Cardiology Flashcards
Define atrial fibrillation
AF is a supraventricular tachyarrhythmia characterised by uncoordinated atrial activity on the surface ECG. AF has an irregularly irregular rhythm.
Describe the aetiology of atrial fibrillation
May be no identifiable cause
Systemic: Advancing age Infection/sepsis Diabetes Hyperthyroidism (thyrotoxicosis) Hypertension Alcohol Electrolyte imbalance Pneumonia
Heart: Ischaemic heart disease e.g. MI, Coronary Artery Disease Congestive heart failure Hypertensive heart disease Heart failure Valvular heart disease Cardiomyopathies Pericarditis Myocarditis Rheumatic heart disease Sick sinus syndrome Atrial myxoma
Lung:
Bronchial carcinoma
Pulmonary embolism
Pneumonia
Summarise the epidemiology of atrial fibrillation
VERY COMMON in the elderly
Present in 5% of those > 65 years
May be paroxysmal
Affects men more than women
What are the presenting symptoms of atrial fibrillation?
Asymptomatic Palpitations Dizziness Syncope SOB Chest pain Fatigue Symptoms of the cause of AF
What are the signs on physical examination of atrial fibrillation?
Irregularly irregular pulse
Hypotension
Tachycardia
Difference in apical beat and radial pulse
Check for signs of thyroid disease and valvular disease
What are the appropriate investigations for atrial fibrillation?
12 lead ECG - shows irregularly irregular tachycardia (QRS complexes), absent P waves
Echocardiogram - determine if any valvular disease, pericardial disease, cardiomyopathies
Bloods:
Cardiac enzymes
TFT - test for hyperthyroidism as the cause (low TSH)
Lipid profile
U&Es, Mg2+ and Ca2+ (there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia)
Serum transaminases - may be deranged if AF due to alcohol
What is the management of atrial fibrillation?
First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection)
If HAEMODYNAMICALLY UNSTABLE - DC CARDIOVERSION
- 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 for patients with paroxysmal AF) strategy for suitable patients
RATE CONTROL in chronic (Permanent) AF Control ventricular rate with: Digoxin Verapamil (rate-limiting CCB) Beta-blockers
Aim for ventricular rate ~ 90 bpm
How is stroke risk stratified in atrial fibrillation?
CHA2DS2VASc Score
C - congestive heart failure (1) H - hypertension (1) A2 - age >75 (2) D - Diabetes Mellitus (1) S2 - previous stroke/TIA/thromboembolism (2) V - vascular disease (1) A - age 64-75 (1) Sc - female sex (1)
If low risk (score of 1) - OAC or aspirin
If high risk (score >2) - anticoagulation with warfarin or other oral anticoagulants eg DOACs
Define aortic regurgitation
The diastolic leakage of blood from the aorta into the left ventricle due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root.
Explain the aetiology of aortic regurgitation
- Primary disease of the aortic valve leaflets
- Rheumatic heart disease (developing countries)
- Congenital bicuspid aortic valve - Aortic root dilation
- Marfan’s syndrome or related connective tissue disease
- Aortitis secondary to syphilis, Behcet’s, Takayasu’s, reactive arthritis, or ankylosing spondylitis.
- Systemic hypertension
- Aortic dissection
- Arthritides (e.g. rheumatoid arthritis, seronegative arthritides)
- Pseudoxanthoma elasticum
- Osteogenesis imperfecta
Acute aortic regurgitation:
Aortic root dissection
Endocarditis can lead to rupture of leaflets or even paravalvular leaks.
Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of blood.
Summarise the epidemiology of aortic regurgitation
Less common than aortic stenosis and mitral regurgitation
Prevalence increases with age
More common in men than women
Chronic AR often begins in the late 50s
Most frequently seen in patients > 80 years
What are the presenting symptoms of aortic regurgitation?
Chronic AR: Initially ASYMPTOMATIC Later on, the patient may develop symptoms of heart failure: - Exertional dyspnoea - Orthopnoea - Fatigue - Paroxysmal nocturnal dyspnoea
Severe Acute AR:
Sudden cardiovascular collapse (LV can’t adapt to the rapid increase in end-diastolic volume). Symptoms related to aetiology (e.g. chest/back pain caused by aortic dissection).
Weakness
Chest pain
What are the signs on physical examination of aortic regurgitation?
End-diastolic murmur heard loudest on expiration, when sitting forwards and in the left sternal edge Collapsing pulse Pallor Rapid and faint peripheral pulse Tachypnoea Wide pulse pressure Thrusting and heaving displaced apex beat Basal lung crepitations
Rare signs:
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/diastolic sounds) heard at 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
What are the appropriate investigations for aortic regurgitation?
ECG - not diagnostic, may show non-specific ST-T wave changes, left axis deviation, or conduction abnormalities 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
CXR - may show cardiomegaly, dilatation of ascending aorta, signs of pulmonary oedema if heart failure also present
Echocardiogram - detection and evaluation of severity of AR. Visualisation of the origin of regurgitant jet and its width. May show underlying cause.
Cardiac catheterisation with angiography - If there is any uncertainty about the functional state of the ventricle or the presence of coronary artery disease
Define rheumatic fever
An autoimmune disease which can affect many systems including the heart, joints, brain and skin following group A streptococcal throat infection.
The effects on the heart can lead to permanent illness known as chronic rheumatic heart disease. Long-term penicillin secondary prophylaxis, acute rheumatic fever can recur causing cumulative damage to cardiac valvular tissue.
Explain the aetiology of rheumatic fever
Acute rheumatic fever is an autoimmune disease.
A group A streptococcal infection triggers an autoimmune response in a susceptible host. The response is targeted against cardiac, synovial, subcutaneous, epidermal and neuronal tissue.
What are the risk factors for rheumatic fever?
Poverty Overcrowded living quarters Family history of rheumatic fever D8/17 B cell antigen Indigenous populations
Summarise the epidemiology of rheumatic fever
Mainly in children aged 4-15 years old
Rare in people over 30 years old
94% of cases are in developing countries
No clear sex predilection, however chronic rheumatic heart disease is more common in females
More than 2.4 million children have rheumatic heart disease worldwide
What are the five hallmarks of rheumatic fever?
Carditis Arthritis Chorea Erythema marginatum Subutaneous nodules
What are the four minor manifestations of rheumatic fever?
Fever
Arthralgia
Elevated inflammatory markers
Prolonged PR interval on ECG
What are the presenting symptoms of rheumatic fever?
Fever
Joint pain (knees, ankles, wrists, elbows, and hips, usually asymmetrical)
Recent sore throat or scarlet fever (2-4 weeks previously)
Chest pain
SOB
Palpitations
Nodules on the skin
Restlessness, clumsiness, emotional lability and personality changes (indicates chorea)
What are the signs on physical examination of rheumatic fever?
Heart murmur - mitral regurgitation is the most common valvular problem caused which results in pan-systolic murmur heard loudest at apex and which radiates to the axilla OR aortic regurgitation causing an early diastolic murmur
Pericardial rub
Signs of congestive heart failure
Jerky, uncoordinated choreiform movements
Red, hot or swollen joints
Small, painless nodules beneath the skin
Erythema marginatum
What are the appropriate investigations for rheumatic fever?
Bloods:
ESR, CRP, WCC may be raised
Blood cultures - show no growth
ECG - prolonged PR interval
Chest X-Ray - may show congestive cardiac failure or chamber enlargement
Echocardiogram: may reveal morphological changes to the mitral and/or aortic valves. Allows you to see the severity of regurg.
Throat culture: growth of beta-haemolytic group A streptococci
Define abdominal aortic aneurysm
A permanent pathologial dilation of the aorta with a diameter >1.5 times the expected anteroposterior diameter of that segment, given the patient’s sex and body size.
Localised enlargement of the abdominal aorta such that the diameter is > 3 cm or > 50% larger than normal. Usually located BELOW the renal arteries.
(Normal abdominal aorta diameter = 2cm)
What are the risk factors for abdominal aortic aneurysm?
SMOKING Family history Increased age Male sex (however rupture more likely in females) Congenital/connective tissue disorders Dyslipidaemia COPD Atherosclerosis Hypetension Centripetal obesity
There are NO specific identifiable causes - may be due to atherosclerosis OR altered tissue metalloproteinases diminish the integrity of the arterial wall
Summarise the epidemiology of abdominal aortic aneurysms
Epidemiology varies by region, age and sex
Highest prevalence in male smokers
Prevalence increases with age
4-6 times more likely in men
What are the presenting symptoms of abdominal aortic aneurysm?
If unruptured: ASYMPTOMATIC and an incidental finding
If ruptured:
Abdominal, back, loin or groin pain which is sudden and severe
Syncope
Shock
What is the triad for the presentation of a ruptured abdominal aortic aneurysm?
Abdominal and/or back pain
Pulsatile abdominal mass
Hypotension
What are the signs on physical examination of abdominal aortic aneurysm?
Palpable, pulsatile, laterally expansile abdominal mass
Hypotension
Abdominal bruit
Retroperitoneal haemorrhage can cause Grey-Turner’s sign
What are the appropriate investigations for abdominal aortic aneurysm?
ABDOMINAL USS - abdominal aorta diameter >3cm. Cannot tell if aneurysm is leaking
Bloods:
ESR/CRP - if elevated, inflammatory AAA
FBC - leukocytosis and anaemia suggest inflectious AAA
Culture - if positive with leukocytosis and anaemia, suggests infectious AAA
CT angiography - shows if ruptured
MRI angiography - anatomical mapping to assist with operative planning
Define aortic dissection
A separation occurs in aortic wall intima, usually by a discrete intimal tear, causing blood flow into a new false channel composed of the inner and outer layers of the media.
Explain the aetiology of aortic dissection
Results from an intimal tear that expands into the media of the aortic wall which is preceded by degenerative changes in the smooth muscle of the media.
- HYPERTENSION
- Bleeding from the vasa vasorum
- Connective tissue disease: Marfan syndrome and Ehlers-Danlos syndrome (weakening of the media)
- Bicuspid aortic valve
- Aortic atherosclerosis
- Iatrogenic (aortic manipulation with cardiac surgery or interventional procedures.)
- Congenital cardiac abnormalities (e.g. coarctation of the aorta)
- Aortitis
- Trauma
How can aortic dissection give rise to organ hypoperfusion and associated symptoms?
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).
What are the risk factors of aortic dissection?
Hypertension Atherosclerotic aneurysmal disease Marfan’s syndrome Ehlers-Danlos syndrome Bicuspid aortic valve Smoking Coarctation Crack cocaine use Family history of aortic dissection Increased age Heavy lifting Pregnancy
What is aortic coarctation?
Congenital abnormality whereby the aorta is narrowed
Summarise the epidemiology of aortic dissection
Mostly affects men over 50 years old (40-60 is most common)
0.5-3 cases per 100,000 people annually
What are the presenting symptoms of aortic dissection?
Acute severe central TEARING chest pain which radiates to back (interscapular and lower pain)
Other symptoms caused by obstruction of branches of the aorta:
Carotid artery - hemiparesis (weakness of half the body), 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
What are the signs on physical examination of aortic dissection?
BLOOD PRESSURE DIFFERENCE BETWEEN THE TWO ARMS >20mmHg
Pulse deficit (reduced or absent due to aortic arch involvement)
Diastolic murmur on back below left scapula descending to abdomen (crescendo murmur common in proximal dissections)
Hypertension
Wide pulse pressure
Hypotension associated with tamponade
Signs of Aortic Regurgitation:
High volume collapsing pulse
Early diastolic murmur over aortic area
Pulsus paradoxus - Abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. May indicate: - Tamponade - Pericarditis - Chronic sleep apnoea - Obstructive lung disease
What are the appropriate investigations for aortic dissection?
CT ANGIOGRAPHY - will show intimal flap
ECG - often normal however if MI, ST segment depression
CXR - may show widened mediastinum
Bloods:
Cardiac enzymes - usually negative
Renal function tests - elevated creatinine and urea if renal perfusion is compromised
LFTs - elevated AST and ALT if liver perfusion is compromised
FBC - may show anaemia if haemorrhage
Type and cross to prepare for surgery
Define aortic stenosis
Obstruction of blood flow across the aortic valve due to pathological narrowing.
A progressive disease that presents after a long subclinical period with symptoms of decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure.
Narrowing of the left ventricular outflow at the level of the aortic valve
Explain the aetiology of aortic stenosis
Calcification of aortic valve - most common cause in adults
Congenital bicuspid valve
Rheumatic heart disease in developing countries
What are the risk factors for aortic stenosis?
Smoking Hypertension Diabetes LDL cholesterol Age >60 years old Congenitally bicuspid valve Rheumatic heart disease Chronic kidney disease
Summarise the epidemiology of aortic stenosis
Most common valvular disease in US and Europe - 3% of 75 year olds
2nd most frequent cause for cardiac surgery
More common in males
Patients typically prevent 70s-80s
Patients with bicuspid aortic valves present two decades earlier
What are the presenting symptoms of aortic stenosis?
May be asymptomatic initially
Dyspnoea on exertion
Exertional chest pain (angina due to increased O2 demand of the hypertrophied left ventricle)
Syncope or dizziness on exercise (due to outflow obstruction)
Symptoms of heart failure (e.g. dyspnoea, orthopnoea)
What are the signs on physical examination of aortic stenosis?
Ejection systolic murmur (crescendo-decrescendo) which radiates to carotids and is loudest at right upper sternal border
Diminished S2 (softened or absent)
Narrow pulse pressure
Slow-rising pulse
Thrill in the aortic area (only if severe)
Forceful sustained thrusting undisplaced apex beat
A bicuspid valve may produce an ejection click
What are the appropriate investigations for aortic stenosis?
Transthoracic echocardiogram with Doppler (visualises structural changes and levels of stenosis) - elevated aortic pressure gradient, measurement of valve and LV ejection fraction
Cardiac MRI - shows stenotic aortic valve
Cardiac catheterisation - shows elevated aortic pressure gradient
ECG - may show left bundle branch block and left ventricular hypertrophy:
- Absent Q waves
- Deep S in V1/V2
- Tall R in V5/V6
- Inverted T waves in I, aVL and V5/6
- Left axis deviation
CXR - Post-stenotic enlargement of ascending aorta, Calcification of aortic valve
Cardiac angiography - Allows differentiation from other causes of angina (e.g. MI) and assessment of concomitant coronary artery disease
Define arterial ulcers
A localised area of damage and breakdown of skin due to inadequate arterial blood supply - an ischaemic ulcer.
Usually seen on the feet of patients with severe atheromatous narrowing of the arteries supplying the legs.
Summarise the aetiology and 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
Summarise the epidemiology of arterial ulcers
22% of leg ulcers are arterial ulcers
Prevalence increases with age and obesity
What are the presenting symptoms of arterial ulcers?
Often DISTAL - at the dorsum of the foot or between the toes (over bony prominences)
Punched-out appearance
Often elliptical with clearly defined edges (sharp demarcation)
The ulcer base contains grey, granulation tissue
NIGHT PAIN - hallmark of arterial ulcers
- Painful, especially at night or when the legs are elevated
- Pain is worse when supine (arterial blood flow is further reduced when supine)
- Pain is relieved by dangling the affected leg off the end of the bed
What are the signs on physical examination of arterial ulcers?
Night pain Punched-out appearance Hairlessness Pale, cold skin Absent pulses Nail dystrophy Wasting of calf muscles
What are the appropriate investigations for arterial ulcers?
Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery
ABPI - < 0.8
Percutaneous angiography
ECG
Bloods:
Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor)
FBC - anaemia can worsen the ischaemia
What is ABPI and what do the results mean?
Highest ankle pressure DIVIDED by highest brachial pressure
>1.2 - Abnormally hard vessel (e.g. calcified - often false negative)
1.2-1.0 - normal
0.8-0.9 - mild arterial disease and claudication
0.5-0.79 - moderate arterial disease with severe claudication
<0.5 - severe arterial disease with pain at rest, ulceration, gangrene and critical ischaemia
What are the 3 types of ulcers and how do you distinguish them?
Arterial ulcer - punched out ulcer, night pain, pain when supine, low ABPI, cold skin
Venous ulcer - painful, worse on standing, normal ABPI, warm skin
Neurotrophic ulcer - painless, abnormal sensation, warm skin
What is atrial flutter and its pathophysiology?
A macro-reentrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm
Wave of muscle contraction through atria
Re-entrant rhythm in atria - overrides sinus node - atria contract repeatedly at fast rate
Between IVC and coronary sinus is CAVOTRICUSPID ISTHMUS which propagates re-entry signal more slowly - allows to get past refractory period
What are the two types of atrial flutter?
Type 1 - TYPICAL ATRIAL FLUTTER - most common
Single re-entrant cycle which moves around the tricuspid valve of RIGHT atrium in counter-clockwise direction
Type 2 - ATYPICAL ATRIAL FLUTTER
Re-entrant cycle in right or left atrium, exact location less clearly defined
What causes atrial flutter?
Underlying disease such as ischaemia makes heart cells irritable and changes properties such as refractory period, making re-entrant circuit more likely
Usually initiated by premature atrial contraction due to unknown cause
What are the appropriate examinations for atrial flutter?
ECG - electrical activity not initiated by SA node so NO P WAVES - F-waves produced instead which have sawtoothed shape most prominent in leads II, III, aVF, and V1.
See 2:1 atrial:ventricular beats, for example as AV node has a much longer refractory period than SA node, therefore not every atrial contraction can cause a ventricular contraction
CXR - may be underlying lung disease
Bloods:
Thyroid function tests - can be underlying thyroid disease
U&Es - may be underlying electrolyte abnormality
What are the atrial and ventricular refractory period times?
Atrial = 150ms Ventricular = 330ms
What are the presenting symptoms of atrial flutter?
If supraventricular tachycardia and underlying condition which means cannot tolerate tachy: Shortness of breath Chest pain Dizziness Nausea Palpitations Fatigue Syncope
Symptoms of heart failure or pulmonary symptoms
What are the possible complications of atrial flutter?
- Prolonged tachycardia leads to ventricular decompensation which leads to HEART FAILURE
- Atria not contracting effectively leads to stasis of blood which can cause clots - embolism to brain causing STROKE
May degenerate into atrial fibrillation
What is the management of atrial flutter?
- Anticoagulation to prevent clotting of blood to prevent stroke
- Rate control to prevent ventricular tachycardia - beta blockers, calcium channel blockers - try this first with anticoagulation
- Electrical cardioversion to stop the episode of flutter by depolarising all atrial tissue at once to allow sinus node to take control IF HAEMODYNAMICALLY UNSTABLE
- Radiofrequency catheter ablation which destroys cavotricuspid isthmus tissue therefore stopping propagation of signal
Treat underlying cause
What are the risk factors for atrial flutter?
Increasing age Valvular dysfunction Atrial septal defect Recent cardiac or thoracic procedures Surgical or post-ablation scarring of atria Heart failure Hyperthyroidism COPD Asthma Pneumonia Diabetes Male Anti-arrhythmic drugs for atrial fibrillation
Summarise the epidemiology of atrial flutter
Prevalence increases with age
2.5 times more common in men
Often co-exists with atrial fibrillation
What are the signs on physical examination of atrial flutter?
Hypotension
Jugular venous pulsations with rapid flutter waves
What are the possible 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
What is the prognosis of atrial fibrillation?
Chronic AF in a diseased heart does not usually return to sinus rhythm
Define cardiac arrest
Sudden cardiac arrest is a sudden state of circulatory failure due to a loss of cardiac systolic function.
Acute cessation of cardiac function.
It is the result of 4 specific cardiac rhythm disturbances:
1. Ventricular fibrillation
2. Pulseless ventricular tachycardia
3. Pulseless electrical activity
4. Asystole.
Torsades de pointes is a sub-group of polymorphic VT in patients with an underlying prolonged QT interval, sometimes related to hypomagnesaemia.
Explain the aetiology of cardiac arrest
Main underlying causes: Ischaemic heart disease Cardiovascular disease Dysrhythmias Cardiomyopathy
Ventricular tachycardia and ventricular fibrillation are the two most common causes
Pulseless electrical activity is caused by myocardial ischaemia/infarction, hypovolaemia, hypoxia, and pulmonary embolism
The REVERSIBLE causes of cardiac arrest are the 4 Hs and 4 Ts: Hypothermia Hypoxia Hypovolaemia Hypokalaemia/Hyperkalaemia
Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis))
Thromboembolic
Tamponade
Tension pneumothorax
Summarise the epidemiology of cardiac arrest
Survival is estimated at <20% for patients presenting out-of-hospital with Ventricular Fibrillation
Survival is <10% overall for patients presenting with out-of-hospital cardiac arrest
What are the presenting symptoms of cardiac arrest?
Patient unresponsive following syncope
Cardiac arrest is usually sudden
May be preceded by: Fatigue Fainting Blackouts Dizziness
What are the signs on physical examination of cardiac arrest?
Unconscious and not breathing
Absent carotid pulses (absence of circulation)
What are the appropriate investigations for cardiac arrest?
Bloods: FBC - low haematocrit in haemorrhage U&Es - may show electrolyte abnormalities eg hyper or hypokalaemia as a cause Cardiac biomarkers - normal or elevated ABG
Continuous cardiac monitoring - identify cardiac rhythm
Echo - assesses cardiac activity and left ventricular function. May show valvular abnormalities, myocardial scarring, cardiomyopathy, pericardial effusion, tamponade
ECG: may show QT interval, ST-segment or T-wave changes; conduction abnormalities; ventricular hypertrophy
Which rhythms are shockable and which are non-shockable?
Shockable:
Ventricular fibrillation
Pulseless Ventricular tachycardia
Non-shockable:
Asystole
Pulseless electrical activity
What is the management of cardiac arrest?
Attach cardiac monitor and defibrillator
If pulseless VT or VF (shockable rhythms): Defibrillate once (150-360 J biphasic, 360 J monophasic) CPR, reassess rhythm, shock again if still in pulseless VT or VF Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins If persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine)
If pulseless electrical activity 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
Treatment of REVERSIBLE causes:
Hypothermia - warm slowly
Hypokalaemia/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 given toxin
What is the rate and ratio of CPR?
Rate: 100-120 compressions per minute
30 compressions:2 rescue breaths
Compression at least 5cm
What are the possible complications of cardiac arrest?
Death
Rib and sternal fractures
Irreversible anoxic brain injury
Recurrent cardiac arrest
What is the prognosis of cardiac arrest?
Generally poor
Early provision of CPR improves prognosis
Worse outcomes: long time to discovery of arrest, short duration of CPR, pre-existing cerebrovascular accident or renal dysfunction
Define cardiac failure
Inability of the cardiac output to meet the body’s demands despite normal venous pressures. The impaired ability of the heart to cope with the metabolic needs of the body.
What are the types of cardiac failure and their risk factors?
LOW OUTPUT Cardiac Failure (reduced cardiac output) 1. Left Heart Failure: IHD Hypertension Cardiomyopathy Aortic valve disease Mitral regurgitation
- Right Heart Failure:
Secondary to left heart failure (congestive cardiac failure)
Infarction
Cardiomyopathy
Pulmonary hypertension/embolus/valve disease
Chronic lung disease
Tricuspid regurgitation
Constrictive pericarditis/pericardial tamponade
3. 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
Summarise the epidemiology of cardiac failure
10% of those over 65 years old have heart failure
What are the presenting symptoms of the different types of heart failure?
Left Heart Failure - symptoms caused by pulmonary congestion causing pulmonary hypertension and oedema
- Dyspnoea
- Orthopnoea (more venous blood back to heart and into pulmonary circulation)
- Paroxysmal nocturnal dyspnoea
- Fatigue
Acute Left Ventricular Failure: Dyspnoea Wheeze Cough Pink frothy sputum
Right Heart Failure: blood backup in body Swollen ankles Fatigue Increased weight (due to oedema) Reduced exercise tolerance Anorexia Nausea
What are the signs on physical examination of cardiac failure?
Left Heart Failure:
Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
S3 gallop (caused by rapid ventricular filling)
Pan-systolic murmur (due to functional mitral regurgitation)
Acute Left Ventricular Failure: Tachypnoea Cyanosis Tachycardia Peripheral shutdown Pulsus alternans Gallop rhythm Wheeze (cardiac asthma) Fine crackles throughout lung
Right Heart Failure:
Raised JVP - > 3cm
Hepatomegaly/splenomegaly due to blood back up
Ascites
Ankle/sacral pitting oedema
Signs of functional tricuspid regurgitation
What is pulsus alternans and why does it occur with acute left ventricular failure?
Pulsus alternans = Arterial pulse waveforms showing alternating strong and weak beats.
It is a sign of LV systolic impairment.
In LV dysfunction, ejection fraction significantly decreases.
Causes reduction in stroke volume therefore more blood remains in ventricle.
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 leads to an increase in the strength of the myocardial contraction.
This results in a stronger systolic pulse.
What are the appropriate investigations for cardiac failure?
Bloods: FBC, U&E, LFTs, CRP, Glucose, Lipids, TFTs
ACUTE Left Ventricular Failure:
ABG
Troponin - rule out MI
BNP - Raised plasma BNP (>400pg/ml) suggests diagnosis of cardiac failure whereas low plasma BNP rules out cardiac failure (<100pg/ml - 90% sensitivity)
CXR: Alveolar shadowing Kerley B lines (interstitial oedema) Cardiomegaly Upper Lobe Diversion Pleural Effusion Fluid in the fissures Perihilar shadowing
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 myocardium causing restrictive filling
Swan-Ganz Catheter - Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures
What is congestive cardiac failure?
The inability of the cardiac output to meet the demands of the body without increasing diastolic pressure which results in breathlessness and abnormal sodium and water retention leading to oedema.
What is the management of cardiac failure?
Acute Left Ventricular Failure:
- Treating Cardiogenic Shock (severe cardiac failure with low blood pressure):
- Use of inotropes (e.g. dobutamine - cardiac stimulant which acts on beta-1 and increases contractility)
- Managed in ITU - Treating Pulmonary Oedema:
- Sit the patient up
- 60-100% Oxygen (and consider CPAP)
- Diamorphine (venodilator + anxiolytic)
- GTN infusion to reduce preload
- IV furosemide if fluid overloaded (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) AND TREAT EXACERBATING FACTORS (e.g. anaemia).
- ACE Inhibitors: Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
- Beta-Blockers: Blocks the effects of a chronically activated sympathetic system!!!
- Loop Diuretics: Alongside dietary salt restriction, can correct fluid overload
- Aldosterone Antagonists (must monitor K+ as these drugs may cause hyperkalaemia)
- Angiotensin Receptor Blockers (must monitor K+ as these drugs may cause hyperkalaemia)
- Digoxin: Positive inotrope, reduces hospitalisation but does NOT improve survival. Increases strength of heart muscle contraction.
Cardiac resynchronization therapy (CRT): Biventricular pacing improves symptoms and survival in patients with LVEF < 35% - stimulates ventricles to contract at same time
Management of underlying associated conditions eg hypertension, IHD, valvular disease, diabetes, rheumatic fever
Lifestyle modifications - smoking and alcohol cessation, decrease sodium intake to <2g/day, maintain healthy weight, decrease fluid intake to <2L/day
What are the possible complications of cardiac failure?
Respiratory failure
Cardiogenic shock
Death
What is the prognosis of cardiac failure?
50% of those with severe cardiac failure die within 2 years
What is ejection fraction and what does it mean?
The portion of blood pumped out of the left ventricle
Ejection fraction = stroke volume divided by total left ventricular volume
50-70% = normal 40-50% = borderline <40% = systolic heart failure
What is the difference between systolic and diastolic heart failure?
Systolic heart failure - ventricles cannot pump enough during systole
Diastolic heart failure - not enough blood fills into the ventricles during diastole. Thick ventricular walls means the chamber doesn’t get an adequate load of blood
- Low stroke volume
- Normal ejection fraction
Define cardiomyopathy
A variety of issues resulting from primary disease of the myocardium (heart muscle)
What are the three types of cardiomyopathy and what do they mean?
- Dilated cardiomyopathy - all 4 chambers of the heart dilate, causing thin walls which produce less contraction force
- Hypertrophic cardiomyopathy - heart walls become thick, heavy and hypercontractile
- Restrictive cardiomyopathy - the heart muscle is stiff and less compliant, meaning the heart cannot fill properly. The muscles and ventricles all stay the same size
Summarise the aetiology of cardiomyopathy
Usually idiopathic
Dilated: Post-viral myocarditis infection Alcohol Drugs - cocaine, chemotherapy agents Thyrotoxicosis Genetic Peripartum
Hypertrophic:
Genetic - autosomal dominant
Restrictive: Sarcoidosis Amyloidosis Haemochromatosis Radiation of heart tissue Endocardial fibroelastosis - children
Summarise the epidemiology of cardiomyopathy
Dilated cardiomyopathy is the most common type
Hypertrophic cardiomyopathy is the main cause of sudden death in young athletes
Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20%
Restrictive is even rarer
What are the presenting symptoms of cardiomyopathy?
Dilated: Heart failure symptoms - fatigue, dyspnoea, ankle oedema Arrhythmias Thromboembolism Family history of sudden death
Hypertrophic: Syncope Usually NO SYMPTOMS Angina Arrhythmias Family history of sudden death
Restrictive: Dyspnoea Fatigue Arrhythmias Ankle or abdominal swelling Family history of sudden death
What are the signs on physical examination of cardiomyopathy?
Dilated:
Pan-systolic murmur due to mitral regurgitation
S3 heart sound after S2
S4 heart sounds before S1
Raised JVP
Displaced apex beat
Functional mitral and tricuspid regurgitations
Hypertrophic:
Crescendo-decrescendo (ejection systolic) murmur
Jerky carotid pulse
Double apex beat
Restrictive: Raised JVP Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles Palpable apex beat Third heart sound Ascites Ankle oedema Hepatomegaly
What are the appropriate investigations for cardiomyopathy?
CXR: May show cardiomegaly, may show signs of heart failure
ECG:
All Types - Non-specific ST changes, conduction defects, arrhythmias
Hypertrophic - Left-axis deviation, signs of left ventricular hypertrophy, Q waves in inferior and lateral leads
Restrictive - Low voltage complexes
Echocardiography: Dilated: Left ventricular dilation Normal or decreased wall thickness Ejection fraction <45%
Hypertrophic:
Ventricular hypertrophy (asymmetrical septal hypertrophy)
Left ventricular volume normal or low
Restrictive:
Non-dilated non-hypertrophied ventricles
Atrial enlargement
Preserved systolic function and diastolic dysfunction (normal ejection fraction)
Cardiac Catheterisation - may be necessary to measure pressures
Endomyocardial Biopsy - find deposits in myocardium in restrictive
Pedigree or Genetic Analysis
Chest MRI/CT - see fat, iron or amyloid deposits in restrictive
Define constrictive pericarditis
Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.
What is the difference between pericarditis and constrictive pericarditis?
Constrictive pericarditis impedes normal diastolic filling and can be a medium to late complication of acute pericarditis.
Explain the aetiology of pericarditis
Can occur after any pericardial disease process Idiopathic Virus (Coxsackie, mumps, EBV, CMV) TB Mediastinal irradiation Post-surgical Connective tissue disease Underlying systemic condition
What are the risk factors of pericarditis?
Male Age 20-50 years Transmural MI Cardiac surgery Neoplasm Viral and bacterial infections Systemic autoimmune disorders Mediastinal radiation Pericardial injury
Summarise the epidemiology of constrictive pericarditis
More common in adults (20-50y/o) but documented in all ages
More common in males
Most common disease of the pericardium
RARE
9% of patients with acute pericarditis will develop constrictive pericarditis
TB has the HIGHEST TOTAL INCIDENCE out of all causes
What are the presenting symptoms of constrictive pericarditis?
Chest pain - sharp, stabbing, pleuritic (worse on inspiration)
Pain is relieved when sitting up or leaning forward.
GTN does not relieve pain and pain is constant, not related to exertion.
Pericardial rub (high-pitched/squeaky)
Fever
Myalgia
Heart failure symptoms - fatigue, dyspnoea, peripheral oedema
What are the signs on physical examination of constrictive pericarditis?
Signs of right sided heart failure: Raised JVP Peripheral oedema Kussmaul's sign (paradoxical rise in JVP on inspiration) Pulsatile hepatomegaly
ADVANCED: jaundice, cachexia, muscle wasting
What are the appropriate investigations for pericarditis?
Bloods: Serum troponin - mildly elevated ESR/CRP - may be elevated Serum urea - elevated if renal failure FBC - elevated WBC
ECG - upwards concave ST-segment elevation globally with PR depressions (SADDLE SHAPED ST-ELEVATION)
Pericardial fluid/blood culture - positive if infectious cause
CXR - normal or cardiomegaly with water-bottle-shaped enlarged cardiac silhouette if large pericardial effusion. May show calcification of the pericardium.
Echocardiogram - helps distinguish from restrictive cardiomyopathy
MRI/CT - allows assessment of thickness of pericardium
Pericardial biopsy - may be indicated (especially if suspected infective cause)
