside - avoid very rapid lowering due to cerebral infarction
Identify the possible complications of hypertension and its management.
- Heart failure
- CAD
- MI
- CVA
- PVD
- DVT
- PE
- Retinopathy
- Renal failure
- Hypertensive encephalopathy
- Posterior reversible encephalopathy syndrome (PRES)
- Malignant hypertension
Summarise the prognosis for patients with hypertension.
Good if BP controlled.
Uncontrolled hypertension linked with increased mortality (6 x stroke risk, 3 x cardiac death risk).
Treatment reduces incidence of renal damage, stroke and heart failure.
Define implanted cardiac defibrillator.
A device fitted surgically into the chest to send electrical pulses to the heart to keep it beating regularly and not too slowly.
Summarise the indications for an implanted cardiac defibrillator.
- Arrhythmia - patients who have survived a 1st episode of life-threatening ventricular arrhythmias, to prevent further events
- Heart failure - where symptoms and cardiac function can no longer be controlled by pharmacological treatment alone
Identify the possible complications of an implanted cardiac defibrillator.
- Infection at implant site
- Allergic reaction to medications used during procedure
- Swelling
- Bleeding
- Bruising
- Damage to vein where the ICD leads are placed
Define infective endocarditis.
Infection of intracardiac endocardial structures - mainly heart valves.
Explain the aetiology / risk factors of infective endocarditis.
Vegetations form as a result of lodging of the organisms on the heart valves during a period of bacteraemia.
- Made of platelets, fibrin, infective organisms
- Poorly penetrated by immune system
- Destroy valve leaflets
- Invade myocardium
- Invade aortic wall
- Abscess cavities form
- Activation of immune system also causes formation of immune complexes –> cutaneous vasculitis, glomerulonephritis, arthritis
Endocardium can be colonized by virtually any organism, but most common are:
1) Streptococci (40%) - mainly alpha-haemolytic Streptococcus viridans or bovis
2) Staphylococci (35%) - aureus or epidermidis (IVDU)
3) Enterococci (20%) - faecalis
4) Others - e.g. Coxiella burnetti, histoplasma, HACEK - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
Risk Factors:
- Abnormal valves - e.g. congenital, post-rheumatic, calcification, degeneration
- Prosthetic heart valves
- Turbulant flow - e.g. patent ductus arteriosus or VSD
- Recent dental work
- Bacteraemia
- S.bovis –> GI Malignancy
Summarise the epidemiology of infective endocarditis.
16-22 per million per year (UK)
Recognise the presenting symptoms of infective endocarditis.
- Fever
- Sweats
- Chills
- Malaise
- Arthralgia
- Myalgia
- Confusion
- Skin lesions
- Ask about recent dental surgery or IV drug use
Recognise the signs of infective endocarditis on physical examination.
- Pyrexia
- Tachycardia
- Signs of anaemia
- Clubbing - if long-standing
- New regurgitant murmur
- Muffled heart sounds
- Splenomegay
NB: Right-sided lesions may imply IV drug use.
Frequency:
Mitral > Aortic > Tricuspid > Pulmonary
Vasculitic Lesions:
- Roth’s spots - petechiae on retina
- Petechiae (especially on pharyngeal and conjunctival mucosa)
- Janeway lesions - painless palmar macules that blanch on pressure
- Osler’s nodes - tender nodules on finger / toe pads
- Splinter haemorrhages - nail-bed haemorrhages
Identfiy appropriate investigations for infective endocarditis and interpret the results.
1) Bloods
2) Urinalysis
3) Blood culture
4) Echocardiography
5) Others
Bloods
- FBC - high neutrophils, normocytic anaemia
- High ESR and CRP
- U&E
- Rheumatoid factor positive
Urinalysis
- Microscopic haematuria
- Proteinuria
Blood Culture
- 3 sets 1 hour apart
- Culture and sensitivity vital but start empirical treatment first
- Culture negative 2-5%
Echocardiography (Transthoracic)
- Transoesophageal echocardiography more sensitive for endocarditis
- Useful for detection of vegetations, valve abscess, diagnosis of prosthetic valve endocarditis, assessment of embolic risk
Others:
- ECG - conduction changes
- CXR - septic pulmonary emboli : focal lung infiltrates, central cavitation - e.g. tricuspid valve endocarditis
Duke’s Classification (2 major, 1 major + 3 minor, all minor):
- MAJOR - positive blood culture in 2 separate samples, positive echocardiogram
- MINOR - high grade pyrexia >38 degrees, risk factors, positive blood culture (no major criteria), positive echocardiogram (not major), vascular signs
+ve echocardiogram = vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation
Risk factors:
- Abnormal valves
- IV drug use
- Dental surgery
Generate a management plan for infective endocarditis.
Antibiotics for 4-6 weeks (at least 6 weeks for prosthetic valve endocarditis).
On clinical suspicion:
- Benzylpenicillin + Gentamycin
- Gentamycin - dose adjusted for peak serum level of 3-4ug/ml, trough <1ug/ml
STREPTOCOCCI
- Continue Benzylpenicillin + Gentamycin
- Alt - Ceftriaxone, Vancomycin
STAPHYLOCOCCI
- Flucloxacillin / Vancomycin + Gentamycin
- Prosthetic - Vancomycin + Gentamicin + Rifampin
ENTEROCOCCI
- Ampicillin + Gentamycin
HACEK
- Ampicillin or Ceftriaxone + Gentamycin
Culture Negative
- Vancomycin + Gentamycin
Surgery
- If poor response or deterioration = urgent valve replacement
- Replacement of prosthees
- Kissing mitral valve vegetations - may be able to salvage
Prophylaxis
- If history of infective endocarditis + undergoing high risk procedures
- High risk procedures - e.g. dental, incision or biopsy of respiratory mucosa, procedures in patients with GI/GU tract infection, procedures on infected skin or musculoskeletal tissue, prosthetic heart valve placement
- Dental - 2g oral amoxicillin 30-60 mins before procedure
Identify the possible complications of infective endocarditis and its management.
- Valve incompetence
- Intracardiac fistulae or abscesses
- Aneurysm formation
- Heart failure
- Renal failure
- Glomerulonephritis
- Arterial emboli from vegetations (brain, kidney, lungs, spleen)
Summarise the prognosis for patients with infective endocarditis.
Fatal if untreated.
When treated, 15-30% mortality.
Define mitral regurgitation.
Retrograde flow of blood from the left ventricle to the left atrium during systole.
Explain the aetiology / risk factors of mitral regurgitation.
Mitral valve damage or dysfunction:
- Rheumatic heart disease
- Infective endocarditis
- Mitral valve prolapse - prolapse of the mitral valve leaflets into the left atrium during systole
- Papillary muscle rupture or dysfunction - secondary to IHD or cardiomyopathy
- Chordal rupture and floppy mitral valve associated with connective tissue diseases (e.g. psuedoxanthoma elasticum), osteogenesis imperfecta, Ehlers-Danlos syndrome, Marfan syndromes, SLE
May also be secondary to left ventricular dilation.
Summarise the epidemiology of mitral regurgitation.
5% of adults.
Prolapse more common in young females.
Recognise the presenting symptoms of mitral regurgitation.
Acute
- Symptoms of left ventricular failure
Chronic
- Asymptomatic
- Exertional dyspnoea
- Palpitations if in AF and fatigue
Mitral Valve Prolapse
- Asymptomatic
- Atypical chest pain
- Palpitations
Recognise the signs of mitral regurgitation on physical examination.
- Normal pulse or irregularly irregular (AF).
- Apex beat laterally displaced and thrusting (left ventricular dilation)
- Pansystolic murmur
- Radiating to axilla
- Palpable as a thrill
- S1 is soft, S3 may be heard (rapid ventricular filling during early diastole)
- Signs of left ventricular failure in acute mitral regurgitation
Mitral Valve Prolapse
- Mid-systolic click
- Late systolic murmur
- Click moves towards 1st heart sound on standing and moves away on lying down
Identify appropriate investigations for mitral regurgitation and interpret the results.
1) ECG
2) CXR
3) Echocardiography
ECG
- Normal
- AF
- Broad bifid p wave - p mitrale
- Delayed activation of left atrium due to enlargement
CXR
- Acute mitral regurgitation = left ventricular failure signs
- Chronic mitral regurgitation = left atrial enlargement, cardiomegaly, left ventricular dilation, mitral valve calcification (rheumatic)
Echocardiography
- 6-12 months for moderate-sever MR to assess left-ventricular ejection fraction and end-systolic dimension
Define mitral stenosis.
Mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle.
Explain the aetiology / risk factors of mitral stenosis.
- Rheumatic heart disease (90%)
- Congenital mitral stenosis
- SLE
- Rheumatoid arthritis
- Endocarditis
- Atrial myxoma - rare cardiac tumour
Summarise the epidemiology of mitral stenosis.
Declining incidence in industrialised countries due to declining incidence of rheumatic fever.
Recognise the presenting symptoms of mitral stenosis.
- Asymptomatic
- Fatigue
- SOB on exertion
- SOB on lying down - orthopnoea
- Palpitations (due to AF)
Rare:
- Cough
- Haemoptysis
- Hoarseness due to compression of left laryngeal nerve by an enlarged left atrium
Recognise the signs of mitral stenosis on physical examination.
- Peripheral or facial cyanosis - malar flush
- Pulse - thready, irregularly irregular (AF)
- Palpation - apex beat undisplaced, tapping, parasternal heave (right ventricular hypertrophy, pulmonary hypertension)
- Auscultation - loud 1st heart sound with opening snap, mid-diastolic murmur (presystolic accentuation if in sinus rhythm), pulmonary oedema (if decompensated)
Identify appropriate investigations for mitral stenosis and interpret the results.
1) ECG
2) CXR
3) Echocardiography
4) Cardiac catheterisation
ECG
- Normal
- Broad bifid p wave (p mitrale) - due to left atrial hypertrophy
- AF
- Evidence of right ventricular hypertrophy in severe pulmonary hypertension
CXR
- Left atrial enlargement
- Cardiac enlargement
- Pulmonary congestion
- Mitral valve calcified in rheumatic cases
Echocardiography
- Assess functional and structural impairments
- Transoesophageal better valve visualisation
Cardiac Catheterisation
- Measures severity of heart failure
Define myocarditis.
Acute inflammation and necrosis of cardiac muscle = myocardium.
Explain the aetiology / risk factors of myocarditis.
Infection:
- Viruses - e.g. Coxackie B, echovirus, EBV, CMV, adenovirus, influenza
- Bacterial - e.g. post-streptococcal, tuberculosis, diptheria, Lyme disease
- Fungal - e.g. candidiasis
- Protozoal - e.g. trypanosomiasis (Chagas disease)
- Helminths - e.g. thrichinosis
Non-infective:
- Systemic disorders - e.g. SLE, sarcoidosis, polymyositis
- Hypersensitivity myocarditis - e.g. sulphonamides
Drugs:
- Chemotherapy agents - e.g. doxorubicin, streptomyocin
- Cocaine abuse
- Heavy metals
- Radiation
Summarise the epidemiology of myocarditis.
Unknown. Many cases not detected at time of acute illness.
Europe & USA - Coxsackie B virus
SA - Chagas disease.
Recognise the presenting symptoms of myocarditis.
- Prodromal ‘flu-like’ illness
- Fever
- Malaise
- Fatigue
- Lethargy
- Breathlessness - pericardial effusion, myocardial dysfunction
- Sharp chest pain - suggesting associated pericarditis
Recognise the signs of myocarditis on physical examination.
Signs of concurrent pericarditis or complications - e.g. heart failure, arrhythmia.
Identify appropriate investigations for myocarditis and interpret the results.
1) Blood
2) ECG
3) CXR
4) Pericardial fluid drainage
5) Echocardiography
6) Myocardial biopsy
Bloods
- FBC - high WCC in infective causes
- U&E
- High ESR or CRP
- Cardiac enzymes high
- Antistreptolysin O titre, ANA, serum ACE, TFT - viral or bacterial serology
ECG
- Non-specific T wave and ST changes
- Widespread saddle-shaped ST elevation in pericarditis
CXR
- Normal
- Cardiomegaly
- Pulmonary oedema
Pericardial fluid drainage
- Glucose
- Protein
- Cytology
- Culture
- Sensitivity
Echocardiography
- Systolic / diastolic function
- Wall motion abnormalities
- Pericardial effusion
Myocardial Biopsy
- Rarely required
- Result does not influence management
Define pericarditis.
Inflammation of the pericardium, may be acute, subacute or chronic.
Explain the aetiology / risk factors of pericarditis.
- Idiopathic
- Infective - commonly Coxsackie B, echovirus, mumps virus, streptococci, fungi, staphylococci, TB
- Connective tissue disease - e.g. sarcoid, SLE, scleroderma
- Post-myocardial infarction (24-72h) in up to 20% of patients
- Dressler’s Syndrome (weeks to months after acute MI)
- Malignancy ( lung, breast, lymphoma, leukaemia, melanoma)
- Metabolic (myxoedema, uraemia)
- Radiotherapy
- Thoracic surgery
- Drugs - e.g. hydralazine, isoniazid
Summarise the epidemiology of pericarditis.
Uncommon
Clinical incidence <1 in 100 hospital admissions.
More common in males.
Recognise the presenting symptoms of pericarditis.
Chest pain:
- Sharp
- Central
- Radiates to neck and shoulders
- Aggravated by coughing, deep inspiration, lying flat
- Relieved by sitting forward
- Dyspnoea
- Nausea
Recognise the signs of pericarditis on physical examination.
- Fever
- Pericardial friction rub - best heard lower left sternal edge, with patient leaning forward in expiration
- Heart sounds may be faint in the presence of an effusion
Cardiac tamponade:
- High JVP (Bell’s Triad)
- Low BP (^^)
- Muffled heart sounds (^^)
- Tachycardia
- Pulsus paradoxus
- Reduced SBP by >10mmHg on inspiration
Constrictive Pericarditis (Chronic):
- High JVP with inspiration - Kussmaul’s sign
- Pulsus paradoxus
- Hepatomegaly
- Ascites
- Oedema
- Pericardial knock - rapid ventricular filing
- AF
Identify appropriate investigations for pericarditis and interpret the results.
1) ECG
2) Echocardiogram
3) Bloods
4) CXR
ECG
- Widespread ST elevation that is saddle shaped
Echocardiogram
- Assess pericardial effusion and cardiac function
Bloods
- FBC
- U&E
- ESR
- CRP
- Cardiac enzymes - normal
- Blood cultures
- ASO titres
- ANA
- Rheumatoid factor
- TFT
- Mantoux test
- Viral serology
CXR
- Normal - globular heart shadow if 250mL effusion
- Pericardial calcification can be seen in constrictive pericarditis - best seen on lateral CXR or CT
Generate a management plan for pericarditis.
- Acute - cardiac tamponade treated by emergency pericardiocentesis
- Medical - treat underlying cause, NSAIDs for relief of pain and fever
- Recurrent - low-dose steroids, immunosuppressants or colchicine
- Surgical - excision of pericardium in constrictive pericarditis
Identify the possible complications of pericarditis and its management.
- Pericardial effusion
- Cardiac tamponade
- Cardiac arrhythmia
Summarise the prognosis for patients with pericarditis.
Depends on underlying cause
Good prognosis in viral cases - recovery within 2 weeks
Poor in malignant pericarditis
Recurrent - particularly in those caused by thoracic surgery
Define peripheral vascular disease (acute and chronic limb ischaemia).
Peripheral Vascular Disease
- Insufficient tissue perfusion initiated by existing atherosclerosis acutely compounded by either emboli or thrombi.
Peripheral Arterial Disease
- A range of arterial syndromes that are caused by atherosclerotic obstruction of lower-extremity arteries
Acute Limb Ischaemia
- Sudden decrease in arterial blood flow to a limb that threatens its viability
- Surgical emergency requiring revascularization in 4-6h to save the limb
Chronic Limb Ischaemia
- Peripheral arterial disease that results in a symptomatic reduced blood supply to the limbs typically caused by atherosclerosis and vasculitis, and affecting lower limbs
Explain the aetiology / risk factors of peripheral vascular disease (acute and chronic limb ischaemia).
Caused by:
- Atherosclerosis
- Vasculitis
- Emboli - due from heart (AF, mural thrombosis) or aneurysms
Acute Limb Ischaemia - may be due to thrombus in situ, emboli, graft/angioplasty occlusion or trauma.
Risk Factors:
- Atherosclerosis
- Smoking
- Diabetes
- Hypertension
- Elevated CRP = inflammation
- Hypertension
- Hyperlipidaemia
- Age 40years+
- History of coronary artery disease / cerebrovascular disease
- Low levels of exercise
Summarise the epidemiology of peripheral vascular disease (acute and chronic limb ischaemia).
Acute Limb Ischaemia - 1.5 cases per 10,000 per year
Recognise the presenting symptoms of peripheral vascular disease (acute and chronic limb ischaemia).
Acute Limb Ischaemia
- 6Ps - pale, pulseless, painful, paralysed, paraesthetic, perishingly cold
- Asymptomatic
- Intermittent claudication
- Thigh or buttock pain with walking that is relieved with rest
- Erectile dysfunction
- Leg pain at rest
- Gangrene
- Non-healing wound / ulcer
Recognise the signs of peripheral vascular disease (acute and chronic limb ischaemia) on physical examination.
Acute Limb Ischaemia - 6Ps - pale, pulseless, painful, paralysed, paraesthetic, perishingly cold - Fixed mottling = irreversibility Gangrene - Non-healing wound/ulcer
Identify appropriate investigations for peripheral vascular disease (acute and chronic limb ischaemia) and interpret the results.
- Ankle-brachial index (ABI)
- Toe-brachial index (TBI)
- Segmental pressure examination
- Pulse volume recording
- Duplex ultrasound
Define ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).
Reduced blood supply to the heart muscle resulting in chest pain (angina pectoris).
May present as stable angina or acute coronary syndrome.
Acute coronary syndrome - divided into unstable angina (no cardiac injury), STEMI, NSTEMI.
MI = cardiac muscle necrosis resulting from ischaemia.
Atherosclerosis:
- Endothelial injury
- Migration of monocytes into sub-endothlial space
- Differentiation into macrophages
- Accumulation of LDL lipids insudated in subendothelium
- Foam cells
- Release of growth factors
- Smooth muscle proliferation
- Production of collagen and proteoglycans
- Formation of atheromatous plaque
Explain the aetiology / risk factors of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).
Angina pectoris = oxygen demand»_space; oxygen supply
- Caused by atherosclerosis, spasm, arteritis, emboli
MI
- Caused by occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation
Risk factors:
- Male
- DM
- Family history
- Hypertension
- Hyperlipidaemia
- Smoking
- Previous history
Atherosclerosis:
- Endothelial injury
- Migration of monocytes into sub-endothlial space
- Differentiation into macrophages
- Accumulation of LDL lipids insudated in subendothelium
- Foam cells
- Release of growth factors
- Smooth muscle proliferation
- Production of collagen and proteoglycans
- Formation of atheromatous plaque
Summarise the epidemiology of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).
2%
Common
More common in males
MI 5 in 1000 incidence UK
Recognise the presenting symptoms of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).
Acute Coronary Syndrome
- Chest pain
- Discomfort of acute onset
- Central heavy tight gripping pain
- Radiation to left arm, neck, jaw or epigastrum
- Increase severity and frequency of previous stable angina
- Breathlessness
- Sweating
- Nausea
- Vomiting
- Silent in elderly or patients with diabetes
Stable Angina
- Brought on by exertion
- Relieved by rest
Recognise the signs of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) on physical examination.
Acute Coronary Syndrome
- No clinical signs
- Pale
- Sweating
- Restless
- Low-grade pyrexia
- Check both radial pulses for aortic dissection
- Arryhthmias
- Disturbances of BP
- New heart murmurs - e.g. pansystolic murmur of mitral regurgitation from papillary muscle rupture or ventricular septal defect
- Signs of complications - e.g. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oligura)
Stable Angina
- Look for signs of risk factors
Identfy appropriate investigations for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and interpret the results.
- Bloods
- ECG
- CXR
- Exercise ECG Testing
- Radionuclide Myocardial Perfusion Imaging (rMPI)
- Echocardiogram
- Pharmacologic Stress Testing
- Cardiac catheterization / angiography
- Coronary Calcium Scoring
Bloods
- FBC
- U&E
- CRP
- Glucose
- Lipid profile
- Cardiac enzymes - CK-MB and troponin -T or I1 (high after 12h)
- Amylase - pancreatitis mimics MI
- TFTs
- AST & LDH - high after 24-48h
ECG
- Unstable Angina or NSTEMI - ST depression, T-wave inversion, Q waves (may indicate old MI)
- STEMI - ST elevation (>1mm in limb leads, >2mm in chest leads), hyperacute T-waves, new-onset LBBB, hours later T-wave invesion, days later Q waves
Location of infarct:
- Inferior walls –> II, III, AVF
- Anterior wall –> Septum (V1-2), Apex (V3-4), Anterolateral Wall (V5-6)
- Lateral wall –> I, AVL
- Posterior infarct –> Tall R wave, ST depression in V1-3
CXR
- Look for signs of heart failure
- Look for differentials - e.g. aortic dissection
Exercise ECG - treadmill test
- Indications - troponin-negative ACS, stable angina with intermediate or high pretest probability of CHD
- Not on digoxin - false-positive result
- Take into account chest pain, cardiac risk factors, age, gender
- Positive Test = >1mm horizontal or downsloping ST-segment depression measured 80ms after end of QRS
- Failed Test = failure to achieve at least 85% of the predicted maximal heart rate (220-age), negative otherwise
- B-blockers reduce maximal heart rate
Radionuclide Myocardial Perfusion Imaging (rMPI)
- Tc-99m sestamibi or tetrofosmin
- Under stress (exercise or pharmacological) or at rest
- Show low uptake in ischaemic myocardium during stress
- Rest testing - used in patient with ACS, no previous MI but non-diagnostic troponin and ECGs
Echocardiogram
- Measure LVEF - myocardial stunning misleading in early measurements
- Exercise or dobutamine stress - detect inducible wall motion abnormalities
Pharmacologic Stress Testing
- Patients who cannot exercise or if exercise test is inconclusive
- E.g. Dipyridamole, adenosine, dobutamine induces tachycardia
- Detect ischaemic myocardium - e.g. rMPI, echocardiography
- Contraindicated in AV block and reactive airway disease (dipyridamole, adenosine)
Cardiac Catheterisation / Angiography
- ACS with positive troponin or TIMI score 5-7 or if high risk on stress testing
- Use Duke treadmill score based on exercise time, maximum ST-segment deviation and exercise angina
Coronary Calcium Scoring
- Using specialized CT
- Role in outpatieints with atypical chest pain or in acute chest pain that is not clearly due to ischaemia - e.g. absence of CAC exclusdes obstructive coornary artery disease
Generate a management plan for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).
Stable Angina
- Mimize cardiac risk factors - e.g. BP, hyperlipidaemia, diabetes, advice on smoking, exercise, weight loss, low-fat diet –> ASPIRIN 75mg/day
- Immediate symptoms relief –> GTN as a spray or sublingually
- Long-term –> B-BLOCKERS (e.g. atenolol), CALCIUM CHANNEL BLOCKERS ( e.g. verapamil, diltiazem), NITRATES (e.g. isosorbide dinrate)
- Percutaneous Coronary Intervenion (PCI) - for localised areas of stenosis, in patients with angina not controlled by therapy, restenosis rate 25% at 6 months, drug-eluting coronary stents reduce rates (release sirolimus or paclitaxel)
- Coronary Artery Bypass Graft (CABG) - for 3-vessel disease, rate of MI and survival similar betwen PCI and CABG
NB: Contraindications of B-blockers - e.g. acute heart failure, cardiogenic shock, bradycardia, heart block, asthma,
Unstable Angina / NSTEMI
- Admit to CCU
- Oxygen
- IV access
- Monitor vitals
- Serial ECG
- Analgesia - e.g. GTN, morphine sulphate / diamorphine, antiemetic (metoclopramide)
- Aspirin - 300mg chewed, 75mg maintenance indefinite
- Clopidogrel - 300mg, 75mg maintenance for 1 year if troponin positive or high risk
- Low molecular weight heparin - e.g. enoxaparin, dalteparin
- B-blocker - e.g. metoprolol
- Glucose-insulin infusion if blood glucose >11 mmol/L
- Glycoprotein IIb/IIIa inhibitors - e.g. tirofiban (initiated on presentation, continued for 48-72h or until PCI) –> for patients undergoing PCI, high risk for further cardiac events
- Urgent angiography & revascularisation if no improvement
High Risk for further cardiac events:
- Troponin positive
- TIMI risk score >4
- Continuing ischaemia
STEMI
- Admit to CCU
- Oxygen
- IV access
- Monitor vitals
- Serial ECG
- Analgesia - GTN, morphine sulphate / diamorphine, antiemetic (metoclopramide)
- Aspirin - 300mg chewed, 75mg maintenance indefinite
- Clopidogrel - 600mg if patient going to primary PCI, 300mg if thrombolysis, <75yrs, 75mg if thrombolysis, >75yrs, 75mg maintenance for 1 year
- B-Blocker - e.g. metoprolol
- Primary PCI route - needs IV heparin + GP IIb/IIIa inhibitor OR bivalirudin (antithrombin)
- Thrombolysis route with recobinant tissue plasminogen activator (rtPA) - IV heparin
- Glucose-insulin infusion if blood glucose>11mmol/L
NB:
Primary PCI with goal <90 mins
Thrombolysis with goal of 30 mins
Rescue PCI if continued pain or elevation after thrombolysis of initial ST-segment elevation on follow up ECG 60-90min after fibrinolytic reaction
Thrombolysis
- Fibrinolytics - e.g. streptokinase, rtPA (alteplase, reteplase, tenecteplase) if within 12h of chest pain with ECG changes
Secondary Prevention:
- Antiplatelet agents - e.g. aspirin, clopidogrel
- ACE inhibitors
- B-Blockers
- Statins
- Control risk factors - e.g. smoking, diabetes, hypertension
Advice
- Do not drive for a month following MI
- Education by cardiac rehabilitation team
- Lifestyle changes - e.g. exercise, stop smoking, changing diet
CABG
- For patients with left main stem or three-vessel disease
Identify the possible complications of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and its management.
At risk of MI and other vasuclar diseases - e.g. stroke, peripheral vascular disease
Cardiac injury can lead secondarily to heart failure and arrhythmias
Early Complications (24-72h)
- Death
- Cardiogenic shock
- Heart failure
- Ventricular arrythmias
- Heart block
- Pericarditis
- Myocardial rupture
- Thromboembolism
Late Complications
- Ventricular wall or septum rupture
- Valvular regurgitation
- Ventricula aneurysms
- Tamponade
- Dressler’s syndrome (pericarditis)
- Thromboembolism
Summarise the prognosis for patients with ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).
Acute Coronary Sydnrome:
- TIMI score used for risk stratification (0-7)
- High score = high risk of cardiac events within 30 days
1) >65 yrs
2) Known CAD
3) Aspirin in last 7 days
4) Severe angina (>2 episodes in 24h)
5) ST deviation >1mm
6) Elevated troponin levels
7) >3 coronary artery disease risk factors - e.g. hypertension, hyperlipidaemia, family history, diabetes, smoking
Killip Classification of Acute MI:
- Class I - no evidence of acute heart failure
- Class II - mild to moderate heart failure (S3, crepitations
Define permanent pacing.
Electronic devices that stimulate the heart with electrical impulses to maintain or restore a normal heartbeat.
Most commonly accomplished through transvenous placement of leads to the endocardium (ie. right atrium or ventricle) or epicardium (i.e. to the left ventricular surface via the coronary sinus), which are subsequently connected to a pacing generator placed subcutaneously in the infraclavicular region.
Summarise the indications for permanent pacing.
- Sinus node dysfunction
- Acquired AV block
- Chronic bifascicular block
- After acute phase of myocardial infarction
- Neurocardiogenic syncope and hypersensitive carotid sinus syndrome
- Post cardiac transplantation
- Hypertrophic cardiomyopathy
- Pacing to detect and terminate tachycardia
- Cardiac resynchronization therapy in patients with severe systolic heart failure
- Patients with congenital heart disease
Identify the possible complications of permanent pacing.
- Infections
- Haematoma formation
- Pericardial effusion
- Pericardial tamponade
- Pneumothorax
- Coronary sinus dissection
- Perforation
Define pulmonary embolism.
Occlusion of pulmonary vessels, most commonly caused by a thrombus that has travelled to the vascular system from another site.
Explain the aetiology/risk factors of pulmonary embolism.
- Thrombus
- 95% originate from DVT of lower limbs
- Rarely from right atrium in patients with AF
- Amniotic fluid embolus
- Air embolus
- Fat emboli
- Tumour emboli
- Mycotic emboli from right-sided endocarditis
Risk factors:
- Surgical patients
- Immobility
- Obesity
- OCP
- Heart failure
- Malignancy
Summarise the epidemiology of pulmonary embolism.
Fairly common, especially in hospitalized patients
Occur in 10-20% of those with a confirmed proximal DVT.
Recognize the presenting symptoms of pulmonary embolism.
Depends on site and size.
Small - may be asymptomatic
Moderate
- Sudden onset dyspnoea
- Cough
- Haemoptysis
- Pleuritic chest pain
Large
- Sudden onset dyspnoea
- Cough
- Haemoptysis
- Severe pleuritic chest pain
- Shock
- Collapse
- Acute right heart failure
- Sudden death
Multiple Small Recurrent
- Symptoms of pulmonary hypertension
Recognize the signs of a pulmonary embolism on physical examination.
Clinical Probability Assessment
- Well’s Score - >4 high probability, <3 probability
Clinically suspected DVT = 3.0 PE is most likely diagnosis = 3.0 Recent surgery (4 weeks) = 1.5 Immobilization = 1.5 Tachycardia = 1.5 History of DVT or PE = 1.5 Haemoptysis = 1 Malignancy = 1
- Raised Geneva Score - >11 high probability, 4-10 intermediate probability, <3 low probability
>65 = 1 Recent surgery or fracture (28 days) = 2 Previous DVT / PE = 3 Active maliganancy = 2 Unilateral leg pain = 3 Haemoptysis = 2 Heart Rate > 75-94/min = 3 Heart Rate >85/min = 5 Unilateral leg oedema and tenderness = 4
Small
- No clinical signs
- Tachycardia
- Tachypnoea
Moderate
- Tachycardia
- Tachypnoea
- Pleural rub
- Low O2 sats - despite O2 supplementation
Large
- Shock
- Cyanosis
- Signs of right heart strain - e.g. raised JVP, left parasternal heave, accentuated S2 heart sound
Multiple Recurrent PE
- Signs of pulmonary hypertension and right heart failure
Identify the appropriate investigations for pulmonary embolism and interpret the results.
Low Probability
- D-dimer blood test - cross-linked fibrin degradation products
- Highly sensitive
- Poor specificity
High Probability
- Requires imaging
Additional:
- Bloods - ABG, thrombophilia screen
- ECG - normal, tachycardia, right axis deviation, RBBB
- CXR - exclude other differentials
NB: Classic Si, QIII, TIII pattern uncommon.
- Spiral CT Pulmonary Angiogram - 1st line, poor sensitivity for small emboli
- Ventilation-Perfusion (VQ) Scan - administration of IV 99mTc macro-aggregated albumin and inhalation of 81 krypton gas to identify areas of ventilation and perfusion mismatch
(If abnormal CXR or co-existing lung disease, do not use due to difficulty in interpretation)
- Pulmonary angiography - gold standard, invasive though
- Doppler USS of lower limb - to examine for VT
- Echocardiogram - right heart strain shown
Define pulmonary hypertension.
A consistently increased pulmonary arterial pressure (>20mmHg) under resting conditions.
Explain the aetiology /risk factors of pulmonary hypertension.
Primary
- Idiopathic
Secondary
- Left heart disease - mitral valve disease, left ventricular failure, left atrial myxoma/thrombosis
- Chronic lung disease - COPD
- Recurrent pulmonary emboli
- Increased pulmonary blood flow - ASD, VSD, patent ductus arteriosus
- Connective tissue disease - SLE, systemic sclerosis
Drugs - e.g. amiodarone
Summarise the epidemiology of pulmonary hypertension.
Primary pulmonary hypertension - young females.
Recognize the presenting symptoms of pulmonary hypertension.
- Dyspnoea - on exertion
- Chest pain
- Syncope
- Tiredness
- Symptoms of the underlying cause - e.g. chronic cough
Recognize the signs of pulmonary hypertension on physical examination.
- Raised JVP - prominent a wave in the JVP waveform
- Left parasternal heave - right ventricular hypertrophy
- Loud pulmonary component of S2 (S3/S4 may be heard)
- Early diastolic murmur - Graham Steell murmur (caused by pulmonary regurgitation if tricuspid regurgitation develops - large CV wave, pansystolic murmur)
- Signs of underlying condition
- Right heart failure signs in severe cases
Identify appropriate investigations for pulmonary hypertension and interpret the results.
- CXR
- ECG
- Echocardiography
- Lung function test
- VQ Scan
- Cardiac catheterization
- High-Resolution CT-Thorax
- Lung Biopsy
CXR
- Cardiomegaly - right ventricular enlargement, right atrial dilation
- Prominent main pulmonary arteries - taper rapidly
- Signs of the cause - e.g. COPD, calcified mitral valves
ECG
- Right ventricular hypertrophy - right-axis deviation
Identify appropriate investigations for pulmonary hypertension and interpret the results.
- CXR
- ECG
- Echocardiography
- Lung function test
- VQ Scan
- Cardiac catheterization
- High-Resolution CT-Thorax
- Lung Biopsy
CXR
- Cardiomegaly - right ventricular enlargement, right atrial dilation
- Prominent main pulmonary arteries - taper rapidly
- Signs of the cause - e.g. COPD, calcified mitral valves
ECG
- Right ventricular hypertrophy - right-axis deviation, prominant R wave in V1, T inversion in V1-2
- Right atrial enlargement - peaked P wave in II (P pulmonale)
- Limb leads exhibit low voltage (R < 5mm) in COPD
Echocardiography
- Visualise right ventricular hypertrophy or dilation
- Possible underlying cause
Lung Function Tests
- Assess for chronic lung disease
VQ Scan
- Assess for PE
Cardiac Catheterisation
- Assess severity, right heart pressures, response to vasodilators
High Resolution CT-Thorax
- Images pulmonary arteries
- Diagnose lung disease
Lung Biopsy
- Assess structural lung changes
Define rheumatic fever.
An inflammatory multisystem disorder, occurring following group A B-haemolytic streptococci (GAS) infection.
Explain the aetiology/risk factors for rheumatic fever.
Unknown.
Streptococcal pharyngeal infection required.
Genetic susceptibility.
Molecular mimicry - role in the initiation of tissue injury - e.g. antibodies directed against GAS antigens cross-react with host antigens
Summarise the epidemiology of rheumatic fever.
5-15 years - peak incidence
Far East, Middle East, Easter Europe, South America
Mean incidence 19/100,000 .
Reduction in incidence in West, non-Western countries incidence is relatively high.
Recognize the presenting symptoms of rheumatic fever.
- 2-5 weeks after GAS infection
- Fever
- Malaise
- Anorexia
- Painful, swollen joints
- Reduced movement and function
- Breathlessness
- Chest pain
- Palpitations
Recognize the signs of rheumatic fever on physical examination.
- Duckett Jones Criteria - positive diagnosis if at least 2 major criteria, or one major plus 2 minor criteria
Major Criteria:
- Arthritis - migratory or fleeting polyarthritis with swelling, redness, tenderness of large joints
- Carditis - new murmur (Carey Coombs murmur - mid-diastolic murmur due to mitral valvulitis), pericarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes
- Chorea - rapid, involuntary, irregular movements with flowing or dancing quality, slurred speech (more common in females)
- Nodules - small, firm, painless, subcutaneous nodules on extensor surfaces, joints and tendons
- Erythema Marginatum (20%) - transient erythematous rash with raised edges, seen on trunk and proximal limbs (cresent or ring-shaped patches)
Minor Criteria
- Pyrexia
- Previous rheumatic fever
- Arthralgia - only if arthritis is not present as major criteria
- Recent streptococcal infection - supported by positive throat cultures or high antitreptolysin O titre
- High ESR, CRP orWCC
- High PR and QT intervals on ECG - if carditis not present as major criteria
Identify appropriate investigations for rheumatic fever and interpret the results.
- Bloods
- Throat swab
- ECG
- Echocardiogram
Bloods
- FBC - raised WCC
- ESR/CRP - raised ESR, CRP
- Raised antitreptolysin O titre
Throat Swab
- Culture for GAS
- Rapid streptococcal antigen test
ECG
- Saddle shaped ST elevation
- PR segment depression
- Arrhythmias
(signs of pericarditis)
Echocardiogram
- Pericardial effusion
- Myocardial thickening or dysfunction
- Valvular dysfunction
Define supraventricular tachycardia.
A dysrhythmia originating at or above the atrioventricular node, and if defined by a narrow complex (QRS < 120ms) at a rate >100bpm.
Atrioventricular nodal reentrant tachycardia (AVNRT) = paroxysmal SVT - defined as intermittent SVT without provoking factors, presenting with a ventricular rhythm of 160 bpm.
Explain the aetiology / risk factors of supraventricular tachycardia.
Most common cause is orthodromic re-entry phenomenon - when the tachycardia is secondary to normal anterograde electrical conduction from the atria to the AV node to the ventricles, with the retrograde conduction via an accessory pathway form the ventricles back to the atria.
Children <12 - accessory AV pathways causes re-entry tachycardia
Narrow QRS complex indicates ventricles are being activated superior to the bundle of His - implies the arrythmia originates from the SA node, atrial myometrium, AV node or within His bundle.
Rarer - anti-dromic conduction passing from atria to ventricles via accessory pathway and then returns retrograde through AV node to atria.
Differential diagnosis:
- Sinus tachycardia
- Atrial tachycardia
- Junctional tachycardia
- Atrial fibrillation
- Atrial flutter
- Multi atrial tachycardia
In patients susceptible, triggers can be:
- Caffeine
- Alcohol
- Physical stress
- Emotional stress
- Cigarette smoking
Risk Factors:
- Children with congenital heart disease
Summarise the epidemiology of supraventricular tachycardia.
AVNRT:
35 per 100,000 - most common non-sinus tachydysrhythmia in young adults
M:F 2:1
Old:Young 5:1
SVT:
Most common symptomatic dysrhymthmia in infants and children.
Recognise the presenting symptoms of supraventricular tachycardia.
- Anxiety
- Palpitations
- Chest discomfort
- Light-headedness
- Syncope
- Dyspnea
- Shock
Recognize the signs of supraventricular tachycardia on physical examination.
- Hypotension
- Signs of heart failure - e.g. bibasilar crackles, 3rd heart sound, JVP raised
- Exercise intolerance
- Tachycardia
Check for Haemodynamic Instability:
- Hypotension
- Hypoxia
- SOB
- Chest pain
- Shock
- Evidence of poor end-organ perfusion
- Altered mental status
Identify appropriate investigations for supraventricular tachycardia and interpret the results.
- ECG - narrow complex, regular tachycardia (180-220bpm), no detectable P waves
(if P waves are detectable, consider sinus tachycardia, atrial fibrillation, atrial flutter)
- Bloods - check electrolyte abnormalities, anaemia, hyperthyroidism, digoxin levels
Generate a management plan for supraventricular tachycardia.
Step 1
- Give O2 if SaO2 < 90%
- Get IV access
- 12-lead ECG
Step 2
- Check for haemodynamic instability - shock, chest pain, ischaemia on ECG, heart failure, syncope
Step 3 - If Haemodynamic Instability
- Get expert help
- Sedation
- Up to 3 synchronized DC shocks - 70-120J for first (if AF 120-150J) then 120-360J
- Check and correct K+, Mg2+,Ca2+
Generate a management plan for supraventricular tachycardia.
Step 1
- Give O2 if SaO2 < 90%
- Get IV access
- 12-lead ECG
Step 2
- Check for haemodynamic instability - shock, chest pain, ischaemia on ECG, heart failure, syncope
Step 3 - If Haemodynamic Instability
- Get expert help
- Sedation
- Up to 3 synchronized DC shocks - 70-120J for first (if AF 120-150J) then 120-360J
- Check and correct K+, Mg2+,Ca2+
Step 3 - if Haemodynamically Stable
- Ask is the rhythm regular?
Step 4 - Rhythm is NOT REGULAR
- Start continuous ECG trace
- Perform vagal manoeuvres (Valsalva Manouvre) but take care if possible digoxin toxicity, acute ischaemia, carotid bruit
Step 4 - Rhythm is REGULAR
- Treat as AF
- Control rate with B-blocker - e.g. metoprolol 1-10mg IV, small increments to slow rate
- Control rate with rate-limiting Ca2+ channel blocker - verapamil 5-10mg IV
- Control rate with digoxin (if heart failure - e.g. load with 500mcg PO then 500mcg PO after 8h and further 250mcg PO after 8h
- Control rate with amiodarine
- Anticoagulation with warfarin or NOAC to reduce risk of stroke
- If onset <48h or effectively anti-coagulated for >3 weeks, consider cardioversion under sedation with DC or chemical cardioversion
- Chemical cardioversion - e.g. flecanide 300mg PO (if no structural heart damage) or amiodarone 300mg IVI over 20-60mins, then 900mg over 24h
Identify the possible complications of supraventricular tachycardia and its management.
- Haematoma
- Pseudoaneurysm of the artery
- Bleeding
- Myocardial infarction
- Heart block and the need for a pacemaker
- Stroke
- Death
Summarise the prognosis for patients with supraventricular tachycardia.
- Good outcome
- Small risk of sudden death
- Depends on the severity of the defect
- Pregnancy - higher risk of death if unrepaired heart defect
Define tricuspid regurgitation.
Backflow of blood from the right ventricle to the right atrium during systole.
Explain the aetiology/risk factors of tricuspid regurgitation.
Congenital
- Ebstein anomaly = malpositioned tricuspid valve
- Cleft valve in ostium primum defect
Functional
- Consequence of right ventricular dilation - e.g. pulmonary hypertension
- Valve prolapse
Rheumatic Heart Disease
- Associated with valvular disease
Infective Endocarditis
- Common in IV drug users
- Usually staphylococcal
Others
- Carcinoid syndrome
- Trauma
- Cirrhosis - long-standing
- Iatrogenic - e.g. radiotherapy to the thorax
Summarise the epidemiology of tricuspid regurgitation.
Differs with various causes
Infective endocarditis probably most common cause
Recognize the presenting symptoms of tricuspid regurgitation.
- Fatigue
- Breathlessness
- Palpitations
- Headaches
- Nausea
- Anorexia
- Epigastric pain made worse by exercise
- Jaundice
- Lower limb swelling
Recognise the signs of tricuspid regurgitation on physical examination.
- Irregular pulse - due to AF, right atrial enlargement
- Raised JVP with giant v waves that may oscillate the earlobe - caused by the transmission of right ventricular pressure (may also be giant a wave if in sinus rhythm)
- Parasternal heave
- Pansystolic murmur best heart at the left lower sternal edge, louder on inspiration (Carvallo sign), loud P2 component of second heart sound
- Pleural effusion
- Causes of pulmonary hypertension - e.g. emphysema
- Palpable liver - tender, smooth, pulsatile
- Ascites
- Pitting oedema
Identify appropriate investigations for tricuspid regurgitation and interpret the results.
- Bloods
- ECG
- CXR
- Echocardiogram
- Right Heart Catheterization
Bloods
- FBC
- LFT
- Cardiac enzymes
- Blood cultures
ECG
- Tall P wave - right atrial hypertrophy if in sinus rhythm
- Changes indicative of other cardiac disease
CXR
- Right-sided enlargement of cardiac shadow
Echocardiography
- Extent of regurgitation estimated by colour flow Doppler
- May be able to detect tricuspid valve abnormality - e.g. prolapse
- Right ventricular dilation
Right Heart Catheterization
- Rarely necessary
- Assess pulmonary artery pressure
Define varicose veins.
Long, tortuous and dilated veins of the superficial venous system.
Explain the aetiology / risk factors of varicose veins.
Blood from superficial veins of the leg passess into deep veins via perforator veins (perforate deep fascia) and at the saphenofemoral and saphenopopliteal junctions. Valves prevent blood from passing from deep to superficial veins. If they become incompetent there is venous hypertension and silatation of the superficial veins occurs.
Risk Factors:
- Prolonged standing
- Obesity
- Pregnancy
- Family history
- Contraceptive pill
Causes:
- Primary mechanical factors (95%)
- Secondary to obstruction (DVT, foetus, pelvic tumour), arteriovenous malformations, overactive muscle pumps (e.g. cyclists), rarely congenital valve absence
Summarise the epidemiology of varicose vein.
Reports of prevalence of chronic venous insufficiency vary from < 1% to 40% in females and from < 1% to 17% in males. Prevalence estimates for varicose veins are higher, <1% to 73% in females and 2% to 56% in males.
Recognize the presenting symptoms of varicose veins.
- My legs are ugly
- Pain
- Cramps
- Tingling
- Heaviness
- Restless legs
Recognize the signs of varicose veins on physical examination.
- Oedema
- Eczema
- Ulcers
- Haemosiderin
- Haemorrhage
- Phlebitis
- Atrophie blanche - white scarring at the site of a previous, healed ulcer
- Lipodermatosclerosis - skin hardness from subcutaneous fibrosis caused by chronic inflammation and fat necrosis
- VVs don’t caused DVTs on their own - except possibly proximally spreading thrombophlebitis of the long sapheneous veins
Identify appropriate investigations for varicose veins and interpret the results.
- Duplex ultrasound - assesses for reversed flow
Generate a management plan for varicose veins.
Criteria for specialist referral of patients with VVs should be: Pain, Bleeding, Ulceration, Superficial Thrombophlebitis, Severe Impact on Quality of Life
- Treat underlying cause
- Education - avoid prolonged standing, elevate legs whenever possible, support stockings, lose weight, regular walks (calf muscle action aids venous return)
- Endovascular Treatment
Endovascualr Treatment
- Radiofrequency ablation - catether inserted into vein, heated to 120 degree, destoys endothelium, closes vein, as good as surgery at 3 months
- Endovenous laser ablation - similar to above, uses laser, similar outcome to surgery at 2 years
- Infection Sclerotherapy - A) Liquid sclerosant is indicated for varicosities below the knee if there is no gross saphenofemoral incompetence, injected at multiple sites, vein compressed for a few weeks to avoid thrombosis (intravascular granulation tissue obliterates lumen). B) Foam sclerosant injected under ultrasound guidance (prevents spread of foam to femoral vein) at single site, spreads rapidly throughout veins, damage endothelium
- Surgery - depends on vein anatomy and surgical preference - e.g. saphenofemoral ligation, multiple avulsions, stripping from groin to upper calf, bandage legs elevated after surgery
Identify the possible complications of varicose veins and its management.
- Bruising
- Swelling
- Skin discolouration
- Pain
- Infection
- Blood clots - e.g. thrombophlebitis, DVT, PE
- Scarring
Summarise the prognosis for patients with varicose veins.
Although varicose veins and venous insufficiency are chronic diseases, their prognosis is essentially benign in the great majority of cases, even without intervention. However, good self-care is especially important in order to decrease the discomfort, complications, and progression.
Define vasovagal syncope.
Fainting when your body overreacts to certain triggers, such as the sight of blood, extreme emotional distress. The vasovagal syncope trigger causes your heart rate and blood pressure to drop suddenly.
Explain the aetiology / risk factors of vasovagal syncope.
Occurs due to reflex bradycardia with/without peripheral vasodilation provoked by emotion, pain or standing too long (cannot occur when you’re lying down).
Onset is over seconds (not instantaneous) and is often preceded by pre-syncopal symptoms - e.g. nausea, pallor, sweating, narrowing of visual fields.
Brief clonic jerking of the limbs may occur due to cerebral hypoperfusion, but there is no tonic/clonic sequence.
Urinary incontinence is uncommon, there is no tongue biting.
Unconsciousness usually lasts for 2 mins, and recovery is rapid.
Summarise the epidemiology of vasovagal syncope.
In the general population, the annual number episodes are 18.1–39.7 per 1000 patients, with similar incidence between genders, and with high prevalence between 10 and 30 years of age, mainly of vasovagal syncope (Moya et al., 2009).
Recognise the presenting symptoms of vasovagal syncope.
- Collapse
- Loss of consciousness
- Nausea
- Pallor
- Sweating
- Narrowing of visual fields
- Clonic jerking of the limbs
- No tonic/clonic sequence
- No urinary incontinence
- No tongue-biting
Recognise the signs of vasovagal syncope on physical examination.
- Collapse
- Loss of consciousness
- Nausea
- Pallor
- Sweating
- Narrowing of visual fields
- Clonic jerking of the limbs
- No tonic/clonic sequence
- No urinary incontinence
- No tongue-biting
Identify appropriate investigations for vasovagal syncope and interpret the results.
- Cardiovascular examination
- Neurological examination
- Measure BP lying and standing
Identify appropriate investigations for vasovagal syncope and interpret the results.
- Cardiovascular examination
- Neurological examination
- Measure BP lying and standing
- ECG & 24h ECG
- Bloods - U&E, FBC, Mg2+, Ca2+, Glucose
- Tilt table test
- EEG
- Sleep EEG
- Echocardiogram
- CT MRI brain
- ABG if practical
Define Wolff-Parkinson-White Syndrome.
Short PR interval and delta-wave on ECG predisposing to supraventricular tachycardias (SVT).
2 Types : Type A - +ve delta wave in V1 Type B - -ve delta wave in V1
Explain the aetiology / risk factors of Wolff-Parkinson-White Syndrome.
Congenital accessory pathway (bundle of Kent) bypasses the atrioventricular node causing ventricular pre-excitation.
Risk Factors:
- Ebstein’s anomaly
- Hypertrophic cardiomyopathy
- Mitral valve prolapse
- Atrial septal defect
Summarise the epidemiology of Wolff-Parkinson-White Syndrome.
Peak incidence has been reported in individuals between 30 and 40 years old in otherwise healthy adults. Some reports suggest that WPW syndrome occurs in males more often than females. The disorder’s estimated prevalence is . 1-3.1 per 1,000 people in the United States.
Recognise the presenting symptoms of Wolff-Parkinson-White Syndrome.
- Asymptomatic
- Atrioventricular re-entrant tachycardia
- Atrial fibrillation
- Sudden cardiac death
- Palpitations
- Dizziness
- Shortness of breath
- Chest pain
Recognise the signs of Wolff-Parkinson-White Syndrome on physical examination.
- Asymptomatic
- Atrioventricular re-entrant tachycardia
- Atrial fibrillation
- Sudden cardiac death
- Palpitations
- Dizziness
- Shortness of breath
- Chest pain
Define venous ulcers.
Wounds that are thought to occur due to improper functioning of venous valves, usually of the legs.
Explain the aetiology / risk factors of venous ulcers.
The main cause of venous leg ulcers is faulty valves inside the leg veins. These valves normally allow the blood to flow up the leg towards the heart, and they also prevent backward flow down the leg. If the valves are faulty, backward flow is not prevented and pressure builds up inside the veins.
Develops after minor injury, where persistently high pressure in the veins of the legs damages the skin.
Risk factors:
- Varicose veins
- History of DVT
- Blockage of the lymph vessels - causes fluid to build up in the legs
- Older age
- Female
- Tall height
- Family history of venous insufficiency
- Obesity
- Pregnancy
- Smoking
- Osteoarthritis
- Leg injury
- Paralysis
Summarise the epidemiology of venous ulcers.
70-90% of leg ulcer cases caused by venous valve dysfunction.
1 in 500 people in the UK
Become more common with age
1 in 50 people >80 yrs.
Recognize the presenting symptoms of venous ulcers.
- Heavy feeling in the legs
- Aching in the legs
- Itchy skin on legs
- Pain
- Fever
Recognise the signs of venous ulcers on physical examination.
- Pedal oedema
- Discolouration and darkening of the skin around the ulcer = hyperpigmentation
- Hardened skin around the ulcer = lipodermatosclerosis
- Varicose eczema - red, flaky, scaley skin on legs
- Enlarged veins on the legs (varicose veins)
- Unpleasant and foul-smelling discharge from ulcer
Identify appropriate investigations for venous ulcers and interpret the results.
1) Duplex ultrasound
- Demonstrates retrograde or reversed flow
- Valve closure time >0.5 seconds indicates venous insufficiency
2) Ascending phlebography - evaluate treatment options for complex cases, as identifies obstruction site and level, presence and location of collaterals
3) CT venography - reveals detailed venous anatomy
4) MR Venography - reveals detailed venous anatomy
5) CT CAP - rule out extrinsic compression for iliac vein compressions (e.g. pelvic or abdominal mass)
6) Intravascular ultrasound - in specialised centres as secondary test to identify iliac vein obstruction
7) Air Plethysmography - identifies reflux and obstruction
Generate a management plan for venous ulcers.
Prevention
- Graded compression stockings - for CVI-related oedema, stasis dermatitis, small venous leg ulcers
In general, there are three classes of compression stockings: class 1 stockings (light compression) control oedema; class 2 (medium compression) and class 3 (high compression) are usually required for more advanced CVI. Patients with severe CVI or previous ulcers generally require lifelong graded compression stockings of at least 30 to 40 mmHg.
- Moisturisers - to combat skin dryness and flaking
- Pentoxifylline - 400mg orally QDS
- Diosmin - consult specialist
With Superficial Venous Reflux:
- Endovenous ablation or saphenectomy
With Angiomata and Varicosities:
- Endovenous ablation or injection sclerotherapy
With Perforating Vein Incompetence:
- Endovenous ablation
With Iliac Vein Obstruction:
- Percutaneous iliac angioplasty and stenting
With Deep Venous Reflux :
- Venous valvular reconstruction - for patients whose conventional therapy has failed
With Leg Pain:
- Horse chesnut seed extract
Identify the possible complications of venous ulcers and its management.
- Osetomyelitis
- Septicaemia
- Cellulitis
- Venous Eczema
- Malignancy
Summarise the prognosis for patients with venous ulcers.
The healing was worst for patients with venous ulcers, only 44% had healed their original ulcers without recurrence. The 5 year survival was 52%, significantly lower than for age- and sex-matched controls (68%) (p = 0.0002).
Define ventricular fibrillation.
Irregular, rapid ventricular activation with no cardiac output.
Explain the aetiology / risk factors of ventricular fibrillation.
The most common cause is a problem in the electrical impulses traveling through your heart after a first heart attack or problems resulting from a scar in your heart’s muscle tissue from a previous heart attack.
Some cases of ventricular fibrillation begin as a rapid heartbeat called ventricular tachycardia (VT). This rapid but regular beating of the heart is caused by abnormal electrical impulses that start in the ventricles.
Most VT occurs in people with a heart-related problem, such as scars or damage from a heart attack. Sometimes VT can last less than 30 seconds (nonsustained) and may not cause symptoms. But VT may be a sign of more-serious heart problems.
If VT lasts more than 30 seconds, it will usually lead to palpitations, dizziness or fainting. Untreated VT will often lead to ventricular fibrillation.
Risk Factors:
- Previous episode of ventricular fibrillation
- Previous heart attack
- Congenital heart disease
- Cardiomyopathy
- Injuries that cause damage to heart muscle - e.g. electrocution
- Cocaine or Methamphetamine use
- Electrolyte abnormalities - e.g. potassium, magnesium
Summarise the epidemiology of ventricular fibrillation.
In the pediatric and adolescent age groups, VF occurs with an annual incidence of 1.3-8.5 cases per 100,000 persons, accounting for approximately 5% of all deaths in this group. VF is often the first expression of coronary artery disease (CAD) and is responsible for approximately 50% of deaths from CAD.
Recognise the presenting symptoms of ventricular fibrillation.
- Chest pain
- Dizziness
- Nausea
- Rapid, fluttering heartbeat
- Shortness of breath
- Fainting
Recognise the signs of ventricular fibrillation on physical examination.
- Loss of consciousness
- Rapid, fluttering heart beat
Identify appropriate investigations for ventricular fibrillation and interpret the results.
- Cardiac Monitor - classification of the rhythm
- Bloods - ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose
Generate a management plan for ventricular fibrillation.
BLS.
If pulseless Ventricular Tachycardia or Ventricular Fibrillation = Shockable Rhythm:
- Defibrillate once - 150-360J biphasic, 360J monophasic
- Resume CPR immediately for 2 min, then return to assess rhythm again
- Administer adrenaline (1mg IV) after second defibrillation and again ever 3-5 minutes
- If shockable rhythm persists after third shock, administer amiodarone 300mg IV bolus or lidocaine.
Identify the possible complications of ventricular fibrillation and its management.
- Sudden cardiac death
- Coma
- Loss of nerve function
- Changes in mental function
Summarise the prognosis for patients with ventricular fibrillation.
Overall survival to 1 month was only 1.6% for patients with non-shockable rhythms and 9.5% for patients found in VF. With increasing time to defibrillation, the survival rate fell rapidly from approximately 50% with a minimal delay to 5% at 15 min.
Define ventricular tachycardia.
> 3 Successive ventricular extrasystoles (broad QRS complexes >120ms) at a rate of >12- bpm
Patients at high risk of recurrent VT should be considered for implantable defibrillator which has been shown to be more effective than amiodarone.
Explain the aetiology / risk factors of ventricular tachycardia.
- MI
- Congenital heart defect
- Hypertrophic or dilated cardiomyopathy
- Myocarditis
- Ischaemic heart disease
- Heart failure
Risk Factors:
- Age
- Heart condition
- Previous MI
- Family history of VT - inherited catecholaminergic polymorphic ventricular tachycardia or arrhythmogenic right ventricular dysplasia
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.
- Lightheadedness
- Dizziness
- Palpitations
- Fatigue
- Chest pressure or pain
- Shortness of breath
- Fainting spells
Recognise the signs of ventricular tachycardia on physical examination.
- Lightheadedness
- Dizziness
- Palpitations
- Fatigue
- Chest pressure or pain
- Shortness of breath
- Fainting spells
Identify appropriate investigations for ventricular tachycardia and interpret the results.
- Cardiac monitor - classification of rhythm
- Bloods - ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose
- ECG
- Transoesophageal echocardiogram - ultrasound probe inserted into oesophagus
- Cardiac MRI
- Cardiac CT
- Coronary angiogram
- CXR
- Stress echocardiogram
Generate a management plan for ventricular tachycardia.
If sustained ventricular tachycardia with haemodynamic stability:
- Amiodarone hydrochloride
- Flecainide acetate
- propafenone hydrochloride
- Lidocaine hydrochloride
- If sinus rhythm not restored, then DC cardioversion or pacing considered
- Catheter ablation option if cessation of arrhythmia is not urgent
If non-sustained ventricular tachycardia with haemodynamic stability:
- Treat with beta-blocker
If unstable sustained Ventricular Tachycardia:
- Watch for deterioration with signs of hypotension or reduced cardiac ouput
- DC cardioversion to restore sinus rhythm
- IV amiodarone hydrochloride and repeat DC cardioversion
If pulseless Ventricular Tachycardia or Ventricular Fibrillation = Shockable Rhythm:
- Defibrillate once - 150-360J biphasic, 360J monophasic
- Resume CPR immediately for 2 min, then return to assess rhythm again
- Administer adrenaline (1mg IV) after second defibrillation and again ever 3-5 minutes
- If shockable rhythm persists after third shock, administer amiodarone 300mg IV bolus or lidocaine.
Maintenance Therapy:
- Implantable cardioverter-defibrillator
- Beta-blockers
- Sotalol hydrochloride - in place of standard beta-blocker
- Amiodarone hydrochloride
Summarise the prognosis for patients with ventricular tachycardia.
At higher risk of ventricular fibrillation.
