Cardiovascular Flashcards
Define abdominal aortic aneurysm.
A permanent pathological dilation of the aorta with diameter >1.5 times the expected anteroposterior (AP) diameter of that segment, given the patient’s sex and body size - e.g. 3cm+
Explain the aetiology / risk factors of an abdominal aortic aneurysm.
Cause - degeneration of the elastic lamellae and smooth muscleloss. also genetic component.
Risk factors:
- Cigarette smoking
- Hereditary / family history
- Increased age
- Male sex (prevalence)
Summarise the epidemiology of an abdominal aortic aneurysm.
3% of those 50+ years .
M:F 3:1
Less common in diabetes
Recognize the presenting symptoms of an abdominal aortic aneurysm.
- Abdominal, back or groin pain
- Presence of risk factors- cigarette smoking, family history, increased age, male sex
Recognize the signs of an abdominal aortic aneurysm on physical examination.
- Palpable pulsatile abdominal mass
- Abdominal, back or groin pain
- Hypotension
Identify appropriate investigations for an abdominal aortic aneurysm and interpret the results.
- Abdominal ultrasound
- Bloods - ESR, CRP, FBC, blood cultures
- CT angiography
Define amyloidosis.
Heterogenous group of diseases characterized by extracellular deposition of amyloid fibrils.
Can be systemic or localised - e.g. pancreatic islets of Langerhans, cerebral cortex, cerebral blood vessels, bones and joints
Pancreatic Islets of Langerhans - T2DM
Cerebral Cortex - Alzheimer’s
Cerebral Blood Vessels - amyloid angiopathy
Bones & Joints - long-term dialysis caused by B2 microglobulin
Explain the aetiology / risk factors of amyloidosis.
Amyloid fibrils are polymers comprising low-molecular-weight subunit proteins.
Amyloid fibril subunits are derived from proteins that undergo conformational changes to adopt anti-parallel B-pleated sheet configuration.
Amyloid fibril subunits associated with GAGs and serum amyloid P-component (SAP), and their sdeposition progressively disrupts the structure and function of nromal tissue.
Classification:
- AA - serum amyloid A protein - e.g. Chronic inflammatory (RA, seronegative arthritides, Crohn’s, familial Mediterranean fever), chronic infections (TB, bronchiectasis, osteomyelitis), malignancy (Hodgkin’s disease, renal cancer)
- AL - monoclonal immunoglobulin light chains fibril protein - e.g. subtle monoclonal plasma cell dyscrasias, multiple myeloma, Waldenstrom’s macroglobulinaemia, B-cell lymphoma
- ATTR (familiar amyloid polyneuropath) - genetic-variant transthyretin - autosomal dominantly transmitted muttaions in the gene for transthyretin (TTR), variable penetrance
Risk factors:
- Monoclonal gammopathy of undetermined significance (MGUS)
- Inflammatory polyarthropathy
- Chronic infections
- IBD
Summarise the epidemiology of amyloidosis.
AA = 1-5% incidence among patients with chronic inflammatory disease
AL = estimated annual incidence of about 3,000 cases in US, 300-600 cases in UK
Hereditary - 5% of patients with systemic amyloidosis
Recognise the presenting symptoms of amyloidosis.
Renal
- Proteinuria
- Nephrotic syndrome
- Renal failure
Cardiac
- Restrictive cardiomyopathy
- Heart failure
- Arrythmia
- Angina - due to accumulation of amyloid in coronary arteries
GI
- Macroglossia - characteristic of AL
- Hepatomegaly
- Splenomegaly
- Gut dysmotility
- Malabsorption
- Bleeding
Neurological
- Sensory and motor neuropathy
- Autonomic neuropathy - symptoms of bowel or bladder dysfunction, postural hypotension
- Carpal tunnel syndrome
Skin
- Waxy skin
- Easy brusing
- Purpura around the eyes - characteristic of AL
- Plaques
- Nodules
Joints
- Painful asymmetrical large joint
- Shoulder pad sign - enlargement of the anterior shoulder
Haematological
- Bleeding diathesis - factor X deficiency due to binding on amyloid fibrils primarily in the liver and spleen and reduce synthesis of coagulation factors in patients with advanced liver disease
Recognise the signs of amyloidosis on physical examination.
Renal
- Proteinuria
- Nephrotic syndrome
- Renal failure
Cardiac
- Restrictive cardiomyopathy
- Heart failure
- Arrythmia
- Angina - due to accumulation of amyloid in coronary arteries
GI
- Macroglossia - characteristic of AL
- Hepatomegaly
- Splenomegaly
- Gut dysmotility
- Malabsorption
- Bleeding
Neurological
- Sensory and motor neuropathy
- Autonomic neuropathy - symptoms of bowel or bladder dysfunction, postural hypotension
- Carpal tunnel syndrome
Skin
- Waxy skin
- Easy brusing
- Purpura around the eyes - characteristic of AL
- Plaques
- Nodules
Joints
- Painful asymmetrical large joint
- Shoulder pad sign - enlargement of the anterior shoulder
Haematological
- Bleeding diathesis - factor X deficiency due to binding on amyloid fibrils primarily in the liver and spleen and reduce synthesis of coagulation factors in patients with advanced liver disease
Identify appropriate investigations for amyloidosis and interpret the results.
- Tissue biopsy - congo red stain, immunohistochemistry (diagnose amyloidosis, identify amyloid fibril protein)
- Urine (proteinuria, free immunoglobi light chains in AL)
- Blood (CRP, ESR, RF, Ig levels, serum protein electrophoresis, LFTs, U&E, SAA levels)
- 123I-SAP Scan - radiolabeled SAP localizes to the deposits enabling quantitative imaging of amyloidotic organs throughout the body
Define aortic dissection.
A condition where a tear in the aortic intima allows blood to surge into the aortic ball, causing a split between the inner and outer tunica media, and creating a false lumen.
Type A Stanford = ascending aorta tear
Type B Standford = descending aorta tear distal to the left subclavian artery
Explain the aetiology / risk factors of aortic dissection.
Degenerative changes in the smooth muscle of the aortic media are the predisposing event.
Risk factors:
- Hypertenison
- Aortic atherosclerosis
- Connective tissue disease - e.g. SLE, Marfan’s, Ehlers-Danlos
- Congenital cardiac abnormalities - e.g. aortic coarctation
- Aortitis - e.g. Takayasu’s aortitis, tertiary syphilis
- Iatrogenic - e.g. during angiography, angioplasty
- Trauma
- Crack cocaine
Summarise the epidemiology of aortic dissection.
Female betwene 40-60 years
Recognise the presenting symptoms of aortic dissection.
- Sudden central ‘tearing’ pain
- Radiates to back - mimics MI
(Can lead to occlusion of the aorta and its branches)
Carotid obstruction = hemiparesis, dysphasia, blackout
Coronary artery obstruction = chest pain, angia, MI
Subclavian obstruction = ataxia, loss of conscioussness
Anterior spinal artery = paraplegia
Coeliac obstruction = severe abdominal pain (ischaemic bowel)
Renal artery obstruction - anuria, renal failure
Recognise the signs of aortic dissection on physical examination .
Murmur on the back below the left scapula, descending to the abdomen.
BP - hypertension (discrepancy between arms of >20mmHg), wide pulse pressure, if hypotensive = ?tamponade - check pulsus paradoxus
Aortia insufficiency - collapsing pulse, early diastolic murmer over aortic area, unequal arm pulses
Palpable abdominal mass?
Identify appropriate investigations for aortic dissetcion and interpret the results.
- Bloods
- CXR
- ECG
- CT-Thorax
- Echocardiography
- Cardiac catheterization and aortography
Bloods
- FBC
- Cross match 10-units of blood
- U&E - renal function
- Clotting
CXR
- Widened mediastinum
- Localized bulge in aortic arch
ECG
- Often nromal
- Signs of left ventricular hypertrophy or inferior MI if dissection compromises the ostia of the right coronary artery
CT-Thorax
- False lumen of dissection can be visualized
Echocardiography
- Transoesophageal highly specific
Define aortic regurgitation.
Reflux of blood from the aorta into the left ventricle during diastole. (also called aortic insuffiency)
Explain the aetiology / risk factors of aortic regurgitation.
- Reflux of the blood into the left ventricle during diastole
- Increase end-diastolic volume
- Incrwase stroke volume
- Low end-diastolic pressure in aorta
- Collapsing pulse & wide pulse pressure
- Acute AR - LV cannot adapt to rapid increase in end-diastolic volume caused by regurgitant blood
1) Aortic Valve Leaflet Abnormalities or Damage
- Bicuspid aortic valve
- Infective endocarditis
- Rheumatic fever
- Trauma
2) Aortic Root / Ascending Aorta Dilation
- Systemic hypertension
- Aortic dissection
- Aortitis - e.g. syphilis, Takayasu’s arteritis
- Arthritides - e.g. RA, seronegative athritides
- Marfan’s Syndrome
- Pseudoxanthoma elasticum
- Ehlers-Danlos Syndrome
- Oestogenesis imperfecta
Risk Factors:
- Bicuspid aortic valve
- Rheumatic fever
- Endocarditis
- Marfan’s Syndrome
- Connective tissue disease
Summarise the epidemiology of aortic regurgitation.
Chronic = late 50s
Documented most frequently in patients >80 years
Recognise the presenting symptoms of aortic regurgitation.
Chronic AR - initially asymptomatic, later symptoms of heart failure = e.g. exertional dyspnoea, orthopnoea, fatigue, angina
Severe acute AR - sudden cardiovascular collapse
Symptoms related to aetiology - e.g. chest or back pain in patients with aortic dissection
Recognise the signs of aortic regurgitation on physical examination.
- Collapsing water-hammer pulse
- Wide pulse pressure
- Thrusting and heavy (volume-loaded) displaced apex beat
- Early distolic murmer at lower left sternal edge - better when sitting forward and expiration
- Ejection systolic murmer heard due to high flow across valve
- AUSTIN-FLINT mid-diastolic murmer - over the apex from turbulent reflex hitting anterior cusp of mitral valvae and causing mitral stenosis
Rare signs:
- Quincke’s sign - visable pulsations on the nail-bed
- de Musset’s sign - head nodding in time with the pulse
- Becker’s sign - visible pulsations of the pupils and retinal arteries
- Muller’s sign - visible pulsation of the uvula
- Corrigan’s sign - visible pulsations in the neck
- Traube’s sign - pistol shot (systolic and diastolic sounds) heard on auscultation of the femoral arteries
- Duroziez’s sign - a systolic and diastolic bruit heard on partial compression of the femoral artery with a stethoscope
- Rosenbach’s sign - systolic pulsations of the liver
- Gerhard’s sign - systolic pulsations of the spleen
- Hill’s sign - popliteal cuff systolic pressure exceeding brachial pressure by >60mmHg
Identfiy appropriate investigations for aortic regurgitation and interpret the results.
- CXR
- ECG
- Echocardiogram
- Cardiac catheterisation with angiography
CXR
- Cardiomegaly
- Dilation of the ascending aorta
- Signs of pulmonary oedema may be seen with left heart failure
ECG
- Left ventricular hypertrophy
- Deep S waves in V1-2
- Tall R wave in V5-6
- Inverted T waves in I, AVL, V5-6
- Left-axis deviation
Echocardiogram
- 2D echo and M-mode - shows underlying cause (e.g. aortic root dilation, bicuspid aortic valve) or effects of AR (left ventricular dilation, dysfunction and fluttering of anterior mitral valve leaflet)
- Doppler echocardiography for detecting AR and assessing severity
- Periodic follow-up echocardiogram for serial meaurements of LV size and function
Cardiac Catheterization with Angiography
- If there is uncertainty about the functional state of the ventricle or the presence of coronary artery disease
Define aortic stenosis.
Narrowing of the left ventricular outflow at the level of the aortic valve.
Explain the aetiology / risk factors of aortic stenosis.
1) Stenosis secondary to rheumatic heart diseas
2) Calcification of a congenital bicuspid aortic valve
3) Calcification and degeneration of a tricuspid aortic valve in the elderly
Risk factors:
- Age 60+years
- Congenitally bicuspid aortic valve
- Rheumatic heart disease
- Chronic kidney disease
Summarise the epidemiology of aortic stenosis.
Prevalence in 3% of 75 year olds
F>M
Bicuspid aortic valve - may present earlier
Recognise the presenting syjmptoms of aortic stenosis.
- Initially asymptomatic
- Angina - due to increased oxygen demand of the hypertrophied ventricles
- Syncope or dizziness on exercise
- Symptoms of heart failure - e.g. dyspnoea
Recognise the signs of aortic stenosis on physical examination.
- BP - narrow pulse pressure
- Pulse - slow rising
- Palpation - thrill in the aortic area, forceful sustained thrusting undisplaced apex beat
- Auscultation - harsh ejection systolic murmer at aortic area, radiates to carotid artery and apex, 2nd heart sound softened or absent, ejection click due to bicuspid valve
Distinguish from Aortic Sclerosis and Hypertorphic Obstructive Cardiomyopathy (HOCM).
Aortic sclerosis - senile degernation with no left ventricular outflow tract obstruction (normal pulse character, no thrill, ejection systolic murmur radiates faintly, S2 heart sound normal)
Identify appropriate investigations for aortic stenosis and interpret the results.
- ECG
- CXR
- Echocardigram
- Cardiac angiography
ECG
- Signs of left ventricular hypertrophy, LBBB
- Deep S wave in V1-2
- Tall R wave in V5-6
- Inverted T waves in I, AVL, V5-6
- Left axis deviation
CXR
- Post-stenotic enlargement of the ascending aorta
- Calcification of aortic valve
Echocardiogram
- Visualises structual changes of the valves and level of stenosis - valvar, supravalvar, subvalvar
- Estimation of the aortic valve area and pressure gradient across valev in systole and left ventricular function assessed
Cardiac Angiography
- Allows differentiation from other causes of angina
- Assessment for concomitant coronary artery disease - 50% of patients
Define arterial ulcers.
A localised area of damage and breakdown of skin due to inadequate aterial blood supply.
Usually seen on the feet of patients with severe artheromatous narrowing of the arteries supplying the legs.
[ischaemic ulcer]
Explain the aetiology / risk factors of arterial ulcers.
Risk Factors:
- Coronary heart disease
- History of stroke or TIA
- Diabetes mellitus
- Peripheral aterial disease - e.g. intermittent claudication
- Obesity
- Immobility
Cause: Lack of blood flow to the capillary beds of the lower extremities.
Summarise the epidemiology of arterial ulcers.
22% of leg ulcers
Prevalence increases with age and obesity
Recognise the presenting symptjoms of arterial ulcers.
- DISTAL - at the dosrum of the foot or between the toes over body prominences
- Punched out appearance
- Elliptical with clearly defined edges - sharp demarcation
- Grey, granulation tissue
- Night Pain - hallmark of arterial ulcers - e.g. at night, when legs are elevated, supine, relieved by dangling leg off the end of the bed
Recognise the signs of arterial ulcers on physical examination.
- Night Pain
- Punched-out appearance
- Hairlessness
- Pale, cold skin
- Absent pulses
- Wasting of calf muscles
- Dry necrotic base
Identfiy appropriate investigations for arterial ulcers and interpret the results.
- Duplex ultrasonography of lower limbs - assess patency of arteries, potential for revascularisation or bypass surgery
- ABPI - <0.8
- Percutaneous angiography
- ECG
- Fasting serum lipids, fasting glucose, HbA1C
- FBC - anaemia can worsen the ischaemia
Define atrial fibrillation / flutter.
Characterized by rapid, chaotic and ineffective atrial electrical conduction.
Permanent, persistent, paroxysmal.
Atrial flutter - characterized by atrial rate of 300/min, ventricular rate 150/min (2:1 heart block as the AV node conducts every second beat = saw tooth baseline
Can be reversed by vagal maneouvres, IV adenosine (with cardiac monitoring) or chemical cardioversion.
Explain the aetiology / risk factors of atrial fibrillation / flutter.
May be no identifiable cause (lone AF)
Secondary causes lead to abnormal atrial electircal pathways.
Systemic
- Thyrotoxicosis
- Hypertension
- Pneumonia
- Alcohol
Heart
- Mitral valve disease
- Ischaemic heart disease
- Rheumatic heart disease
- Cardiomyopathy
- Pericarditis
- Sick sinus syndrome
- Atrial myxoma
Lung
- Bronchial carcinoma
- Pulmonary embolism
Risk Factors (Chornic):
- Hypertension
- CAD
- CHF
- Advancing age
Risk Factors (Acute):
- Increasing age
- DM
- Hypertension
- CHF
Summarise the epidemiology of atrial fibrillation / flutter.
Very common in the elderly - 5% of those >65 years
May be paroxysmal
Recognise the presenting symptoms of atrial fibrillation / flutter.
- Asymptomatic
- Palpitations
- Syncope
- Symptoms of the cause of AF
Recognise the signs of atrial fibrillation / flutter on physical examination.
- Irregularly irregular pulse
- Difference in apical beat and radial pulse
- Look for thyroid disease
- Look for valvular heart disease
Identify appropriate investigations for arterial fibrillation / flutter and interpret the results.
- ECG
- Blood
- Echocardiogram
ECG
- Uneven baseline (fibrillations)
- Absent P waves
- Irregular QRS complexes
- Saw-tooth baseline
- Consider atrial flutter
Bloods
- Cardiac enzymes
- TFT
- Lipid profile
- U&E
- Mg2+
- Ca2+
NB: Risk of digoxin toxicity increased with hypokalaemia, hypomagnesaemia or hypercalcaemia
Echocardiogram
- ?Mitral valve disease
- ?Left atrial dilation
- ?Left ventricular dysfunction
- ?Structural abnormalities
Generate a management plan for arterial fibrillation / flutter.
- Treat reversible causes - e.g. thyrotoxicosis, chest infection
1) Rhythm Control
- AF > 48 from onset, anticoagulate (3-4 weeks) before attempting cardioversion
- DC cardioversion - synchronized DCshock (2x100J, 1x200J)
- Chemical cardioversion - flecainide (contraindicated if IHD) or amiodarone
- Prophylaxis against AF - sotalol, amiodarone, flecainide (pill in pocket strategy?)
2) Rate Control
- Chronic AF - ventricular rate control with digoxin, verapamil and B-blockers (90/min rate aim)
3) Stroke Risk Stratification
- Low risk - with aspirin
- High risk - with anticoagulation with warfarin
Risk Factors:
- Previous TBE
- Age 75 years+
- Hypertension
- Diabetes
- Vascular disease
- Valve disease
- Heart Failure
- Impaired Left Ventricular Function
Identify the possible complications of arterial fibrillation / flutter and its management.
- TBE - 4% per year, increased risk with left atrial enlargement or left ventricular dysfunction
- Worsens existing heart failure
Summarise the prognosis for patients with arterial fibrillation / flutter.
Chronic AF in a diseasedheart does not usually return to sinus rhythm.
Define cardiac arrest.
Acute cessation of cardiac function.
Explain the aetiology / risk factors of cardiac arrest.
4 H’s:
- Hypoxia
- Hypothermia
- Hypovolaemia
- Hypo or hyperkalaemia
4 T’s:
- Tamponade
- Tension pneumothorax
- Thromboembolism (TBE)
- Toxins (drugs, therapeutic agents, sepsis)
Recognise the presenting symptoms of cardiac arrest.
Management precedes or is concurrent to history (e.g. from witnesses)
Recognise the signs of cardiac arrest on physical examination.
- Unconscious
- Not breathing
- Absent carotid pulses
Identfiy apporpriate investigations for cardiac arrest and interpret the results.
1) Cardiac monitor - classifcation of rhythm directs management
2) Bloods - ABG, U&E, FBC, cross-match,clotting, toxicology screen, glucose
Generate a management plan for cardiac arrest.
Safety
- Approprach with caution
- Cause of arrest may still pose a threat
- Defibrillators and oxygen = hazards
- Help summoned as soon as possible
BLS
- If arrest is witnessed and monitored, consider giving a precordial thump if no defibrillators avaliable
- Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift
- Assess breathing by look, listen and feel
- If not breathing, give 2 effective breaths immediately
- Assess circulation at carotid pulse for 10s
- If absent, give 30 chest compressions at a rate of 100/min
- Continue cycles of 30 compressions for every two breaths
- Proceed to advanced life support as soon as possible
ALS
- Attach cardiac monitor and defibrillator
- Assess rhthym
A) If pulseless ventricular tachycardia or ventricularfibrillation (SHOCKABLE)
- Defibrillate once - 150-360J biphasic, 360J monophasic
- Resume CPR immediately for 2 mins and then return to 2
- Administer adrenaline (1mg IV) after 2nd defibrillation and again every 3-5 mins
- If SHOCKABLE persists, administer amiodarone 300mg IV bolus or lidocaine
B) If pulseless electrical activity (PEA) or asystole:
- CPR for 2 minutes then return to 2
- Administer adrenaline 1mg IV every 3-5 minutes
- Atropine (3mg IV) if asystole or PEA with rate <60/min
C) During CPR
- Check electrodes, paddle positions and contacts
- Secure the airway - e.g. attempt ET intubation, high-flow oxygen
- Once airway secure, give continuous compresisons and breaths
- Consider Mg, HCO3, external pacing
- Stop CPR and check pulse only if change in rhythm or signs of life
Treatment of Reversible Causes:
- Hypothermia - warm slowly
- Hypo/hyperkalaemia - correction of electrolytes
- Hypovolaemia - IV colloids, crystalloids or blood products
- Tamponade - pericardiocentesis under xiphisterum up and leftwards
- Tension pneumothorax - needle into second intercostal space, mid-clavicular line
Identify the possible complications of cardiac arrest and its management.
- Irreversible hypoxic brain damage
- Death
Summarise the prognosis for patients with cardiac arrest.
- Less successful outside hospital
- Duration of inadequate effective cardiac output is associated with poor prognosis
Define cardiac failure (acute and chronic).
Inability of the cardiac output to meet the body’s demands despite normal venous pressures.
Explain the aetiology /risk factors of cardiac failure (acute and chronic).
LOW CARDIAC OUTPUT
- Left heart failure - ischaemic heart disease, hypertesion, cardiomyopathy aortic valve disease, mitral regurgitation
- Right heart failure - secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade
- Biventricular failure - arrhythmia, cardiomyopathy (dilated or restirctive), myocarditis, drug toxicity
HIGH DEMAND
- Anaemia
- Berberi
- Pregnancy
- Paget’s disease
- Hyperthyroidism
- Arteriovenous malformation
Summarise the epidemiology of cardiac failure (acute and chronic).
10% of 65 year olds
Recognise the presenting symptoms of cardiac failure (acute and chronic).
Left - caused by pulmonary congestion
- Dyspnoea
- Orthopnea
- Paroxysmal nocturnal dyspnoea
- Fatigue
Acute LVF
- Dyspnoea
- Wheeze
- Cough
- Pink frothy sputum
Right
- Swollen ankles
- Fatigue
- Increased weight - due to oedema
- Reduced exercise tolerace
- Anorexia
- Nausea
NB: New York Heart Association Classification
- No dyspnoea
- Dyspnoea or ordinary activities
- Dyspnoea on less than ordinary activities
- Dyspnoea at rest
Recognise the signs of cardiac failure (acute and chronic) on physical examination.
Left
- Tachycardia
- Tachypnoea
- Displaced apex beat
- Bilateral basal crackles
- 3rd heart sound - gallop rhythm, rapid ventricular filling
- Pansystolic murmuer - functional mitral regurgitation
Acute Left
- Tachyhypnoea
- Cyanosis
- Tachycardia
- Peripheral shutdown
- Pulsus alternans
- Gallop rhythm
- Wheeze cardiac asthma
- Fine crackles throughout the lung
Right
- High JVP
- Hepatomegaly
- Ascites
- Ankle/sacral pitting
- Oedema
- Signs of functional tricuspid regurgitation
Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results.
- Bloods
- CXR
- ECF
- Echocardiogram
- Swan-Ganz Catheter
Bloods
- FBC
- U&E
- LFTs
- CRP
- Glucose
- Lipids
- TFTs
- Acute LVF - ABG, troponin, brain natriuretic peptide (BNP)
- High plasma BNP suggests cardiac failure
CXR (Acute LVF)
- Cardiomegaly - heart >50% of thoracic width
- Prominent upper lobe vessels
- Pleural effusion
- Intestitial oedema - Kerley B lines
- Perihilar shadowing - bat’s wings
- Fluid in fissures
ECG
- May be normal
- Ischaemic changes
- Arrhthmia
- Left ventricular hypertrophy
Echocardiogram
- LVEF <40% = systolic dysfunction
- Diastolic dysfunction - reduced compliance leading to a restrictive filling defect
Swan-Ganz Catheter
- Allows measurements of right atrial, right ventricular, pulonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Generate a management plan for cardiac failure (acute and chronic) and its management.
Acute LVF
- Cardiogenic shock - severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine), manage in ITU
- Pulmonary oedema - sit up patient, 60-10% oxygen, CPAP.
- Monitor BP, respiatory rate, sats, urine output, ECG
- Treat the cause - e.g. MI, arrythmia
Also consider: diamorphine (venodilator and axiolytic), GTN infusion (reduce preload) IV furosemide if fluid overloaded (venodilator and diuretic)
Chronic LVF
- Treat the cause - e.g. hypertension
- Treat exacerbating factors - e.g. anaemia
- ACE inhibitors - e.g. enalapril, perindopril, ramipril
- B-Blockers - e.g. bisprolol, carvidolol
- Loop diuretics - e.g. furosemide - and dietary salt restritcion to correct fluid overload
- Aldosterone Antagonists - e.g. spironolactone, eplerenone
- Angiotensin Receptor Blokcers - e.g. candesartan
- Hydralazine and Nitrate
- Digoxin
- N-3 Polyunsaturated Fatty Acids
- Cardiac Resynchroniszation Therapy (CRT)
- Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction - e.g. NSAIDs, non-dihydropyridine calcium channel blockers - e.g. diltiazem and verapamil.
Identify the possible complications of cardiac failure (acute and chronic) and its management.
- Respiratory failure
- Cardiogenic shock
- Death
Summarise the prognosis for patients with cardiac failure (acute and chronic).
50% of patients with severe heart failure die within 2 years.
Outline the mechanism of action of ACE-Inhibitors in heart failure patients.
- Inhibit intracardiac renin-angiotensin system that may contribute to myocardial hypertrophy and remodelling
- Slow progression of heart failure and improves survival
- Additive benefits of ACE inhibitors and beta-blockers
Outline the mechanism of action of Beta-Blockers in heart failure patients.
- Block the effects of chronically activated sympathetic system
- Slows progresion of heart failure and improves survival
- Additive benefits of ACE inhibitors + Beta-blockers
Outline the mechanism of action of Aldosterone Antagonists in heart failure patients.
- Improve survival in patients with NYHA class II/IV symptoms and on standard therapy
- Monitor K+ - may cause hyperkalaemia
- Used to assist with management of diuretic induced hypokalaemia
Outline the mechanism of action of Angiotensin Receptor Blockers in heart failure patients.
- May be added in pateints with persistent symptoms despite ACE inhibitors and B-blockers
- Monitor K+ - may cause hyperkalaemia
Outline the mechanism of action of Hydralazine and Nitrates in heart failure patients.
- May be added in patients (Afro-Carribeans) with persistent symptomsdespite therapy with ACE inhibitor and beta-blocker
Outline the mechanism of action of Digoxin in heart failure patients.
- Positive ionotrope
- Reduced hospitalisation
- Does not improve survival
Outline the mechanism of action of N-3 Polyunsaturated Fatty Acids in heart failure patients.
- Provide small beneficial advantage in terms of mortality
Outline the mechanism of action of CRT in heart failure patients.
- Biventricular pacing
- Improves symptoms and survival in patients with LVEF<35%, cardiac dyssynchrony (QRS>120msec) and moderate to severe symptoms despite optimal medical therapy
- Most patients who meet these criteria are also candidates for implanatable cardiac defibrillator (ICD) and recieve combined device
Define cardiomyopathy.
Primary disease of the myocardium.
May be dilated, hypertrophic or restrictive.
Explain the aetiology /risk factors of cardiomyopathy.
Dilated - post-viral myocarditis, alcohol, drugs (doxorubicine, cocaine), familial (autosomal dominant), thyrotoxicosis, haemochromatosis, peripartum
Hypertrophic - genetic (autosomal dominant) mutations in beta-myosin, troponin T or alpha-tropomyosin
Restrictive - amyloidosis, sarcoidosis, haemachromatosis.
Summarise the epidemiology of cardiomyopathy.
0.05-0.20% prevalence - dilated and hypertrophic
Restrictive cardiomyopaty is very rare
Recognise the presenting symptoms of cardiomyopathy.
Dilated:
- Symptoms of heart failure
- Arrythmias
- Thromboembolism
- Family history of sudden death
Hypertrophic:
- Usually none
- Syncope
- Angina
- Arrythmias
- Family history of sudden death
Restrictive:
- Dyspnoea
- Fatigue
- Arrythmia
- Ankle or abdominal swelling
- Enquire about family history of sudden death
Recognise the signs of cardiomyopathy on physical examination.
Dilated:
- Raised JVP
- Displaced apex beat
- Functional mitral and tricuspid regurgitations
- 3rd heart sound
Hypertrophic
- Jerky carotid pulse
- Double apex beat
- Ejection systolic murmur
Restrictive
- Raised JVP
- Kussmaul’s sign - further raised JVP on inspiration
- Palpable apex beat
- 3rd heart sound
- Ascites
- Ankle oedema
- Hepatomegaly
Identify appropriate investigations for cardiomyopathy and interpret the results.
- CXR - show cardiomegaly, heart failure signs
- ECG
- Echocardiography
- Cardiac catheterization - measure pressures
- Endomyocardial biopsy - restrictive cardiomyopathy
- Pedigree or Genetic Analysis - rare
ECG:
- All types –> non-specific ST changes, conduction defects, arrythmias
- Hypertrophic –> left axis deviation, signs of left ventricular hypertrophy (aortic stenosis), Q waves in inferior and lateral leads
- Restrictive - low voltage complexes
Echocardiography:
- Dilated –> dilated ventricles with global hyookinesia
- Hypertrophic –> ventricular hypertrophy (disproportionate septal involvement)
- Restritcive –> non-dilated non-hypertrophied ventricles, atrial enlargement, preserved systolic function, diastolic dysfunction, gradular or sparkling appearance of myocardium in amyloidosis
Define constrictive percarditis.
The heart is incased in a rigid pericardium.
Explain the aetiology / risk factors of constrictive pericarditis.
Unknown. (UK)
TB or after any pericarditis (elsewhere).
Risk Factors:
- 1% = idiopathic and viral pericarditis
- 2-5% = autoimmune, immunemediated and neoplastic aetiology
- 20-30% = bacterial aetiology (e.g. TB, purulent percarditis).
Summarise the epidemiology of constrictive pericarditis.
- 76 cases per 1000 person-years after acute idiopathic or viral pericarditis.
- 7 cases per 1000 person-years for acute tuberculous pericarditis.
- 7 cases per 1000 person-years for purulent pericarditis.
Recognise the presenting symptoms of constrictive pericarditis.
- Difficulty breathing that develops slowly and becomes worse
- Fatigue
- Swollen abdomen
- Chronic, severe swelling in legs and ankles
- Weakness
- Low grade fever
- Chest pain
Recognise the signs of constrictive pericarditis on physical examination.
- Raised JVP
- Kussmaul’s sign - raised JVP paradoxically with inspiration
- Soft, diffuse apex beat
- Quiet heart signs
- S3
- Diastolic percardial knock
- Hepatosplenomegaly
- Ascites
- Oedema
Identfiy appropriate investigations forconstrictive pericarditis and interpret the results.
- CXR - small heart + pericardial calcification
- CT/MRI - distinguish from restrictive cardiomyopathy
- Echocardiography
- Cardiac catheterisation
Define coronary angiography and PCI.
Coronary angiography - a procedure that uses contrast dye, usually containing iodine, and X-rays to detect blockages in the coronary arteries that are caused by plaque buildup.
PCI = Percutaneous Coronary Intervention (Coronary Angioplasty) - a non-surgical procedure that improves blood flow to your heart, requiring cardiac catheterisation.
Cardiac Catheterisation - the insertion of a catheter tube and injection of contrast dye (usually iodine-based) into your coronary arteries
Summarise the indications for coronary angiography and PCI.
Coronary angiography:
- Symptoms of coronary artery disease - e.g. angina
- Pain in your chest, jaw, neck or arm
- New or increasing chest pain (unstable angina)
- Unexplained congestive heart failure
- Acute myocardial infarction with mechanical complications requiring cardiac surgery
PCI:
- Acute ST-elevated myocardial infarction (STEMI)
- Non-ST-elevated acute coronary syndrome (NSTE-ACS)
- Unstable angina
- Stable angina
- Anginal equivalent - e.g. dyspnea, arrythmia, dizziness, cyncope
- High risk stress test findings
Identify the possible complications of coronary angiography and PCI.
Coronary Angiography:
- Heart attack
- Stroke
- Injury to catheterized artery
- Arrhythmias
- Allergic reactions to the dye or medications used during the procedure
- Kidney damage
- Excessive bleeding
- Infection
PCI:
- Bleeding
- Haematoma
- Pseudoaneurysm at access site
- Heart attack
- Stroke
Identify appropriate investigations for cardiomyopathy and interpret the results.
- CXR - show cardiomegaly, heart failure signs
- ECG
- Echocardiography
- Cardiac catheterization - measure pressures
- Endomyocardial biopsy - restrictive cardiomyopathy
- Pedigree or Genetic Analysis - rare
ECG:
- All types –> non-specific ST changes, conduction defects, arrythmias
- Hypertrophic –> left axis deviation, signs of left ventricular hypertrophy (aortic stenosis), Q waves in inferior and lateral leads
- Restrictive - low voltage complexes
Echocardiography:
- Dilated –> dilated ventricles with global hyookinesia
- Hypertrophic –> ventricular hypertrophy (disproportionate septal involvement)
- Restritcive –> non-dilated non-hypertrophied ventricles, atrial enlargement, preserved systolic function, diastolic dysfunction, gradular or sparkling appearance of myocardium in amyloidosis
Define constrictive percarditis.
The heart is incased in a rigid pericardium.
Explain the aetiology / risk factors of constrictive pericarditis.
Unknown. (UK)
TB or after any pericarditis (elsewhere).
Risk Factors:
- 1% = idiopathic and viral pericarditis
- 2-5% = autoimmune, immunemediated and neoplastic aetiology
- 20-30% = bacterial aetiology (e.g. TB, purulent percarditis).
Summarise the epidemiology of constrictive pericarditis.
- 76 cases per 1000 person-years after acute idiopathic or viral pericarditis.
- 7 cases per 1000 person-years for acute tuberculous pericarditis.
- 7 cases per 1000 person-years for purulent pericarditis.
Recognise the presenting symptoms of constrictive pericarditis.
- Difficulty breathing that develops slowly and becomes worse
- Fatigue
- Swollen abdomen
- Chronic, severe swelling in legs and ankles
- Weakness
- Low grade fever
- Chest pain
Identify the possible complications of DC cardioversion.
[Direct Current Cardioversion]
- Dislodged blood clots
- Abnormal heart rhythm dollowing the procedure
- Skin burns
- Ventricular fibrillation due to general anaesthetia or lack of synchronisation between DC shock and QRS
- Thromboembolus - insufficient anticoagulant therapy
- Non-sustained ventricular tachycardia
- Atrial arrhthmia
- Heart block
- Bradycardia
- Transient left bundle branch block
- Myocardial necrosis
- Myocardial dysfunction
- Transient hypotension
- Pulmonary oedema
- Pain at application site
Define coronary artery bypass graft (CABG).
A healthy artery or vein from the body is grafted to the blocked coronary artery. The grafted artery or vein bypasses the blocked portion of the coronary artery, creating a new passage for oxygen-rich blood to be routed around the blockage to the heart muscle.
Summarise the indications for a coornary artery bypass graft (CABG).
- Triple coronary vessel disease
- Left main stem coronary artery disease
- Two coronary vessel disease with a proximal left anterior descending artery lesion
Identify the possible complications of a coronary artery bypass graft (CABG).
- Stroke
- Neurocognitie dysfunction
- Intraoperative myocardial infarction
- Temporary conduction abnormalities
- Arrhythmias - e.g. atrial fibrillation
- Pericardial effusion / tamponade
- Haemorrhage
- Mediastinitis
- Steral wound infection
- Renal dysfunction
- Death
Define DC cardioversion.
[Direct Current Cardioversion]
A procedure to convert an abnormal heart rhythm to a normal heart rhythm.
Atrial fibrillation - most common arrhythmia
Aim to completely depolarize the heart using a direct current.
Summarise the indications for DC cardioversion.
[Direct Current Cardioversion]
To restore sinus rhythm if Ventricular Fibrillation / Ventricular Tachycardia, Atrial Fibrillation, Flutter, Supraventricular Tachycardias.
If other treatments have failured or there is haemodynamic compromise.
Emergency or electively.
Emergency = VF, VT
Electively = AF
Define deep vein thrombosis (DVT).
Formation of a thrombus within the deep veins - most comonly of the calf or thigh.
Generate a management plan for deep vein thrombosis (DVT).
Anticoagulation:
- Heparin - whilst awaiting therapeutic INR from warfarin anti-coag
- DVT below knee treated with anti-coagulation for 3 months
- DVT above knee treated with anticoagulation for 6 months
- Recurrent DVT - long term warfarin
- If active anticoagulation is contraindicated and/or high risk of embolisation - place IVC filter by IVR to prevent embolus in lungs
Prevention:
- Use of graduated compression stockings
- Mobilisation if possible
- At-risk groups should have prophylactic heparin - e.g. low-molecular weight heparin if no contraindications
Identify the possible complications of deep vein thrombosis (DVT) and its management.
Of the disease:
- PE
- Damage to vein valves
- Chornic venous insufficiency of the lower limb (pro-thrombotic syndrome)
- Venous infarction - phlegmasia cerulea dolens
Of the treatment:
- Heparin-induced thrombocytopaenia
- Bleeding
Summarise the prognosis for patients with deep vein thrombosis (DVT).
Depends on extent of DVT, below-knee DVTs lower risk of embolus.
More proximal DVTs have higher risk of propagation and embolisation, which if large, may be fatal.
Recognise the signs of deep vein thrombosis (DVT) on physical examination.
- Examine for swelling
- Examine for calf tenderness
- Severe leg oedema and cyanosis (phlegmasia cerulea dolens) is rare
- Respiratory examination for signs of a PE
Use Wells Clinical Prediction Score
Identify appropriate investigations for deep vein thrombosis (DVT).
- Doppler ultrasound
- Bloods
- ECG, CXR, ABG - if PE?
Doppler US
- Gold standard
- Good sensitivity for femoral veins
- Less sensitive for calf veins
Bloods
- D-dimers = fibrinogen degradation products - sensitive but non-specific and only useful as a negative predictor in low-risk patinets
- Thrombophilia screen, prior to starting anticoagulation - if recurrent episodes
- FBC - platelet count prior to starting heparin
- U&E
- Clotting
Generate a management plan for deep vein thrombosis (DVT).
Anticoagulation:
- Heparin - whilst awaiting therapeutic INR from warfarin anti-coag
- DVT below knee treated with anti-coagulation for 3 months
- DVT above knee treated with anticoagulation for 6 months
- Recurrent DVT - long term warfarin
- If active anticoagulation is contraindicated and/or high risk of embolisation - place IVC filter by IVR to prevent embolus in lungs
Define dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
Elevation of one or more plasma lipid fractions.
Explain the aetiology / risk factors of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
LDL accummulates in the intima of systemic arteries.
Taken up by LDLR on macrophage = foam cell.
HDL is a shuttle in periphery for transport of cholesterol esters back to the liver –> cardioprotective
Primary - molecular genetic basis, some unknown
- Familial hypercholesterolaemia - reduced functional hepatic LDLR
- Familial hypertriglyceridaemia - unknown, autosomal dominant
- Hypertriglyceridaemia - lipoprotein lipase or apo-CII deficiency
- Familial combined hyperlipidaemia - unknown
- Remnant hyperlipidaemia - apo-E2 genotype inheritance, accumulation of LDL remnants
Secondary - subdivided depending on abnormality
- HIGH CHOLESTEROL - hypothyroidism, nephrotic syndrome, cholestatic liver disease, anorexia nervosa
- HIGH TRIGLYCERIDES - diabetes, drugs (e.g. B-blockers, thiazides, oestrogens), alcohol, obesty, chronic renal disease, hepatocellular disease
Summarise the epidemiology of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
50% of UK population have a cholesterol level high enough to be a risk for CHD.
Recognise the presenting symptoms of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
- Asymptomatic
- Symptoms of complications
Ask about other CVS risk factors:
- Diabetes
- Smoking
- Hypertension
- Family history
Recognise the signs of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) on physical examination.
Usually normal - examine for secondary causes.
Lipid deposits:
- Xanthelasmas - around eyes
- Corneal arcus
- Tendons xanthomas - e.g. extensor tendons of the hands, Achilles, patella
- Tuberous xanthomas on knees and elbows
- Xanthomas in palmar creases - in remnant hyperlipidaemia
- Eruptive xanthomas and lipidaemia retinalis (pale retinal vessels) - severe hypertriglyceridaemia
Signs of Complications:
- Reduced peripheral pulses
- Carotid bruits
- CVD risks
- High BP
Identify appropriate investigations for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and interpret the results.
- Bloods
- Cardiovascular Risk Assessment
Bloods
- Fasting lipid profile
- Exclude secondary causes - e.g. glucose, TFT, LFT, U&E
CVD Risk Assessment
- Algorithms
- E.g. Framingham risk equation, QRISK, ASSIGN
Generate a management plan for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia).
Treat secondary causes.
Advice
- Exercise
- Lose weight
- Control BP
- Control diabetes
- Low alcohol
- Dietary modification
Lipid-lowering Drugs
- Primary prevention - if multiple risk factors + no atherosclerosis + risk CHD >20% in 10 years
- Secondary prevention - if established atherosclerosis (e.g. CHD, CAD, AA)
- Target: total cholesterol <4mmol/L, LDL <2mmol/L
Drugs for HIGH Total Cholesterol or HIGH LDL:
- HMG-CoA Reductase Inhibitors - potently lowers mortality and CVS morbidity is demonstrated in numerous trials - high dose recommended as first line - e.g. 40mg simvastatin
- Ezetimibe - inhibits cholesterol absorption in gut, used if statin not tolerated or as adjunctive agent
Drugs for HIGH Triglycerides:
- Fibrates - stimulates lipoprotein lipase activity via specific transcription factors
- Fish oil - rich in omega-3 marine triglycerides, not recommended as can aggravate
Others:
- Anion-exchange resins - e.g. colestyramine, colestipol - binds bile acids and reduces reabsorption, increases hepatic cholesterol conversion to bile acids, increases LDLR on hepatocytes
- Nicotinic acid - reduced hepatic VLDL release, reduces TG, reduces cholesterol, increases HDL, bad side effectes (PG-mediated vasodilation, flushing, dizziness, palpitations), increases glucose and urate.
