Cardiovascular Flashcards
Learning objectives
Answer
Define abdominal aortic aneurysm
• A localised enlargement of the abdominal aorta such that the diameter is > 3 cm or > 50% larger than normal diameter.
o NOTE: normal diameter of the aorta = 2 cm
Explain the aetiology / risk factors of an abdominal aortic aneurysm
• There are NO specific identifiable causes
• Risk Factors
o Severe atherosclerotic damage to aortic wall
o Family history
o Smoking
o Male
o Age
o Hypertension
o Hyperlipidaemia
o Connective tissue disorders: Marfan’s syndrome, Ehlers-Danlos syndrome
o Inflammatory disorders: Behcet’s disease, Takayasu’s arteritis
Summarise the epidemiology of an abdominal aortic aneurysm
Around 4% of men aged between 65 and 74 in England have an AAA (approx. 80,000 men) this results in approximately 6000 deaths per year in England and Wales.
Deaths from AAA account for around 2% of all deaths in men aged 65 and over
Women are much less likely to develop abdominal aortic aneurysms. They are about three times more common in men than in women.
Recognise the presenting symptoms of an abdominal aortic aneurysm
• Unruptured o NO SYMPTOMS o Usually an incidental finding o May have pain in the back, abdomen, loin or groin • RUPTURED o Pain in the abdomen, back or loin o Pain may be sudden or severe o Syncope o Shock • NOTE: degree of shock depends on site of rupture and whether it is contained
Recognise the signs of an abdominal aortic aneurysm on physical examination
- Pulsatile and laterally expansile mass on bimanual palpation of the abdominal aorta
- Abdominal bruit
- Retroperitoneal haemorrhage can cause Grey-Turner’s sign
Identify appropriate investigations for an abdominal aortic aneurysm and interpret the results
• Bloods
o FBC, clotting screen, renal function and liver function
o Cross-match if surgery is planned
• Scans
o Ultrasound - can detect aneurysm but CANNOT tell whether it is leaking or not
o CT with contrast - can show whether an aneurysm has ruptured
o MRI angiography
Define amyloidosis
• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils
Explain the aetiology / risk factors of amyloidosis
• Amyloid fibrils are polymers of low-molecular-weight subunit proteins
• These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration
• Their deposition progressively disrupts the structure and function of normal tissue
• Amyloidosis is classified according to the fibril subunit proteins
o Type AA - serum amyloid A protein
o Type AL - monoclonal immunoglobulin light chains
o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin
Summarise the epidemiology of amyloidosis
- AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
- AL - 300-600 cases in the UK per year
- Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis
Recognise the presenting symptoms & signs of amyloidosis
- Renal - proteinuria, nephrotic syndrome, renal failure
- Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
- GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
- Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
- Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
- Joints - painful asymmetrical large joints, enlargement of anterior shoulder
- Haematological - bleeding tendency
Identify appropriate investigations for amyloidosis and interpret the results
• Tissue Biopsy • Urine - check for proteinuria, free immunoglobulin light chains (in AL) • Bloods o CRP/ESR o Rheumatoid factor o Immunoglobulin levels o Serum protein electrophoresis o LFTs o U&Es • SAP Scan - radiolabelled SAP will localise the deposits of amyloid
Define aortic dissection
- A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, creating a false lumen
- Classification of aortic dissection:
o Type A: ASCENDING aorta (MOST COMMON)
o Type B: DESCENDING aorta (distal to the left subclavian artery)
Explain the aetiology / risk factors of aortic dissection
• Aortic dissection is usually preceded by degenerative changes in the smooth muscle of the aortic media
• Common causes and risk factors:
o HYPERTENSION
o Aortic atherosclerosis
o Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos, SLE)
o Congenital cardiac abnormalities (e.g. coarctation of the aorta)
o Aortitis
o Iatrogenic (e.g. during angioplasty/angiography)
o Trauma
o Crack cocaine
• NOTE: expansion of the false lumen can lead to obstruction of the subclavian, carotid, coeliac and renal arteries
o Hypoperfusion of the target organs of these major arteries can give rise to other symptoms (e.g. carotid artery –> collapse)
Summarise the epidemiology of aortic dissection
• Most common in males aged 40-60 yrsB20B20A18:B20A18:B20
Recognise the presenting symptoms of aortic dissection
• MAIN SYMPTOM: sudden central ‘tearing’ pain, it may radiate to the back in between the shoulder blades (it can mimic MI)
• Other symptoms caused by obstruction of branches of the aorta:
o Carotid artery –> hemiparesis, dysphasia, blackout
o Coronary artery –> chest pain (angina or MI)
o Subclavian artery –> ataxia, loss of consciousness
o Anterior spinal artery –> paraplegia
o Coeliac axis –> severe abdominal pain (due to ischaemic bowel)
o Renal artery –> anuria, renal failure
Recognise the signs of aortic dissection on physical examination
• Murmur on the back (below the left scapula), descending to the abdomen
• Hypertension
• Blood pressure difference between the two arms > 20 mm Hg
• Wide pulse pressure
• Hypotension may suggest tamponade
o Check for pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration
o This may indicate:
• Tamponade
• Pericarditis
• Chronic sleep apnoea
• Obstructive lung disease
• Signs of Aortic Regurgitation
o High volume collapsing pulse
o+B21 Early diastolic murmur over aortic area
• Unequal arm pulses
• There may be a palpable abdominal mass A18:B20
Identify appropriate investigations for aortic dissection and interpret the results
• Bloods o FBC o X-match 10 units of blood o U&E - check renal function o Clotting screen • CXR
o Widened mediastinum • ECG o Often NORMAL o If the ostia of the right coronary artery is compromised you may get signs of: • Left ventricular hypertrophy • Inferior MI
• CT Thorax
o Shows false lumen
• Echocardiography
o Transoesophageal allows visualisation
• Cardiac catheterisation and aortography
Define aortic regurgitation
• Reflux of blood from the aorta into the left ventricle during diastole. Also known as aortic insufficiency
Explain the aetiology / risk factors of aortic regurgitation
• Aortic valve leaflet abnormalities or damage
o Bicuspid aortic valve
o Infective endocarditis
o Rheumatic fever
o Trauma
• Aortic root/ascending aorta dilatation
o Systemic hypertension
o Aortic dissection
o Aortitis
o Arthritides (e.g. rheumatoid arthritis, seronegative arthritides)
o Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos)
o Pseudoxanthoma elasticum
o Osteogenesis imperfecta
• Pathophysiology
o Reflux of blood into the left ventricle results in left ventricular dilatation
o This means increased end diastolic volume and increased stroke volume
o The combination of increased stroke volume and low end-diastolic AORTIC pressure may explain the high-volume collapsing pulse
Summarise the epidemiology of aortic regurgitation
- Chronic AR often begins in the late 50s
* It is most frequently seen in patients > 80 yrs
Recognise the presenting symptoms of aortic regurgitation
• Chronic AR
o Initially ASYMPTOMATIC
o Later on, the patient may develop symptoms of heart failure (e.g. exertional dyspnoea, orthopnoea, fatigue)
• Severe Acute AR
o Sudden cardiovascular collapse (left ventricle cannot adapt to the rapid increase in end-diastolic volume)
• Symptoms related to aetiology (e.g. chest or back pain caused by aortic dissection)
Recognise the signs of aortic regurgitation on physical examination
• Collapsing (water-hammer) pulse
• Wide pulse pressure
• Thrusting and heaving displaced apex beat
• Early diastolic murmur over the aortic valve region
o Heard better at the left sternal edge when the patient is sitting forward with the breath held at the top of expiration
• NOTE: an ejection systolic murmur may also be heard because of increased flow across the valve (due to increased stroke volume)
• Austin Flint mid-diastolic murmur
o Heard over the apex
o Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis
• Rare signs associated with aortic regurgitation:
o Quincke’s Sign - visible pulsation on nail bed
o de Musset’s Sign - head nodding in time with the pulse
o Becker’s Sign - visible pulsation of the pupils and retinal arteries
o Muller’s Sign - visible pulsation of the uvula
o Corrigan’s Sign - visible pulsation in the neck
o Traube’s Sign - pistol shot (loud systolic and diastolic sounds) heard on auscultation of the femoral arteries
o Duroziez’s Sign - systolic and diastolic bruit heard on partial compression of the femoral artery with the stethoscope
o Rosenbach’s Sign - systolic pulsations of the liver
o Gerhard’s Sign - systolic pulsations of the spleen
o Hill’s Sign - popliteal cuff systolic pressure exceeding brachial pressure by > 60 mm Hg
Identify appropriate investigations for aortic regurgitation and interpret the results
• CXR
o Cardiomegaly
o Dilatation of ascending aorta
o Signs of pulmonary oedema (if accompanied by left heart failure)
• ECG
o May show left ventricular hypertrophy
• Deep S in V1/2
• Tall R in V5/6
• Inverted T waves in lead I, aVL, V5/6
• Left axis deviation
• Echocardiogram
o May show underlying cause (e.g. aortic root dilatation, bicuspid aortic valve)
o May show the effects of aortic regurgitation (e.g. left ventricular dilatation, fluttering of the anterior mitral valve leaflet)
o Doppler echocardiogram can show AR and indicate severity
o Repeat echos allow monitoring of progression (LV size and function)
• Cardiac catheterisation with angiography
o If there is any 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
- Stenosis can be secondary to rheumatic heart disease (MOST COMMON WORLDWIDE)
- Calcification of a congenital bicuspid aortic valve
- Calcification/degeneration of a tricuspid aortic valve in the elderly
Summarise the epidemiology of aortic stenosis
- Present in 3% of 75 yr olds
- More common in males
- Those with bicuspid aortic valve present earlier
Recognise the presenting symptoms of aortic stenosis
- May be ASYMPTOMATIC initially
- Angina (due to increased oxygen demand of the hypertrophied left ventricle)
- Syncope or dizziness on exercise (due to outflow obstruction)
- Symptoms of heart failure (e.g. dyspnoea, orthopnoea)
Recognise the signs of aortic stenosis on physical examination
- Narrow pulse pressure
- Slow-rising pulse
- Thrill in the aortic area (only if severe)
- Forceful sustained thrusting undisplaced apex beat
- Ejection systolic murmur at the aortic area, radiating to the carotid artery
- Second heart sound may be softened or absent (due to calcification)
- A bicuspid valve may produce an ejection click
Identify appropriate investigations for aortic stenosis and interpret the results
• ECG
o Signs of left ventricular hypertrophy
• Deep S in V1/2
• Tall R in V5/6
• Inverted T waves in I, aVL and V5/6
• Left axis deviation
o LBBB
• CXR
o Post-stenotic enlargement of ascending aorta
o Calcification of aortic valve
• Echocardiogram
o Visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar)
o Estimation of aortic valve area and pressure gradient across the valve in systole
o Assess left ventricular function
• Cardiac angiography
o Allows differentiation from other causes of angina (e.g. MI)
o Allows assessment of concomitant coronary artery disease
• NOTE: 50% of patients with severe aortic stenosis have significant coronary artery disease
Define arterial ulcers
• A localised area of damage and breakdown of skin due to inadequate arterial blood supply. Usually seen on the feet of patients with severe atheromatous narrowing of the arteries supplying the legs.
Explain the aetiology / risk factors of arterial ulcers
• The ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities
• Risk Factors
o Coronary heart disease
o History of stroke or TIA
o Diabetes mellitus
o Peripheral arterial disease (e.g. intermittent claudication)
o Obesity and immobility
Summarise the epidemiology of arterial ulcers
- 22% of leg ulcers
* Prevalence increases with age and obesity
Recognise the presenting symptoms of arterial ulcers
• Often DISTAL - at the dorsum of the foot or between the toes
• Punched-out appearance
• Often elliptical with clearly defined edges
• The ulcer base contains grey, granulation tissue
• NIGHT PAIN - hallmark of arterial ulcers
o Pain is worse when supine (because arterial blood flow is further reduced when supine)
o Pain is relieved by dangling the affected leg off the end of the bed
Recognise the signs of arterial ulcers on physical examination
- Night pain
- Punched-out appearance
- Hairlessness
- Pale skin
- Absent pulses
- Nail dystrophy
- Wasting of calf muscles
Identify appropriate investigations for arterial ulcers and interpret the results
- Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery
- ABPI
- Percutaneous angiography
- ECG
- Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor)
- FBC - anaemia can worsen the ischaemia
Define atrial fibrillation/flutter
• Characterised by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into:
o Permanent
o Persistent
o Paroxysmal
Explain the aetiology / risk factors of atrial fibrillation/flutter
• There may be no identifiable cause • Secondary causes lead to an abnormal atrial electrical pathway that results in AF • Systemic Causes o Thyrotoxicosis o Hypertension o Pneumonia o Alcohol • Heart Causes o Mitral valve disease o Ischaemic heart disease o Rheumatic heart disease o Cardiomyopathy o Pericarditis o Sick sinus syndrome o Atrial myxoma • Lung Causes o Bronchial carcinoma o PE
Summarise the epidemiology of atrial fibrillation/flutter
- VERY COMMON in the elderly
- Present in 5% of those > 65 years
- May be paroxysmal
Recognise the presenting symptoms of atrial fibrillation/flutter
- Often ASYMPTOMATIC
- Palpitations
- Syncope (if low output)
- 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
- Check for signs of thyroid disease and valvular disease
Identify appropriate investigations for atrial fibrillation/flutter and interpret the results
• ECG o Uneven baseline with absent p waves o Irregular intervals between QRS complexes o Atrial flutter = saw-tooth • Bloods o Cardiac enzymes o TFT o Lipid profile o U&Es, Mg2+ and Ca2+ • Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia • Echocardiogram o May show: • Mitral valve disease • Left atrial dilatation • Left ventricular dysfunction • Structural abnormalities
Generate a management plan for atrial fibrillation/flutter
First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection)
There are TWO main components to AF management:
• RHYTHM CONTROL
o If > 48 hrs since onset of AF
• Anticoagulate for 3-4 weeks before attempting cardioversion
o If < 48 hrs since onset of AF
• DC cardioversion (2 x 100 J, 1 x 200 J)
• Chemical cardioversion: flecainide or amiodarone
NOTE: flecainide is contraindicated if there is a history of ischaemic heart disease
o Prophylaxis against AF
• Sotalol
• Amiodarone
• Flecainide
• Consider pill-in-the-pocket (single dose of a cardioverting drug (e.g. flecainide) for patients with paroxysmal AF) strategy for suitable patients
• RATE CONTROL
o Chronic (Permanent) AF
• Control ventricular rate with:
Digoxin
Verapamil
Beta-blockers
• Aim for ventricular rate ~ 90 bpm
• STROKE RISK STRATIFICATION
o LOW RISK patients can be managed with aspirin
o HIGH RISK patients require anticoagulation with warfarin
o This is based on the CHADS-Vasc Score
o Risk factors include:
• Previous thromboembolic event
• Age > 75 yrs
• Hypertension
• Diabetes
• Vascular disease
• Valvular disease
• Heart failure
• Impaired left ventricular function
Identify the possible complications of atrial fibrillation/flutter and its management
• THROMBOEMBOLISM
o Embolic stroke risk of 4% per year
o Risk is increased with left atrial enlargement or left ventricular dysfunction
• Worsening of existing heart failure
Summarise the prognosis for patients with atrial fibrillation/flutter
• Chronic AF in a disease heart does not usually return to sinus rhythm
Define cardiac arrest
• Acute cessation of cardiac function
Explain the aetiology / risk factors of cardiac arrest
The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts • FOUR Hs o Hypothermia o Hypoxia o Hypovolaemia o Hypokalaemia/Hyperkalaemia • FOUR Ts o Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis)) o Thromboembolic o Tamponade o Tension pneumothorax
Summarise the epidemiology of cardiac arrest
• None available
Recognise the presenting symptoms of cardiac arrest
- Management precedes or is concurrent to history
* Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness
Recognise the signs of cardiac arrest on physical examination
- Unconscious
- Not breathing
- Absent carotid pulses
Identify appropriate investigations for cardiac arrest and interpret the results
• Cardiac Monitor o Allows classification of the rhythm • Bloods o ABG o U&E o FBC o X-match o Clotting o Toxicology screen o Blood glucose
Generate a management plan for cardiac arrest
• SAFETY IS IMPORTANT
o Approach any arrest scene with caution
o The cause of the arrest may pose a threat
o Defibrillators and oxygen are hazards
• Basic Life Support
o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist)
o Clear and maintain the airway with head tilt, jaw thrust and chin lift
o Assess breathing by look, listen and feel
• If they are not breathing, give two rescue breaths
o Assess circulation at carotid pulse for 10 seconds
• If absent - give 30 chest compressions at around 100/min
• Continue cycle of 30 chest compressions for every 2 rescue breaths
o Proceed to advanced life support as soon as possible
• Advanced Life Support
o Attach cardiac monitor and defibrillator
o Assess rhythm
• If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms)
Defibrillate once (150-360 J biphasic, 360 J monophasic)
• Make sure no one is touching the patient or the bed
Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF
Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins
If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine)
• If pulseless electrical activity (PEA) or asystole (non-shockable rhythms)
CPR for 2, and then reassess rhythm
Administer adrenaline (1 mg IV) every 3-5 mins
Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm
o During CPR:
• Check electrodes, paddle positions and contacts
• Secure airway
Once secure, give continuous compressions and breaths
• Consider magnesium, bicarbonate and external pacing
• Stop CPR and check pulse only if change in rhythm or signs of life
• Treatment of REVERSIBLE causes
o Hypothermia - warm slowly
o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels
o Hypovolaemia - IV colloids, crystalloids and blood products
o Tamponade - pericardiocentesis
o Tension Pneumothorax - aspiration or chest drain
o Thromboembolism - treat as PE or MI
o Toxins - use antidote for given toxin
Identify the possible complications of cardiac arrest and its management
- Irreversible hypoxic brain damage
* Death
Summarise the prognosis for patients with cardiac arrest
- Resuscitation is less successful if cardiac arrest happens outside the hospital
- Increased duration of inadequate effective cardiac output –> 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 OUTPUT Cardiac Failure (reduced cardiac output) o Left Heart Failure • Ischaemic heart disease • Hypertension • Cardiomyopathy • Aortic valve disease • Mitral regurgitation o Right Heart Failure • Secondary to left heart failure (in which case it is called congestive cardiac failure) • Infarction • Cardiomyopathy • Pulmonary hypertension/embolus/valve disease • Chronic lung disease • Tricuspid regurgitation • Constrictive pericarditis/pericardial tamponade o Biventricular Failure • Arrhythmia • Cardiomyopathy (dilated or restrictive) • Myocarditis • Drug toxicity • HIGH OUTPUT Cardiac Failure (increased demand) o Anaemia o Beri beri o Pregnancy o Paget's disease o Hyperthyroidism o Arteriovenous malformation
Summarise the epidemiology of cardiac failure (acute and chronic)
• 10% > 65 yrs old
Recognise the presenting symptoms of cardiac failure (acute and chronic)
• Left Heart Failure - symptoms caused by pulmonary congestion o Dyspnoea - divided based on the New York Heart Association classification: • 1 - no dyspnoea • 2 - dyspnoea on ordinary activities • 3 - dyspnoea on less than ordinary activities • 4 - dyspnoea at rest o Orthopnoea o Paroxysmal nocturnal dyspnoea o Fatigue • Acute Left Ventricular Failure o Dyspnoea o Wheeze o Cough o Pink frothy sputum • Right Heart Failure o Swollen ankles o Fatigue o Increased weight (due to oedema) o Reduced exercise tolerance o Anorexia o Nausea
Recognise the signs of cardiac failure (acute and chronic) on physical examination
• Left Heart Failure
o Tachycardia
o Tachypnoea
o Displaced apex beat
o Bilateral basal crackles
o S3 gallop (caused by rapid ventricular filling)
o Pansystolic murmur (due to functional mitral regurgitation)
• Acute Left Ventricular Failure
o Tachypnoea
o Cyanosis
o Tachycardia
o Peripheral shutdown
o Pulsus alternans
• Arterial pulse waveforms showing alternating strong and weak beats
• Sign of left ventricular systolic impairment
• Explanation:
In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume
This causes an increase in end-diastolic volume
This means that the left ventricle is stretched more for the next contraction
Due to Starling’s Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction
This results in a stronger systolic pulse
o Gallop rhythm
o Wheeze (cardiac asthma)
o Fine crackles throughout lung
• Right Heart Failure
o Raised JVP
o Hepatomegaly
o Ascites
o Ankle/sacral pitting oedema
o Signs of functional tricuspid regurgitation
Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results
• Bloods o FBC o U&E o LFTs o CRP o Glucose o Lipids o TFTs • In ACUTE Left Ventricular Failure o ABG o Troponin o BNP • Raised plasma BNP suggests diagnosis of cardiac failure • Low plasma BNP rules out cardiac failure (90% sensitivity) • CXR o Alveolar shadowing o Kerley B lines o Cardiomegaly o Upper Lobe Diversion o Pleural Effusion • ECG o May be normal o May show ischaemic changes (pathological q waves, t wave inversion) o May show arrhythmia or left ventricular hypertrophy • Echocardiogram o Assess ventricular contraction o Systolic dysfunction = LV ejection fraction < 40% o Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect • Swan-Ganz Catheter o Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Generate a management plan for cardiac failure (acute and chronic)
• Acute Left Ventricular Failure
o Treating Cardiogenic Shock:
• This is severe cardiac failure with low blood pressure
• Requires the use of inotropes (e.g. dobutamine)
• Managed in ITU
o Treating Pulmonary Oedema:
• Sit the patient up
• 60-100% Oxygen (and consider CPAP)
• Diamorphine (venodilator + anxiolytic)
• GTN infusion (venodilator –> reduced preload)
• IV furosemide (venodilator and later diuretic effect)
• Monitor:
BP
Respiratory rate
Oxygen saturation
Urine output
ECG
• TREAT THE CAUSE! (e.g. MI, arrhythmia)
• Chronic Left Ventricular Failure
o TREAT THE CAUSE (e.g. hypertension)
o TREAT EXACERBATING FACTORS (e.g. anaemia)
o ACE Inhibitors
• Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
• They slow down the progression of heart failure and improve survival
o Beta-Blockers
• Blocks the effects of a chronically activated sympathetic system
• Slows progression of heart failure and improves survival
• The benefits of ACE inhibitors and beta-blockers are additive
o Loop Diuretics
• Alongside dietary salt restriction, can correct fluid overload
o Aldosterone Antagonists
• Improves survival in patients with NYHA class III/IV symptoms on standard therapy
• Monitor K+ (as these drugs may cause hyperkalaemia)
o Angiotensin Receptor Blockers
• May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers
• Monitor K+ (as these drugs may cause hyperkalaemia)
o Hydralazine and a Nitrate
• May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers
o Digoxin
• Positive inotrope
• Reduces hospitalisation but does NOT improve survival
o N-3 Polyunsaturated Fatty Acids
• Provide a small beneficial advantage in terms of survival
o Cardiac Resynchronisation Therapy
• Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms
• These patients are also candidates for implantable cardioverter defibrillator (ICD)
• They may receive a combined device
o CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)
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% with cardiac failure die within 2 years
Define cardiomyopathy
• Primary disease of the myocardium. Cardiomyopathy may be:
o Dilated
o Hypertrophic
o Restrictive
Explain the aetiology / risk factors of cardiomyopathy
• The majority are IDIOPATHIC • Dilated Cardiomyopathy o Post-viral myocarditis o Alcohol o Drugs (e.g. doxorubicin, cocaine) o Familial o Thyrotoxicosis o Haemochromatosis o Peripartum • Hypertrophic Cardiomyopathy
o Up to 50% are genetic
• Restrictive Cardiomyopathy
o Amyloidosis
o Sarcoidosis
o Haemochromatosis
Summarise the epidemiology of cardiomyopathy
- Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20%
- Restrictive is even rarer
Recognise the presenting symptoms of cardiomyopathy
• Dilated o Symptoms of heart failure o Arrhythmias o Thromboembolism o Family history of sudden death • Hypertrophic o Usually NO SYMPTOMS o Syncope o Angina o Arrhythmias o Family history of sudden death • Restrictive o Dyspnoea o Fatigue o Arrhythmias o Ankle or abdominal swelling o Family history of sudden death
Recognise the signs of cardiomyopathy on physical examination
• Dilated o Raised JVP o Displaced apex beat o Functional mitral and tricuspid regurgitations o Third heart sound • Hypertrophic o Jerky carotid pulse o Double apex beat o Ejection systolic murmur • Restrictive o Raised JVP • Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles o Palpable apex beat o Third heart sound o Ascites o Ankle oedema o Hepatomegaly
Identify appropriate investigations for cardiomyopathy and interpret the results
• CXR
o May show cardiomegaly o May show signs of heart failure • ECG o All Types • Non-specific ST changes • Conduction defects • Arrhythmias o Hypertrophic • Left-axis deviation • Signs of left ventricular hypertrophy • Q waves in inferior and lateral leads o Restrictive • Low voltage complexes • Echocardiography o Dilated • Dilated ventricles with global hypokinesia o Hypertrophic • Ventricular hypertrophy (asymmetrical septal hypertrophy) o Restrictive • Non-dilated non-hypertrophied ventricles • Atrial enlargement • Preserved systolic function • Diastolic dysfunction • Granular or sparkling appearance of myocardium in amyloidosis • Cardiac Catheterisation • Endomyocardial Biopsy • Pedigree or Genetic Analysis
Define constrictive pericarditis
• Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.
Explain the aetiology / risk factors of constrictive pericarditis
• NOTE: it is often underdiagnosed because it is difficult to distinguish it from restrictive cardiomyopathy and other causes of right heart failure • Can occur after any pericardial disease process • More common causes of pericarditis: o Idiopathic o Virus o TB o Mediastinal irradiation o Post-surgical o Connective tissue disease
Summarise the epidemiology of constrictive pericarditis
- RARE
- Documented in all ages
- 9% of patients with acute pericarditis will develop constrictive pericarditis
- TB has the HIGHEST TOTAL INCIDENCE out of all causes
- More common in MALES
Recognise the presenting symptoms & signs of constrictive pericarditis
• Gradual-onset of symptoms
• EARLY - symptoms and signs may be very subtle
• ADVANCED - jaundice, cachexia, muscle wasting
• Right Heart Failure Signs
o Dyspnoea
o Peripheral oedema
o Raised JVP
o Kussmaul’s sign (paradoxical rise in JVP on inspiration)
o Pulsatile hepatomegaly
Identify appropriate investigations for constrictive pericarditis and interpret the results
- CXR - may show calcification of the pericardium
- Echocardiogram - usually diagnostic and helps distinguish from restrictive cardiomyopathy
- MRI - allows assessment of thickness of pericardium
- CT - same role as MRI
- Pericardial biopsy - may be indicated (especially if suspected infective cause)
Define deep vein thrombosis (DVT)
• Formation of a thrombus within the deep veins (most commonly in the calf or thigh)
Explain the aetiology / risk factors of deep vein thrombosis (DVT)
• Deep veins in the legs are more prone to blood stasis, hence clots are more likely to form (look up Virchow's triad) • Risk Factors o COCP o Post-surgery o Prolonged immobility o Obesity o Pregnancy o Dehydration o Smoking o Polycythaemia o Thrombophilia (e.g. protein C deficiency) o Malignancy
Summarise the epidemiology of deep vein thrombosis (DVT)
- VERY COMMON
* Especially in hospitalised patients
Recognise the presenting symptoms of deep vein thrombosis (DVT)
- Swollen limb
* May be painless
Recognise the signs of deep vein thrombosis (DVT) on physical examination
• Examination of the Leg
o Local erythema, warmth and swelling
o Measure the leg circumference
o Varicosities (swollen/tortuous vessels)
o Skin colour changes
o NOTE: Homan’s Sign - forced passive dorsiflexion of the ankle causes deep calf pain
• Risk is stratified using the WELLS CRITERIA (NOTE: this is different from the PE Wells criteria)
o Score 2 or more = high risk
• Examine for PE
o Check respiratory rate, pulse oximetry and pulse rate
Identify appropriate investigations for deep vein thrombosis (DVT) and interpret the results
• Doppler Ultrasound - GOLD STANDARD • Impedance Plethysmography - changes in blood volume results in changes of electrical resistance • Bloods o D-dimer: can be used as a negative predictor o Thrombophilia screen if indicated • If PE suspected o ECG o CXR o ABG
Generate a management plan for deep vein thrombosis (DVT)
• ANTICOAGULATION
o Heparin whilst waiting for warfarin to increase INR to the target range of 2-3
o DVTs that do NOT extend above the knee may be observed and anticoagulated for 3 months
o DVTs extending beyond the knee require anticoagulation for 6 months
o Recurrent DVTs require long-term warfarin
• IVC Filter
o May be used if anticoagulation is contraindicated and there is a risk of embolisation
• Prevention
o Graduated compression stockings
o Mobilisation
o Prophylactic heparin (if high risk e.g. hospitalised patients)
Identify the possible complications of deep vein thrombosis (DVT) and its management
- PE
- Venous infarction (phlegmasia cerulea dolens)
- Thrombophlebitis (results from recurrent DVT)
- Chronic venous insufficiency
Summarise the prognosis for patients with deep vein thrombosis (DVT)
- Depends on extent of DVT
- Below-knee DVTs have a GOOD prognosis
- Proximal DVTs have a greater risk of embolisation
Define dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)
Dyslipidemia is an abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood.
Explain the aetiology / risk factors of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)
Primary dyslipidemia
Blood sample being tested by lab technician.
Dyslipidemia can be diagnosed with a blood test.
Genetic factors cause primary dyslipidemia, and it is inherited. Common causes of primary dyslipidemia include:
Familial combined hyperlipidemia, which develops in teenagers and young adults and can lead to high cholesterol.
Familial hyperapobetalipoproteinemia, a mutation in a group of LDL lipoproteins called apolipoproteins.
Familial hypertriglyceridemia, which leads to high triglyceride levels.
Homozygous familial or polygenic hypercholesterolemia, a mutation in LDL receptors.
Secondary dyslipidemia
Secondary dyslipidemia is caused by lifestyle factors or medical conditions that interfere with blood lipid levels over time.
Common causes of secondary dyslipidemia include:
obesity, especially excess weight around the waist
diabetes
hypothyroidism
alcohol use disorder, also known as alcoholism
polycystic ovary syndrome
metabolic syndrome
excessive consumption of fats, especially saturated and trans fats
Cushing’s syndrome
inflammatory bowel disease, commonly known as IBS
severe infections, such as HIV
an abdominal aortic aneurysm
Several factors are known to increase the chances of developing dyslipidemia and related conditions. These risk factors include:
obesity a sedentary lifestyle a lack of regular physical exercise alcohol use tobacco use use of illegal or illicit drugs sexually transmitted infections type 2 diabetes hypothyroidism chronic kidney or liver conditions digestive conditions older age a diet rich in saturated and trans fats a parent or grandparent with dyslipidemia female sex, as women tend to experience higher LDL levels after menopause
Summarise the epidemiology of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)
In high-income countries, over 50% of adults had raised total cholesterol; more than double the level of the low-income countries.
Recognise the presenting symptoms & signs of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)
Unless it is severe, most people with dyslipidemia are unaware that they have it. A doctor will usually diagnose dyslipidemia during a routine blood test or a test for another condition.
Severe or untreated dyslipidemia can lead to other conditions, including coronary artery disease (CAD) and peripheral artery disease (PAD).
Both CAD and PAD can cause serious health complications, including heart attacks and strokes. Common symptoms of these conditions include:
leg pain, especially when walking or standing
chest pain
tightness or pressure in the chest and shortness of breath
pain, tightness, and pressure in the neck, jaw, shoulders, and back
indigestion and heartburn
sleep problems and daytime exhaustion
dizziness
heart palpitations
cold sweats
vomiting and nausea
swelling in the legs, ankles, feet, stomach, and veins of the neck
fainting
These symptoms may get worse with activity or stress and get better when a person rests.
Anyone who experiences severe chest pain, dizziness, and fainting, or problems breathing should seek emergency care.
Identify appropriate investigations for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and interpret the results
The most common goals are:
Total cholesterol: Below 200 mg/dL
HDL cholesterol: Men - above 40 mg/dL; Women - above 50 mg/dL
LDL cholesterol: Below 100 mg/dL; Below 70 mg/dL for people with diabetes or heart disease.
Triglycerides: Below 150 mg/dL
Generate a management plan for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)
A doctor will usually focus on lowering a person’s levels of triglycerides and LDL. However, treatment can vary, depending on the underlying cause of dyslipidemia and how severe it is.
Doctors may prescribe one or more lipid-modifying medications for people with very high total cholesterol levels of at least 200 milligrams per deciliter of blood.
High cholesterol is usually treated with statins, which interfere with the production of cholesterol in the liver.
If statins fail to lower LDL and triglyceride levels, a doctor may recommend additional medications, including:
ezetimibe niacin fibrates bile acid sequestrants evolocumab and alirocumab lomitapide and mipomersen Some lifestyle changes and supplements can help to encourage healthy blood lipid levels.
Natural treatments include:
reducing the consumption of unhealthy fats, such as those found in red meats, full-fat dairy products, refined carbohydrates, chocolate, chips, and fried foods
exercising regularly
maintaining a healthy body weight, by losing weight if necessary
reducing or avoiding alcohol consumption
quitting smoking and other use of tobacco products
avoiding sitting for long periods of time
increasing consumption of healthy polyunsaturated fats, such as those found in nuts, seeds, legumes, fish, whole grains, and olive oil
taking omega-3 oil, either as a liquid or in capsules
eating plenty of dietary fiber from whole fruits, vegetables, and whole grains
getting at least 6– 8 hours of sleep a night
drinking plenty of water
Identify the possible complications of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and its management
People with minor dyslipidemia usually have no symptoms. They can often manage or resolve the condition by making lifestyle adjustments.
People with dyslipidemia should contact a doctor if they experience symptoms relating to the heart or circulation, including:
chest pains or tightness dizziness heart palpitations exhaustion swelling of the ankles and feet trouble breathing cold sweats nausea and heartburn People who have severe dyslipidemia, especially those with other medical conditions, may need to manage their blood lipid levels with medication, in addition to making lifestyle changes.
Summarise the prognosis for patients with dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)
Significantly reduced risk of CHD if managed well.
Define gangrene
- Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene
- Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes
Explain the aetiology / risk factors of gangrene
o Tissue ischaemia and infarction o Physical trauma o Thermal injury o Gas gangrene is caused by Clostridia perfringens • Necrotising Fasciitis o Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms • Risk Factors o Diabetes o Peripheral vascular disease o Leg ulcers o Malignancy o Immunosuppression o Steroid use o Puncture/surgical wounds
Summarise the epidemiology of gangrene
- Gangrene - relatively COMMON
* Necrotising fasciitis and gas gangrene - RARE
Recognise the presenting symptoms of gangrene
• Gangrene
o Pain
o Discolouration of affected area
o Often affects extremities or areas subject to high pressure
• Necrotising Fasciitis
o Pain
• Often seems SEVERE and out of proportion to the apparent physical signs
o Predisposing event (e.g. trauma, ulcer, surgery)
Recognise the signs of gangrene on physical examination
• Gangrene
o Painful area = erythematous region around gangrenous tissue
o Gangrenous tissue = BLACK because of haemoglobin break down products
o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes
o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)
• Necrotising Fasciitis
o Area of erythema and oedema
o Haemorrhagic blisters may be present
o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)
Identify appropriate investigations for gangrene and interpret the results
- Bloods - FBC, U&Es, glucose, CRP and blood culture
- Wound Swab, Pus/Fluid Aspirate - MC&S
- X-ray of affected area - may show gas produced in gas gangrene
Define heart block (1st, 2nd, 3rd degree)
• 1st Degree AV Block: prolonged conduction through the AV node
• 2nd Degree AV Block:
o Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle ten begins again.
o Mobitz Type II: intermittent or regular failure of conduction through the AV node. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)
• 3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle
Explain the aetiology / risk factors of heart block (1st, 2nd, 3rd degree)
• 250,000 pacemakers are implanted every year and they are mostly for heart block
