CARDIO Flashcards
Define Abdominal Aortic Aneurysm (AAA)
A localised enlargement of the abdominal aorta such that the diameter is >3cm or >50% larger than the normal diameter
(normal diameter of the aorta is 2cm)
Aetiology/ Risk Factors for AAA
- no specific identifiable causes
Risk FACtors: - Severe atherosclerotic damage to aortic wall
-Family history
-Smoking
-Male
-Age
-Hypertension
-Hyperlipidaemia
-Connective tissue disorders: Marfan’s syndrome, Ehlers-Danlos syndrome
-Inflammatory disorders: Behcet’s disease, Takayasu’s arteritis
Presenting symptoms of AAA (ruptured and unruptured)
• Unruptured - NO SYMPTOMS - Usually an incidental finding - May have pain in the back, abdomen, loin or groin • RUPTURED - Pain in the abdomen, back or loin -Pain may be sudden or severe -Syncope -Shock • NOTE: degree of shock depends on site of rupture and whether it is contained
Signs of AAA on physical examination
- pulsatile laterally expansile mass on bimanual palpation of the abdominal aorta
- abdominal bruit
- retroperitoneal haemorrhage causes Grey- Turner’s sign
Investigations of AAA
• Bloods
-FBC, clotting screen, renal function and liver function
-Cross-match if surgery is planned
• Scans
- Ultrasound - can detect aneurysm but CANNOT tell whether it is leaking or not
- CT with contrast - can show whether an aneurysm has ruptured
-MRI angiography
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 :
- Type A: ascending aorta (most common)
- Type B: descending aorta (distal to the left subclavian artery )
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:
-HYPERTENSION
-Aortic atherosclerosis
- Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos, SLE)
-Congenital cardiac abnormalities (e.g. coarctation of the aorta)
-Aortitis
-Iatrogenic (e.g. during angioplasty/angiography)
-Trauma
-Crack cocaine
• NOTE: expansion of the false lumen can lead to obstruction of the subclavian, carotid, coeliac and renal arteries
Hypoperfusion of the target organs of these major arteries can give rise to other symptoms (e.g. carotid artery –> collapse)
Epidemiology of aortic dissection
most common in males aged 40-60yrs
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:
- Carotid artery –> hemiparesis, dysphasia, blackout
-Coronary artery –> chest pain (angina or MI)
- Subclavian artery –> ataxia, loss of consciousness
- Anterior spinal artery –> paraplegia
-Coeliac axis –> severe abdominal pain (due to ischaemic bowel)
- Renal artery –> anuria, renal failure
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 -Check for pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration -This may indicate: • Tamponade • Pericarditis • Chronic sleep apnoea • Obstructive lung disease • Signs of Aortic Regurgitation High volume collapsing pulse Early diastolic murmur over aortic area • Unequal arm pulses • There may be a palpable abdominal mass
Investigations for aortic dissection
• Bloods
- FBC
- X-match 10 units of blood
- U&E - check renal function
- Clotting screen
• CXR
- Widened mediastinum
• ECG - Often NORMAL - If the ostia of the right coronary artery is compromised you may get signs of: • Left ventricular hypertrophy • Inferior MI
• CT Thorax
- Shows false lumen
• Echocardiography
- 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
Aetiology and Risk factors of aortic regurgitation
• Aortic valve leaflet abnormalities or damage - Bicuspid aortic valve -Infective endocarditis - Rheumatic fever -Trauma • Aortic root/ascending aorta dilatation -Systemic hypertension - Aortic dissection - Aortitis - Arthritides (e.g. rheumatoid arthritis, seronegative arthritides) -Connective tissue disease (e.g. Marfan's, Ehlers-Danlos) - Pseudoxanthoma elasticum -Osteogenesis imperfecta
• Pathophysiology
Reflux of blood into the left ventricle results in left ventricular dilatation This means increased end diastolic volume and increased stroke volume 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 beings in the late 50s
- Most frequent in patients >50years
Presenting symptoms of aortic regurgitation
• Chronic AR
Initially ASYMPTOMATIC
Later on, the patient may develop symptoms of heart failure (e.g. exertional dyspnoea, orthopnoea, fatigue)
• Severe Acute AR
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)
Signs of aortic regurgitation on examination
• Collapsing (water-hammer) pulse
• Wide pulse pressure
• Thrusting and heaving displaced apex beat
• Early diastolic murmur over the aortic valve region
- 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
Heard over the apex
Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis
• Rare signs associated with aortic regurgitation:
Quincke’s Sign - visible pulsation on nail bed
de Musset’s Sign - head nodding in time with the pulse
Becker’s Sign - visible pulsation of the pupils and retinal arteries
Muller’s Sign - visible pulsation of the uvula
Corrigan’s Sign - visible pulsation in the neck
Traube’s Sign - pistol shot (loud systolic and diastolic sounds) heard on auscultation of the femoral arteries
Duroziez’s Sign - systolic and diastolic bruit heard on partial compression of the femoral artery with the 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 > 60 mm Hg
Identify investigations for aortic regurgitation
• CXR - Cardiomegaly - Dilatation of ascending aorta - Signs of pulmonary oedema (if accompanied by left heart failure) • ECG - may show left ventricular hypertrophy •deep S in V1/2 •Tall R in V5/6 •Inverted T waves in lead 1, aVL, V5/6 •Left axis deviation
• Echocardiogram
- May show underlying cause (e.g. aortic root dilatation, bicuspid aortic valve)
-May show the effects of aortic regurgitation (e.g. left ventricular dilatation, fluttering of the anterior mitral valve leaflet)
-Doppler echocardiogram can show AR and indicate severity
-Repeat echos allow monitoring of progression (LV size and function)
• Cardiac catheterisation with angiography
- 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
Aetiology and risk factors of aortic stenosis
- Stenosis can be secondary to rheumatic heart disease
- Calcification of a congenital bicuspid aortic valve
- Calcification/ degeneration of a tricuspid aortic valve in the elderly
Epidemiology of aortic stenosis
- Present in 3% of 75 yr olds
- More common in males
- Those with bicuspid aortic valve present earlier
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)
Signs of aortic stenosis on 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
Investigations for aortic stenosis
• ECG - 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 LBBB
• CXR
- post-stenotic enlargement of ascending aorta
- calcification of aortic valve
• Echocardiogram
- Visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar)
- Estimation of aortic valve area and pressure gradient across the valve in systole
- Assess left ventricular function
• Cardiac angiography
- Allows differentiation from other causes of angina (e.g. MI)
- Allows assessment of concomitant coronary artery disease
• NOTE: 50% of patients with severe aortic stenosis have significant coronary artery disease
Define Arterial Ulcer
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
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
-Coronary heart disease
-History of stroke or TIA
-Diabetes Mellitus
- Peripheral arterial disease (e.g. intermittent claudication)
- obesity and immobility
Epidemiology of arterial ulcers
- 22% of leg ulcers
* Prevalence increases with age and obesity
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
- Pain is worse when supine (because arterial blood flow is further reduced when supine)
- Pain is relieved by dangling the affected leg off the end of the bed
Signs of arterial ulcers on physical examination
- Night pain
- Punched-out appearance
- Hairlessness
- Pale skin
- Absent pulses
- Nail dystrophy
- Wasting of calf muscles
Appropriate investigations for arterial ulcers
• 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:
- permanent
- persistent
- paroxysmal
Aetiology & Risk Factors of atrial fibrillation
• There may be no identifiable cause
• Secondary causes lead to an abnormal atrial electrical pathway that results in AF
• Systemic Causes:
Thyrotoxicosis, Hypertension, Pneumonia, Alcohol
• Heart Causes:
Mitral valve disease, Ischaemic heart disease, Rheumatic heart disease, Cardiomyopathy, Pericarditis, Sick sinus syndrome, Atrial myxoma
• Lung Causes:
Bronchial carcinoma, PE
Epidemiology of atrial fibrillation
- very common in the elderly
- present in 5% of those >65 years
- may be paroxysmal
Presenting symptoms of atrial fibrillation
- often asymptomatic
- palpitations
- syncope (if low output)
- symptoms of the cause of AF
Signs of atrial fibrillation on physical examination
- irregularly irregular pulse
- difference in apical beat and radial pulse
- check for signs of thyroid disease and valvular disease
Investigations for atrial fibrillation
• ECG - uneven baseline with absent p waves - irregular intervals between QRS complexes • Bloods -Cardiac enzymes - TFT - Lipid profile - U&Es, Mg2+ and Ca2+ • Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia
• Echocardiogram May show: • Mitral valve disease • Left atrial dilatation • Left ventricular dysfunction • Structural abnormalities
Management plan for atrial fibrillation
First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection) There are TWO main components to AF management:
• RHYTHM CONTROL
-If > 48 hrs since onset of AF:
• Anticoagulate for 3-4 weeks before attempting cardioversion
-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
-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
Chronic (Permanent) AF
• Control ventricular rate with: -Digoxin
- Verapamil
-Beta-blockers
Aim for ventricular rate of roughly 90bpm
• STROKE RISK STRATIFICATION: -LOW RISK patients can be managed with aspirin -HIGH RISK patients require anticoagulation with warfarin -This is based on the CHADS-Vasc Score Risk factors include: • Previous thromboembolic event • Age>75yrs • Hypertension • Diabetes • Vascular disease • Valvular disease • Heart failure • Impaired left ventricular function
Complications of atrial fibrillation
• THROMBOEMBOLISM
-Embolic stroke risk of 4% per year
-Risk is increased with left atrial enlargement or left ventricular dysfunction
• Worsening of existing heart failure
Summarise the prognosis for patients with atrial fibrillation
• Chronic AF in a disease heart does not usually return to sinus rhythm
Define Cardiac Arrest
Acute cessation of cardiac function
Explain the aetiology and risk factors of cardiac arrest
The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts
• FOUR Ts
- Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis))
- Thromboembolic
- Tamponade
- Tension pneumothorax
• FOUR Hs
- Hypothermia
- Hypoxia
- Hypovolaemia
- Hypokalaemia/Hyperkalaemia
Recognise the presenting symptoms of cardiac arrest
- management precedes or is concurrent to history
- usually sudden but some symptoms that me precede are fatigue, fainting, blackouts and dizziness
Signs of cardiac arrest on physical examination
- Unconscious
- Not breathing
- Absent carotid pulses
Investigations for cardiac arrest
• Cardiac Monitor - Allows classification of the rhythm • Bloods - ABG - U&E - FBC - X-match - Clotting -Toxicology screen - Blood glucose
Generate a management plan for cardiac arrest
• SAFETY IS IMPORTANT
- Approach any arrest scene with caution
- The cause of the arrest may pose a threat
-Defibrillators and oxygen are hazards
• Basic Life Support
-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)
-Clear and maintain the airway with head tilt, jaw thrust and chin lift
-Assess breathing by look, listen and feel
• If they are not breathing, give two rescue breaths
-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 Proceed to advanced life support as soon as possible
• Advanced Life Support
-Attach cardiac monitor and defibrillator
-Assess rhythm
• If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms)
- Defibrillate once(150-360 J biphasic, 360J 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(1mgIV) after second defibrillation and again every 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) :
- CPRfor2,and then reassess rhythm
- Administe radrenaline (1mgIV) every3-5mins
- Atropine (3mgIV, once only) if asystole or PEA with rate <60bpm
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:
- Hypothermia : warm slowly
- Hypokalaemia and hyperkalaemia : correction of electrolyte levels
- hypovolaemia : IV colloids, crystalloids and blood products
- tamponade :pericardiocentesis
- tension pneumothorax - aspiration or chest drain
- thromboembolism : treat as PE or MI
- toxins : use antidote for toxin
Possible complications of cardiac arrest
- 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
inability of the cardiac output to meet the body’s demands despite normal venous pressures
Aetiology and risk factors of cardiac failure
• LOW OUTPUT Cardiac Failure (reduced cardiac output) - Left Heart Failure • Ischaemic heart disease • Hypertension • Cardiomyopathy • Aortic valve disease • Mitral regurgitation
- 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
-Biventricular Failure • Arrhythmia • Cardiomyopathy (dilated or restrictive) • Myocarditis • Drug toxicity
• HIGH OUTPUT Cardiac Failure (increased demand)
- Anaemia
- Beri beri
- Pregnancy
- Paget’s disease
- Hyperthyroidism
- Arteriovenous malformation
Epidemiology of cardiac failure
10% >65 years old
Presenting symptoms of cardiac failure
• Left Heart Failure - symptoms caused by pulmonary congestion - 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 -Orthopnoea -Paroxysmal nocturnal dyspnoea - Fatigue • Acute Left Ventricular Failure - Dyspnoea - Wheeze - Cough - Pink frothy sputum • Right Heart Failure - Swollen ankles - Fatigue - Increased weight (due to oedema) -Reduced exercise tolerance -Anorexia -Nausea
Signs of cardiac failure on physical examination
• Left Heart Failure
- Tachycardia
- Tachypnoea
- Displaced apex beat
- Bilateral basal crackles
- S3 gallop (caused by rapid ventricular filling)
- Pansystolic murmur (due to functional mitral regurgitation)
• Acute Left Ventricular Failure
-Tachypnoea
-Cyanosis
-Tachycardia
-Peripheral shutdown
-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
- This results in a stronger systolic pulse
- 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
- Gallop rhythm
- Wheeze (cardiac asthma)
- Fine crackles throughout lung
• Right Heart Failure
- Raised JVP
- Hepatomegaly
- Ascites
- Ankle/sacral pitting oedema
- Signs of functional tricuspid regurgitation
Investigations for cardiac failure
• Bloods -FBC -U&E -LFTs -CRP -Glucose -Lipids -TFTs • In ACUTE Left Ventricular Failure - ABG -Troponin -BNP • Raised plasma BNP suggests diagnosis of cardiac failure • Low plasma BNP rules out cardiac failure (90% sensitivity) • CXR - Alveolar shadowing -Kerley B lines -Cardiomegaly -Upper Lobe Diversion -Pleural Effusion • ECG - may be normal - may show ischaemic changes (pathological q waves, t wave inversion) - may show arrhythmia or left ventricular hypertrophy • Echocardiogram - Assess ventricular contraction - Systolic dysfunction = LV ejection fraction < 40% - Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect • Swan-Ganz Catheter - Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Management plan for cardiac failure (Acute Left Ventricular Failure & Chronic Left Ventricular Failure)
**Acute Left Ventricular Failure
- Treating Cardiogenic Shock:
• This is severe cardiac failure with low blood pressure
• Requires the use of inotropes (e.g. dobutamine)
• Managed in ITU
-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
-TREAT THE CAUSE (e.g. hypertension)
-TREAT EXACERBATING FACTORS (e.g. anaemia)
-ACE Inhibitors
• Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
• They slow down the progression of heart failure and improve survival
-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
-Loop Diuretics
• Alongside dietary salt restriction, can correct fluid overload
-Aldosterone Antagonists
• Improves survival in patients with NYHA class III/IV symptoms on standard therapy
• Monitor K+ (as these drugs may cause hyperkalaemia)
- 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)
-Hydralazine and a Nitrate
• May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers
Digoxin
• Positive inotrope
• Reduces hospitalisation but does NOT improve survival N-3 Polyunsaturated Fatty Acids
• Provide a small beneficial advantage in terms of survival 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
CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)
Identify possible complications of cardiac failure
- Respiratory failure
- Cardiogenic Shock
- Death
Summarise the prognosis for a patient with cardiac failure
- 50% with cardiac failure die within 2 years
Define Cardiomyopathy
Primary disease of the myocardium. Cardiomyopathy may be:
- dilated
- hypertrophic
- restrictive
Aetiology/ Risk factors of cardiomyopathy
• The majority are IDIOPATHIC • Dilated Cardiomyopathy o PostMviral 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%
- restricted is even rarer
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
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 M 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
Investigations for cardiomyopathy
• 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 • LeftMaxis 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 and signs of constrictive pericarditis
• GradualMonset 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
Investigations for constrictive pericarditis
• 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 DVT
Formation of a thrombus within the deep veins (most commonly in the calf or thigh)
Explain the aetiology/risk factors of 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 OCP
o PostMsurgery
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 DVT
- Very common
- Especially in hospitalised patients
Recognise the signs of 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 M 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 DVT
• 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
Management plan for 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 possible complications of DVT
- PE
- Venous infarction (phlegmasia cerulea dolens) • Thrombophlebitis (results from recurrent DVT)
- Chronic venous insufficiency
Summarise the prognosis for patients with DVT
- Depends on extent of DVT
- Below-knee DVTs have a GOOD prognosis
- Proximal DVTs have a greater risk of embolisation
Define Gangrene and Necrotising Fasciitis
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 necrotising fasciitis
• 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 and necrotising fasciitis
- Gangrene - relatively COMMON
* Necrotising fasciitis and gas gangrene - RARE
Recognise the presenting symptoms of gangrene and necrotising fasciitis
–• 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 and necrotising fasciitis on examination
• Gangrene
o Painful area = erythematous region around gangrenous tissue
o Gangrenous tissue = BLACK because of haemoglobin break down products
o Wet Gangrene M tissue becomes boggy with associated pus and a strong odour
caused by the activity of anaerobes
o Gas Gangrene M 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)
Investigations for gangrene and necrotising fasciitis
- 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
Epidemiology of heart block
250,000 pacemakers are implanted every year and they are mostly for heart block
Aetiology/ Risk Factors for heart block
- MI or ischaemic heart disease (MOST COMMON)
- Infection (e.g. rheumatic fever, infective endocarditis) • Drugs (e.g. digoxin)
- Metabolic (e.g. hyperkalaemia)
- Infiltration of conducting system (e.g. sarcoidosis)
- Degeneration of the conducting system
Presenting symptoms of heart block
• 1st Degree - asymptomatic
• 2nd Degree - usually asymptomatic
• Mobitz Type II and 3rd Degree - may cause Stokes-Adams Attacks (syncope caused by ventricular asystole)
o May also cause dizziness, palpitations, chest pain and heart failure
Recognise signs of heart block on physical examination
• Often NORMAL
• Check for signs of a potential cause of heart block
• Complete Heart Block
o Slow large volume pulse
o JVP may show cannon a waves
• Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously
• Mobitz Type II and 3rd Degree Heart Block
o Signs of reduced cardiac output (e.g. hypotension, heart failure)
Identify appropriate investigations for heart block
• ECG J GOLD STANDARD
o First Degree- fixed prolonged PR interval (> 0.2 s)
o Mobitz Type I (Wenckebach) M progressively prolonged PR interval, culminating
in a P wave that is NOT followed by a QRS complex. The pattern then begins again. ‘Going, going, gone’.
o Mobitz Type II M intermittently a P wave is NOT followed by a QRS. There may be
a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
o Complete Heart Block M no relationship between P waves and QRS complexes. If
QRS is initiated in the:
• Bundle of His M narrow complex
• More distally M wide complex and slow rate (~ 30 bpm)
• CXR
o Cardiac enlargement
o Pulmonary oedema
• Bloods
o TFTs
o Digoxin level
o Cardiac enzymes
o Troponin
• Echocardiogram
o Wall motion abnormalities o Aortic valve disease
o Vegetations
Generate a management plan for heart block
• Chronic Block
o Permanent pacemaker is recommended in:
• Complete heart block
• Advanced Mobitz Type II
• Symptomatic Mobitz Type I
• Acute Block
o If associated with clinical deterioration use IV atropine o Consider temporary (external) pacemaker
