Cardiovascular Flashcards
Define gangrene compared to nectrotising fasciitis.
What are the 3 types of gangrene.
What is the cause of gas gangrene
Gangrene is tissue necrosis, may result from ischaemia, infection, or trauma (or a combination of these processes).
3 types: infectious gangrene (wet gangrene) and ischaemic gangrene (dry gangrene) and gas gangrene
- Wet gangrene infection and liquefaction of “dry gangrenous” tissue by saprophytic bacteria. This makes the area swell, drain fluid, and smell bad.
- Dry: Coagulation necrosis of extremity due to slowly developing vascular occlusion. Area becomes dry, shrinks, and turns black.
- Gas gangrene: is caused by clostridia perfringens
Explain the aetiology / risk factors of gangrene & necrotising fasciitis. Include the bugs that cause them
Type 1 vs type 2 necrotising fasciitis
Gangrene:
Critically insufficient blood supply is the most common cause of gangrene, and is often associated with diabetes and long-term smoking
Aetiology…
Infectious gangrene (=wet gangrene): 1. Necrotising fasciitis-Type I (polymicrobial i.e. more than one bacteria involved) Type II (due to haemolytic group A streptococcus (major cause), staphylococci including methicillin resistant strains/MRSA) Type III (gas gangrene, eg due to clostridium).
- Gas gangrene- Clostridium perfringens is the most common aetiological agent (also some non-clostridial organisms)
Ischaemic (=dry gangrene):
1. Atherosclerosis underlies most PAD; diabetic microangiopathy; thrombosis, vasculitis, malignancy, or antiphospholipid syndrome
Gas gangrene is a subset of necrotizing myositis caused by spore-forming clostridial species. There is rapid onset of myonecrosis, muscle swelling, gas production, sepsis, and severe pain. Risk factors include diabetes, trauma, and malignancy.
Epidemiology….
Type I necrotising fasciitis occurs most commonly in patients with diabetes and patients with peripheral vascular disease
Atherosclerosis due to development of atheroembolism
Summarise the epidemiology of gangrene
Gas:
- Severe penetrating trauma or crush injuries associated with interruption of the blood supply
Recognise the presenting symptoms of gangrene
loss of sensation or severe pain in the affected area
sores or blisters that bleed or release a dirty-looking or foul-smelling discharge
Recognise the signs of gangrene on physical examination
redness and swelling
foul smelling discharge
crepitus when pressed, caused by gas under the skin
Identify appropriate investigations for gangrene and interpret the results
Investigations:
FBC: leukocytosis, haemoconcentration, or anaemia
Comprehensive metabolic panel: may indicate metabolic acidosis, liver derangement, renal failure
Serum LDH: elevated if haemolytic anaemia (Rapidly developing haemolytic anaemia with an increased lactate dehydrogenase level is common in patients with gas gangrene)
Coagulation panel: should be normal
CRP: raised
X-ray/CT/MRI
Define peripheral vascular disease. (chronic and then acute)
….
Explain aetiology/risk factors of PVD (chronic and then acute)
Aetiology: Peripheral vascular disease (PVD) is commonly caused by atherosclerosis and usually affects the aorto-iliac or infra-inguinal arteries.
Aetiology (acute): Embolic or thrombotic disease:
- Embolic commonly due to cardiac thrombus and cardiac arrhythmias (now rare)
- ALI is now often due to thrombotic disease . Acute thrombus usually forms on a chronic atherosclerotic stenosis in a patient who has previously reported symptoms of claudication. BUT Thrombus may also form in normal vessels in individuals who are hypercoagulable because of malignancy or thrombophilia defects.
Acute upper limb ischaemia may be caused by similar processes or occur secondary to external compression with a cervical rib/band.
Risk factors (chronic):
- Smoking
- Diabetes
- Hypercholesterolaemia
- HTN
Premature atherosclerosis in patients aged <45 years may be associated with thrombophilia and hyperhomocysteinaemia.
Summarise epidemiology of PVD (chronic and then acute)
It is present in 7% of middle-aged men and 4.5% of middle-aged women, but these patients are more likely to die of MI or stroke than lose their leg.
Recognise presenting symptoms of PVD (chronic and then acute)
-Which classification is used for chronic
What is the difference between critical limb ischaemia and acute limb ischaemia
CHRONIC- Fontaine
Stage I- Asymptomatic
Stage II – intermittent claudication (exertional discomfort rlieved by rest)
Stage III – rest pain/nocturnal pain (severe, unremitting pain in the foot which stops you from sleeping, partially relived by dangling foot over edge of bed)
Stage IV – necrosis/gangrene.
ACUTE 5 Ps: pain , the fact that the leg looks white ( pallor ), paraesthesia , paralysis and the sensation that it is perishingly cold.
The pain is unbearable and normally requires opioids for relief.
CRITICAL LIMB ISCHAEMIA- Pain even at rest (=equivalent of unstable angina)
ACUTE LIMB ISCHAEMIA- fully blocked artery resulting in lack o
Recognise the signs of PVD on physical examination (chronic and then acute)
CHRONIC
- lower limbs are cold with dry skin and lack of hair
- Pulses may be diminished or absent
- Ulceration may occur in association with dark discoloration of the toes or gangrene
- abdomen should be examined for a possible aneurysm.
ACUTE:
The limb is cold, with mottling or marbling of the skin.
Pulses are diminished or absent. The sensation and movement of the leg are reduced in severe ischaemia.
Patients may develop a compartment syndrome with pain in the calf on compression.
Identify appropriate invesitgations for PVD (chronic and then acute)
Imaging
Both acute and chronic:
-Examine pulses to identify anatomical level of disease
-Ankle/brachial pressure index (ABPI) (see other box)- 1st INVESTIGATION
First investigation: Duplex ultrasound using B-mode ultrasound and colour Doppler.
CT angiography (but extensive calcification may obscure stenoses. CTA requires ionizing radiation and iodinated contrast media)- GOLD STANDARD
- Digital subtraction angiography (DSA) provides arteral map but requires peripheral arterial cannulation and exposes the individual to iodinated contrast; it should be reserved for use in patients immediately prior to intervention.
- 3D contrast enhanced MR angiography
Explain the ankle/brachial pressure index
When might the ABPI be wrong
Compares cuff pressure at which blood flow is detectable by doppler in posterior/anterior tibial artery compared to brachial artery
Intermettint claudication associated with ABPI 0.5-0.9. <0.5 associated with critical limb ischaemia
If the arteries are heavily calcified and incompressible – that is, in renal or diabetic disease, the ABPI will be falsely elevated. In these patients, toe pressure values are more sensitive.
TBI should be measured to diagnose patients with suspected PAD when the ABI is >1.40
Management of PVD (chronic and then acute)
Chronic:
Risk factor management- even if cholesterol is normal, reducing it still reduces mortality from cardiovascular disease
What ABPI values might suggest PVD, what about critical limb ischaemia
PVD can be diagnosed using ABPI:
0.5-0.9 = peripheral vascular disease;
< 0.5 =
critical limb ischaemia.
Define arterial ulcer
an ulcer caused by a reduction in arterial blood flow, leading to decreased perfusion of the tissues and subsequent poor healing.
https://teachmesurgery.com/vascular/venous/ulcers/
Explain aetiology/risk factors of arterial ulcers
They often form as small deep lesions with well-defined borders and a necrotic base. They most commonly occur distally at sites of trauma and in pressure areas (e.g the heel).
The main risk factors are those of peripheral arterial disease, including:
smoking, diabetes mellitus, hypertension, hyperlipidaemia, increasing age, positive family history, and obesity and physical inactivity
Recognise presenting symptoms of arterial ulcer/signs of arterial ulcer on physical examination
A patient with a suspected arterial ulcer is likely to give a preceding history of intermittent claudication (pain when they walk) or critical limb ischaemia (pain at night).
No healing, so little or no granulation tissue
Cold limbs, thickened nails, nectrotic toes and hair loss
Limb cold and reduced or absent pulses. In pure arterial ulcer, sensation maintained unlike neuropathic ulcers
arterial ulcers commonly occur on both the dorsal and plantar aspects of the foot (in contrast to medial malleolus for venous ulcers)
Identify appropriate invesitgations for arterial ulcer
ABPI to further quantify the extent of any peripheral arterial disease
The anatomical location of any arterial disease can be assessed by clinical examination, followed by imaging. This includes duplex ultrasound, CT Angiography, and / or Magnetic Resonance Angiogram (MRA).
Identify management of arterial ulcer
Vascular review, combination of:
- Conservative: lifestyle change e.g. smoking cessation, weight loss, increased exercise
- Medical: Suitable pharmacological cardiovascular risk factor modification should also be prescribed, including statin therapy, an antiplatelet agent (aspirin or clopidogrel), and optimisation of blood pressure and glucose. Add an antibiotic if there is infection
-Surgical: Angioplasty (with or without stenting) or bypass grafting (usually for more extensive disease).
Any non-healing ulcers despite a good blood supply may also be offered skin reconstruction with grafts.
To improve the blood supply to the ulcer an angioplasty is often used, or surgery to clear out a blockage from a leg artery (endarterectomy) or a bypass operation to put in a new route for blood flow in the leg.
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, and creating a false lumen.
The layers of arteries are tunica intima (endothelium), media (smooth muscle, collagen and elastic) and adventitia (=externa) (collagen and elastic tissue)
Explain the aetiology / risk factors of aortic dissection
Standard classification of aortic dissection
AETIOLOGY Degenerative changes in the smooth muscle of the aortic media are the predisposing event.
Common causes and predisposing factors are:
1) Most common: uncontrolled hypertension;
2) Congenital cardiac abnormalities (e.g. aortic coarctation, Turner’s, bicuspid aortic valve, E-D syndrome, Marfan);
3) Crack cocaine usage
4) Pregnancy
5) High intensity weightlifting.
Type A Affects Ascending Aorta and Arch, affects 60% of aortic dissections and management is surgical.
Type B Begins beyond brachiocephalic vessels (commences distal to the left subclavian artery), affects 40% of aortic dissections and is managed medically with blood pressure control.
Summarise the epidemiology of aortic dissection
Most common in males between 40-60
Recognise the presenting symptoms of aortic dissection
Sudden central ‘tearing’ pain, may radiate to the back (may mimic an MI) OR jaw depending on the location. Aortic dissection can lead to occlusion of the aorta and its branches:
1) Carotid obstruction: hemiparesis (=hemiplegia, paralysis of one side of body); blackout
2) Coronary artery obstruction: chest pain (angina/MI)
3) Subclavian obstruction (ataxia, loss of consciousness, remember the vertebral arteries arise from subclavian)
4) Anterior spinal artery obstruction (paraplegia, impairment in motor or sensory function of the lower extremities.)
5) Coeliac obstruction (severe abdominal pain, ischaemic bowel)
6) Renal artery obstruction (anuria, renal failure)
Signs of aortic dissection on physical examination
Murmur on the back below left scapula, descending to abdomen.
Blood pressure (BP) : Hypertension (BP discrepancy between arms of > 20 mmHg), wide pulse pressure. If hypotensive may signify tamponade, check for pulsus paradoxus (dip in BP during inspiration of >10mmHg)
Aortic valve insufficiency : Collapsing pulse, early diastolic murmur over aortic area. Unequal arm pulses.
There may be a palpable abdominal mass.
https://www.youtube.com/watch?v=dZLX2MD_w78 –> watch do understand why you get aortic insufficiency/cardiac tamponade
(cause of pulsus parodoxus -https://www.youtube.com/watch?v=7AXIYQK5BBM)
Identify appropriate investigations for aortic dissection and interpret the results
You would do:
CT with angiography is the gold standard for diagnosing an aortic dissection. See intimal flap.
MRI imaging currently gold standard can be used to diagnose aortic dissection with high specifictiy for patients that are contraindicated for CT with angriography (E.G. renal insufficiency)
Bloods : FBC, cross-match 10 units of blood, U&E (renal function), clotting.
CXR: Widened mediastinum, localized bulge in the aortic arch.
ECG : Often normal. 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 (TOE, it’s ultrasound) is highly specific.
Cardiac catheterisation and aortography
Define cardiac failure (acute and chronic)
Inability of the cardiac output to meet the body’s demands despite normal venous pressures.
Explain the aetiology / risk factors of cardiac failure (acute and chronic)
LOW OUTPUT (i.e. the cause is reduced cardiac output):
- Left heart failure: ischaemic heart disease, HTN, cardiomyopathy, aortic valve disease, mitral regurg
- R 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 restrictive), myocarditis, drug toxicity
HIGH OUTPUT (i.e. the cause is increased demand). Anaemia, beriberi, 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 (symptoms caused by pulmonary congestion):
Dyspnoea (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 LVF: Dyspnoea, wheeze, cough and pink frothy sputum.
Right: Swollen ankles, fatigue, increased weight (resulting from oedema), reduced exercise tolerance, anorexia, nausea.
Recognise the signs of cardiac failure (acute and chronic) on physical examination
(left and right)
Left: Tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles, third heart sound ( “gallop” rhythm: rapid ventricular filling), pansystolic murmur (functional mitral regurgitation).
Acute LVF : Tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans, gallop rhythm, wheeze “cardiac asthma”, fine crackles throughout the lung.
Right: raised JVP, hepatomegaly, ascites, ankle/sacral pitting, oedema, signs of functional tricuspid regurgitation (see Tricuspid regurgitation).
Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results
Investigations:
Echocardiogram: To assess ventricular contraction. If left ventricular ejection fraction (LVEF) < 40%: systolic dysfunction. Diastolic dysfunction: reduced compliance leading to a restrictive filling defect.
- Blood: FBC, U&Es, LFTs, CRP, glucose, lipids, TFTs.
In acute LVF: ABG, troponin, brain natriuretic peptide (BNP). Raised Plasma BNP suggests the diagnosis of cardiac failure. A low plasma BNP rules out cardiac failure (90% sensitivity).
CXR (in acute LVF): ABCDE. A= alveolar oedema B= kerley B lines C=cardiomegaly D= upper lobe Diversion E=pleural Effusion
“bat’s wings” perihilar shadowing
ECG: May be normal. May have ischaemic changes, arrhythmia, left ventricular hypertrophy (seen in hypertension).
Swan–Ganz catheter: Allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures.
Generate a management plan for cardiac failure (acute and chronic)
Acute heart failure (from DPD):
-Sit up, o2, IV furosemide, GTN infusion
Pulmonary oedema: sit up patient, 60-100% o2, consider CPAP. Other 1st line are diamorphone (venodilator and anxiolytic), GTN infusion (reduces preload), IV furesomide (venodilator and later diuretic). Monitor BP, RR, sat o2, urine output, ECG. Treat cause
Chronic LVF: treat cause e.g. HTN. Treat exacerbating factors e.g. anaemia.
Drug therapies: ACEi; b blockers; loop diuretics; aldosterone antagonists; ARBs; hydralazine and a nitrate, digoxin and n-3 polyunsaturated fatty acids.
Cardiac resyndronisation therapy (CRT)
Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil) (note this is why you use digoxin instead of a CCB in treatment of AF in patients with heart failure- CCB is contraindicated!)
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)
Fifty per cent of patients with severe heart failure die within 2 years.
Mechanism of action of following for use in cardiac failure: ACEi, b blockers loop diuretic aldosterone antagonists Hydralazine and a nitrate Digoxin n-3 polyunsaturated fats
see rapid medicine page
Define pericarditis
Constrictive?
Inflammation of the pericardium, may be acute, subacute or chronic.
Constrictive pericarditis is a chronic condition characterized by a thickened, fibrotic pericardium, limiting the heart’s ability to function normally
The pericardium is a double-walled sac containing the heart and the roots of the great vessels. The pericardial sac has two layers, a serous layer and a fibrous layer
Explain the aetiology / risk factors of pericarditis
Overall categories
Idiopathic;
Viral infection is the most common cause of acute pericarditis and accounts for 1-10% of cases
infective (especially, coxsackie B and influenza. Also echovirus, mumps virus, streptococci, fungi, staphylococci, TB);
DURING FLARE UPS connective tissue disease (e.g. sarcoid, SLE, scleroderma, rheumatoid);
post-myocardial infarction (24– 72 h) in up to 20% of patients;
Dressler’s syndrome (weeks to months after acute MI=when contents of damaged cardiomyocytes released into circulation due to MI, there is an AI response against it cause dresslers’s);
malignancy (lung, breast, lymphoma, leukaemia, melanoma);
metabolic (myxoedema, uraemia);
radiotherapy;
thoracic surgery;
drugs (e.g. hydralazine, isoniazid).
Mnemonic:
CARDIAC, but without As
C=cancer A= nil R=radiotherapy D=dressler's syndrome, drugs I=infection A=nil C=connective tissue diseases
Summarise the epidemiology of pericarditis
Uncommon, <1 in 100 admissions. More common in males
Recognise the presenting symptoms of pericarditis
Chest pain: sharp and central, which may radiate to back or shoulder. Aggravated by coughing, deep inspiration and lying flat.
Relieved by sitting forward. This position (seated, leaning forward) tends to reduce pressure on the parietal pericardium, particularly with inspiration.
Dypnoea, nausea
Recognise the signs of pericarditis on physical examination
(how best heard)
What about if it leads to: cardiac tamponade, what about constrictive pericarditis
Fever (if due to flu)
pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration),
heart sounds may be faint in the presence of an effusion.
If cardiac tamponade: raised JVP, reduced BP and muffled heart sounds (Beck’s triad). Tachycardia, pulsus parodoxus.
Constrictive pericarditis (chronic): raised JVP with inspiration (Kussmaul’s sign), pulsus paradoxus, hepatomegaly, ascites, oedema, pericardial knock (rapid ventricular filling), AF
Identify appropriate investigations for pericarditis and interpret the results
ECG:
- Widespread saddle shaped ST elevation
- Shallow T-wave inversion may also be seen when adjacent cardiac muscle is affected by the inflammatory process (then strictly a ‘myopericaditis’)
Echocardiogram: for assessment of pericardial effusion and cardiac function
Blood: FBC, U&E, ESR, CRP, cardiac enzymes (usually normal, can be mildly elevated with myopericarditis). Repeat troponin to exclude myocardial insult.
Where appropriate: blood cultures, ASO titres, ANA, rheumatoid factor, TFT, Mantoux test, viral serology.
CXR: Usually normal (globular heart shadow if > 250 mL effusion). Pericardial calcification can be seen in constrictive pericarditis (best seen on lateral CXR or CT).
Generate a management plan for pericarditis
Extra considerations about physical activity?
Acute pericarditis is often self-limited but NSAIDs can alleviate symptoms and prevent a recurrence
Acute : Cardiac tamponade treated by emergency pericardiocentesis.
Medical : Treat the underlying cause, NSAIDs for relief of pain and fever.
Consider prednisolone only in severe cases or if caused by uraemia, connective tissue disease or autoreactivity
Recurrent : Low-dose steroids, immunosuppressants or colchicine.
Surgical: Surgical excision of the pericardium (pericardiectomy) in constrictive pericarditis.
Physical activity:
-Athletes: until symptoms have resolved, CRP has normalized, and ECG and echocardiogram findings have normalized
Non-athletes: until symptoms have resolved and CRP has normalized
Identify the possible complications of pericarditis and its management
Pericardial effusion, cardiac tamponade, cardiac arrythmias.
Some forms of acute pericarditis can lead to a chronic constrictive pericarditis, which in turn can lead to heart failure because of chronic, limited ventricular filling, caused by the thickened and inflexible pericardium.
Summarise the prognosis for patients with pericarditis
depends on underlying cause. Good prognosis in viral cases (recovery within ~2 weeks), poor in malignant pericarditis. Pericarditis may be recurrent (particularly in those caused by thoracic surgery).
Define pulmonary hypertension
A consistently increased pulmonary arterial pressure ( > 20 mmHg) under resting conditions.
Explain the aetiology / risk factors of pulmonary hypertension
Primary : Idiopathic.
Secondary :
Left heart disease (mitral valve disease, left ventricular failure, left atrial myxoma/ thrombosis),
chronic lung disease (COPD),
recurrent pulmonary emboli,
Increased pulmonary blood flow (ASD, VSD, patent ductus arteriosus),
connective tissue disease (e.g. SLE, systemic sclerosis),
drugs (e.g. amiodarone).
Summarise the epidemiology of pulmonary hypertension
Primary pulmonary hypertension is usually seen in young females.
Recognise the presenting symptoms of pulmonary hypertension
Dyspnoea (on exertion),
chest pain,
syncope,
tiredness,
symptoms of the underlying cause (e.g. chronic cough)
Recognise the signs of pulmonary hypertension on physical examination
Raised JVP (prominent a wave in the JVP wave form
Palpation: Left parasternal heave (right ventricular hypertrophy)
Auscultation:
- Loud pulmonary component of S2 (S3/4 may be heard)
- Early diastolic murmur (Graham-Steell murmur) caused by pulmonary regurgitation (due to weak pulmonary valve)
- If tricuspid regurg develops, vould be large cv wave and pansystolic murmur
Identify appropriate investigations for pulmonary hypertension and interpret the results
CXR: Cardiomegaly (right ventricular enlargement, right atrial dilation), prominent main pulmonary arteries (which taper rapidly), signs of the cause (COPD, calcified mitral valve)
ECG: Right ventricular hypertrophy (right-axis deviation, prominent R wave in V1 , T inversion in V 1 , V 2), right atrial enlargement (peaked P wave in II, called ‘P pulmonale’); limb leads exhibit low voltage (R < 5 mm) in COPD.
Echocardiography: To visualise ventricular hypertrophy or dilation and possible underlying cause
Lung function tests: to assess for chronic lung disease
VQ scan: to assess for pulmonary embolism
Cardiac catheterisation: assess severity, right heart pressures and response to vasodilators
High resolution CT thorax: images pulmonary arteries and to diagnose lung disease
Lung biopsy: to assess structural lung changes
Why might an ASD cause pulmonary HTN
An ASD is characterised by a left-to-right shunt with volume overload of the right heart and pulmonary overcirculation. This might result in arrhythmias, right heart failure, pulmonary arterial hypertension, and paradoxical embolism, the last mentioned due to a right-to-left shunt
Why might a left atrial myxoma cause pulmonary HTN?
When situated in the left side of the heart, they may cause symptoms of left atrial outflow obstruction such as pulmonary hypertension.
Why does COPD cause pulmonary HTN
In patients with COPD, pulmonary artery pressure increases due to pulmonary vascular remodeling, which is caused by the combinations of hypoxia, inflammation, and loss of capillaries in severe emphysema.
CTPA vs V/Q scan for assessment of PE
VQ scans are often preferred during pregnancy because they give a lower radiation dose to your breast tissue (which is more sensitive than usual to radiation during pregnancy). However, a CTPA scan will give a smaller radiation dose to your baby, and it can be more accurate in detecting blood clots in your lung.
Define mitral regurgitation
Explain the aetiology / risk factors of mitral regurgitation
Retrograde flow of blood from the left ventricle back into the left atrium during systole
Aetiology:
- Mitral valve prolapse (most common)
This happens because the connective tissue of the leaflets and surrrounding tissue (Including the papillary muscles and the chordae tendineae) is weakened. Known as myxomatous degeneration.
That can be caused by connective tissue diseases:
-Marfans, ehlers danlos syndrome
It results in increased leaflet area and length of chordae tenineae, which can rupture (especially in posterior leaflet)
- Functional mitral regurgitation may be secondary to left ventricular dilation.
- Mitral valve damage/dysfunction
- Rheumatic heart disease (most common)
- Infective endocarditis
- Mitral valve prolapse (prolapse of mitral valve leaflets into the left atrium during systole)
- Papillary muscle rupture of dysfunction (secondary to ischaemic heart disease or cardiomyopathy)
- chordal rupture and floppy mitral valve associated with connective tissue diseases
(e.g. pseudoxanthoma elasticum, osteogenesis imperfecta, Ehlers– Danlos syndrome, Marfan syndromes, SLE).
Drugs like appetite suppressants (fenfluramine, phentermine)
Summarise the epidemiology of mitral regurgitation
Affects 5% of adults. Mitral valve prolapse is more common in young females
Recognise the presenting symptoms of mitral regurgitation
In acute MR, chronic MR and mitral valve proplapse?
A complication related to MR?
Acute MR: may present with symptoms of left ventricular failure
Chronic MR: May be asymptomatic or present with exertional dyspnoea, palpitations if in AF (AF is a complication of MR that can occur because the extra blood in right atrium causes it to enlarge, and an enlarged atrium may develop a rapid and disorganized movement) and fatigue
Mitral valve prolapse: asymptomatic or atypical chest pain or palpitations
Recognise the signs of mitral regurgitation on physical examination
Pulse may be normal or irregularly irregular (if they are in AF)
Apex beat may be laterally displaced and thrusting (because left ventricular dilation may be the CAUSE of the mitral regurg)
Pansystolic murmur, loudest at apex, radiating to axilla (palpable as a thrill). S1 is soft, S3 may be heard (rapid ventricular filling in early diastole)
Signs of left ventricular failure in acute mitral regurgitation
In mitral valve prolapse: mid systolic click and late systolic murmur. The click moves towards the first hearts sound on standing and moves away on lying down.
Identify appropriate investigations for mitral regurgitation and interpret the results
ECG: Noraml or may show AF or broad bifid p wave (p mitrale) indicating delayed activation of left atrium due to left atrial enlargement
CXR: Acute mitral regurgitation may produce signs of left ventricular failure. Chronic mitral regurgitation shows left atrial enlargement, cardiomegaly (caused by left ventricular dilation) or mitral valve calcification in rheumatic cases.
Echocardiography : Every 6– 12 months for moderate– severe MR to assess the LV ejection fraction and end-systolic dimension.
Management:
Surgical : Indicated in patients with chronic MR with symptoms or LV enlargement or dysfunction, pulmonary hypertension, or new-onset AF.
Define rheumatic fever
An inflammatory multisystem disorder occurring following group A b-haemolytic streptococci (GAS) infection.
A complication of <1% streptococcal pharyngitis, developing 2-3 weeks after onset of sore throat
Occurs in children and young adults (first attack usually between 5 and 15 years old)
Explain the aetiology / risk factors for rheumatic fever
Thought to develop because of an AI reaction triggered by streptococci (as it is a complication of <1% streptotoccal pharyngitis).
IT IS NOT THE RESULT OF A DIRECT INFECTION TO THE HEART
Molecular mimicry is thought to play an important role in the initiation of the tissue injury (antibodies directed against GAS antigens cross-react with host antigens)
Summarise the epidemiology of rheumatic fever
Occurs in children and young adults (first attack usually between 5 and 15 years old)
Incidence in developed countries has decreased dramatically since 1920
Recognise the presenting symptoms of rheumatic fever
2-5 weeks after GAS infection:
Presents suddenly
General: fever malaise, anorexia
Joints: Painful, swollen, reduced function
Cardiac: Breathless, chest pain, palpitations
Loss of appetite
Recognise the signs of rheumatic fever on physical examination
What is the skin manifestation
Joints-arthritis
O(looks like a heart)- carditis (tachycardia, murmurs)
N-subcut Nodules,
Erythema marginatum (rash with red, raised edges and clear centre)
Sydenhams’s chorea (involuntary, semi-purposeful movements)
AUSCULTATION: mitral stenosis and aortic regurg are the most common mumurs caused by rheumatic fever
Identify appropriate investigations for rheumatic fever and interpret the results
First: ESR and CRP, WCC (elevated), blood culture (NEGATIVE- do if you suspect infective endocarditis)
ECG (prolonged PR interval), chest x-ray (CCF), echo
Throat culture (usually no longer positive), rapid antigen test froup GAS, anti-streptococcal titre
Bloods: FBC (raised WCC), ESR/CRP raised, raised or rising ANTISTREPTOLYSIN O TITRE
Throat swab: culture for GAS, rapid streptococcal antigen test
ECG: saddle shaped ST elevation and PR segment depression/increased (features of pericarditis) + arrhythmias
Echocardiogram: pericardial effusion, myocardial thickening, valvular dysfunction. Stenoses are late complications
PLEASE SEE JONES’ CRITERIA BELOW
NOTE : Clubbing/hepatosplenomegaly occur in infective endocarditis NOT rheumatic fever
Management: strict bed rest for around 4 months. High dose aspirin.IM dose of benzylpenicillin followed by oral penicillin is needed for primary treatment of streptococcal infection, and then long term to all patients with persistent cardiac damage
DIAGNOSIS: recent strep infection AND 2 major, or 1 major AND 2 minor criteria.
Define pulmonary embolism
Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site.
Explain the aetiology / risk factors of pulmonary embolism
Thrombus ( > 95% originating from DVT of the lower limbs and rarely from right atrium in patients with AF).
Other agents that can embolize to pulmonary vessels include:
- amniotic fluid embolus,
- air embolus,
- fat emboli,
- tumour emboli and
- mycotic emboli from right-sided endocarditis. (this would make a good SBA!)
Groups at risk include: surgical patients, immobility, obesity, OCP, heart failure, malignancy.
Summarise the epidemiology of pulmonary embolism
Relatively common, especially in hospitalized patients, they occur in 10– 20% of those with a confirmed proximal DVT.
Recognise the presenting symptoms of pulmonary embolism
Small?Moderate?Large (or proximal)?Multiple small recurrent?
Small: May be asymptomatic.
Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain.
Large (or proximal): All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death.
Multiple small recurrent: Symptoms of pulmonary hypertension.,
Recognise the signs of pulmonary embolism on physical examination
Small: often no clinical signs
Moderate: Tachypnoea, tachycardia, pleural rub, low o2 sats
Massive PE: shock, cyanosis, signs of right heart strain (raised JVP, parasternal heave, accentuated S2 heart sound)
Multiple recurrent PE: signs of pulmonary HTN and right sided heart failure
Identify appropriate investigations for pulmonary embolism and interpret the results
What are the x ray and ecg signs
You need to calculate a well’s score:
- clinical signs and symptoms of DVT
- PE is #1 diagnosis or equally likely
- Heart rate>100
- Immobilisation at least 3 days or surgery last 4 weeks
- Previous, objectively diagnosed PE/DVT
- Haemoptysis
- Malignancy w/treatment within 6 months or palliative
Normally if score is low you;d do a d-dimer and if it’s high then you’d do a CTPA (1st line investigation of choice, but small sensitivity for small emboli)
VQ scan: Administration of IV 99mTc macro-aggregated albumin and inhalation of 81 krypton gas. NOT suitable if abnormal CXR or coexisting lung disease
Pulmonary angiography is GOLD STANDARD but rarely necessary!!!!!!!
Doppler USS of lower limb
Echocardiogram
Additional investigations:
- Bloods: ANG, consider thrombophilia screen
- ECG: may be normal, show tachycardia, RAD or RBBB, the CLASSICAL SI, QIII, TIII pattern relatively uncommon
- Simultaneous T wave inversions in the inferior (II, III, aVF) and right precordial leads (V1-4) is the most specific finding in favour of PE
CXR TO EXCLUDE other diagnoses….
May have: Hamptoms hump (peripheral wedge of opacity)
Westermark sign (regional oligaemia)
Fleishner sign (enlarged pulnonary artery)
Generate a management plan for pulmonary embolism
..
Identify the possible complications of pulmonary embolism and its management
Death, pulmonary infarction, pulmonary hypertension, right heart
Summarise the prognosis for patients with pulmonary embolism
Thirty percent untreated mortality, 8% with treatment (due to recurrent emboli or underlying disease). Patients have “ risk of future thromboembolic disease.
Comment on the sensitivity and specificity of d-dimer
Highly sensitive but not very specific
A patient with a blood culture indentifying group D streptococcal, gamma haemolytic and optochin resistant infective agent and mitral valve vegitations have what
What other tests need to be done
Likely have an infection with Streptococcus Bovis.
It is a clinically important cause of bacteraemia and infective endocarditis.
GI tract is the most likely portal of entry
GDS bacteraemia associated with liver disease, primarily related to compromised liver function in the setting of Hep C/cirrhosis, and can lead to spontaneous bacterial peritonitis.
Also a link between S Bovis and colonic neiplasia or diverticulitis
So they would need to ve evaluated for colonic and liver disease
Treat with penicillin adn ceftriaxone
How is streptococcus viridans differentiated from streptococcus pneumonia
Strep viridans and strep pneumoniae are both beta haemolytic.
However, viridans is optochin resistant and bile insoluble, whereas s pneumoniae die with optochin and are bile soluble
Infective endocarditis is associated with which pathogen in the following cases:
i. Recent dental procedures involving manipulation of the gingiva
ii. Urinary tract infection
iii. Recent mitral valve replacement
iv. IVDU
v. Spontaneous bacterial peritonitis
i. Viridans streptococci (it’s own group)
ii. Enterococci faecalis cause 5-20% of IEs. Most frequent sauce of infection is genitourinary tract. Can affect normal and previously damaged heart valves
iii. Within 2 months of implantation, prosthetic valve endocarditis is most often caused by S Aureus and coagulase negative staphylococci such as S epidermidis
iv. The affected valve is usually right-sided. S. aureus is the most common agent.
iv. Streptococcus bovis (group D streptotoccus) species that displays γ hemolysis and optochin resistance when cultured from a blood sample.
What causes damage to heart and valves in rheumatic fever
A type II hypersensitivity reaction to the M protein damages the heart and valves. M protein binds with factor H to decrease complement activation.
Which pathogens are associated with the following, and what virulence factor does it therefore cause:
i. ADP-ribosylates Gi thereby increasing cAMP
ii. Activates T cells to release IFN-gamma and IL-2
iii. Binds with factor H to decrease complement activation
iv. Causes an exfoliative rash
v. inactivates elongation factor 2
i. The toxin of Bordetella pertussis ADP-ribosylates Gi, inactivating it and thereby increasing cAMP. This leads to the characteristic symptom whooping cough.
ii. Staphylococcus aureus makes toxic shock syndrome toxin-1, which is a superantigen that activates T cells to release interferon-gamma and IL 2.
iii. Rheumatic fever is an inflammatory disease that typically develops two to four weeks after a throat infection with Streptococcus pyogenes. A type II hypersensitivity reaction to the M protein damages the heart and valves. M protein binds with factor H to decrease complement activation.
iv. Staphylococcus aureus also makes exfoliative toxins A and B, which cause scalded-skin syndrome, a condition seen most often in infants. It often looks worse than it really is.
v. Corynebacterium diphtheriae toxin ADP-ribosylates elongation factor 2. This interrupts protein synthesis, which kills the host cells and creates a mat of debris (pseudomembrane) in the oropharynx.
What condition is associated with mitral valve prolapse
Mitral valve prolapse (MVP) is the most common valvular defect in the United States, and 15-40% of people with panic disorder have associated mitral valve prolapse
Patent ductus arteriosus is associated with which murmur
Can cause a continuous “machine-like” murmur which is accentuated in systole. Gibson.
Define cardiomyopathy
Primary disease of the myocardium.
1) Dilated
2) Hypertrophic
3) Restrictive
Explain the aetiology / risk factors of cardiomyopathy
Majority idiopathic
Dilated: post-viral myocarditis, alcohol, drugs (doxorubicin, cocaine), familial (usually autosomal dominant), thryotoxicosis, haemochromatosis, peripartum
Hypertrophic: Up to 50% of cases are genetic (autosomal dominant) with mutations in b -myosin, troponin T or a -tropomyosin (components of the contractile apparatus).
Restrictive: Amyloidosis, sarcoidosis, haemochromatosis.
Summarise the epidemiology of cardiomyopathy
Restrictive rare
Recognise the presenting symptoms of cardiomyopathy
Dilated: Heart failure signs, FHx of sudden death, thromboembolism, arrythmias
Hypertrophic: Usually none. Syncope, angina, arrhythmias, family Hx sudden death
Restrictive: Dyspnoea, fatigue, arrhythmias, ankle/abdo swelling
Recognise the signs of cardiomyopathy on physical examination
.Dilated: Raised JVP, displaced apex beat, functional mitral and tricuspid, 3rd HS.
Hypertrophic: jerky carotid pulse, double apex beat, ESM
Restrictive: raised JVP (jussmaul’s sign, further increase on inspiration), palpable apex beat, 3rd HS, ascites, ankle oedema, hepatomegaly
Identify appropriate investigations for cardiomyopathy and interpret the results
CXR : May show cardiomegaly, and signs of heart failure.
ECG :
All types : Non-specific ST changes, conduction defects, arrhythmias
Hypertrophic : Left-axis deviation, signs of left ventricular hypertrophy ( see Aortic stenosis), Q waves in inferior and lateral leads.
Restrictive : Low voltage complexes.
Echocardiography :
Dilated : Dilated ventricles with ‘global’ hypokinesia.
Hypertrophic: Ventricular hypertrophy (disproportionate septal involvement)
Restrictive: Non-dilated non-hypertrophied ventricles. Atrial enlargement, preserved systolic function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium in amyloidosis.
Cardiac catheterization : May be necessary for measurement of pressures.
Endomyocardial biopsy : May be helpful in restrictive cardiomyopathy.
Pedigree or genetic analysis : Rarely necessary.
Define aortic regurgitation
What is acute AR
Reflux of blood from aorta into left ventricle (LV) during diastole. Aortic regurgitation (AR) is also called aortic insufficiency.
In acute AR, the LV cannot adapt to the rapid increase in end-diastolic volume caused by regurgitant blood.
Explain the aetiology / risk factors of aortic regurgitation
- Aortic valve leaflet abnormalities or damage:
- Bicuspid aortic valve, IE, rheumatic fever, trauma - Aortic root/ascending aorta dilation
- Systemic hypertension, aortic dissection, aortitis (e.g. syphilis, Takayasu’s arteritis), arthritides (rheumatoid arthritis, seronegative arthritides), Marfan’s syndrome, pseudoxanthoma elasticum, Ehlers– Danlos syndrome, osteogenesis imperfecta.
Summarise the epidemiology of aortic regurgitation
Often begins in late 50s, documented most frequently in patients >80yo
Recognise the presenting symptoms of aortic regurgitation
Chronic AR: Initially asymptomatic.
Later, HF symptoms: exertional dyspnoea, orthopnea, fatigue. Occasionally angina
Sever acute AR: sudden cardiovascular collapse
Recognise the signs of aortic regurgitation on physical examination
Collapsing water hammer pulse and wide pulse pressure .
Thrusting and heaving (heavy loaded) displaced apex beat
Early decrescendo diastolic murmur at lower left sternal edge, better heard with patient SITTING FORWARD with the breath held in expiration. Ejection systolic murmur often heard due to increased flow across the valve.
Austin flint mid-diastolic murmur (see box below on what that is)
Identify appropriate investigations for aortic regurgitation and interpret the results
CXR: Cardiomegaly. Dilation of ascending aorta. Signs of pulmonary oedema with left heart failure
ECG: Signs of left ventricular hypertrophy (deep S wave in V1-2, tall R wave in V5-6, inverted T waves in I, aVL, v5-6 and left axis deviation)
Echocardiogram: 2D echo and M-mode may indicate underlying cause (e.g. aortic root dilation, bicuspid aortic valve) ro effects of AR (LV dilation/dysfunction and fulttering of the anterior mitral valve leaflet).
Doppler echocardiogram for detecting AR and assessing severity
Cardiac catheterisation with angriography: if there is uncertainty about functional state of teh ventricle or the presence of coronary artery disease
What might explain the collapsing pulse and wide pulse pressure in aortic regurgitation
Reflux of blood into the LV during diastole results in left ventricular dilation and increased end-diastolic volume and increased stroke volume.
The combination of increased stroke volume and low end-diastolic pressure in the aorta may explain the collapsing pulse and the wide pulse pressure. In acute AR, the LV cannot adapt to the rapid increase in end-diastolic volume caused by regurgitant blood.
Differentiate the type of hypertrophy in aortic stenosis vs regurgitation
Stenosis= concentric (new sarcomeres deposited in parallel)
Regurg: eccentric (new sarcomeres deposited side by side)
Which condition gives you canon waves
3rd degree heart block
Canon wave happens when, in 3rd degree heart block, the ventricle is contracting at the same time as the atria.
The ventricles cause the AV valves to close. When the atria contract against the closed AV valve, the blood can only flow back into the venous system. Which causes a canon pulse in the neck
What is fibrinoid necrosis and when can it occur
Fibrinoid necrosis is an inflammatory type of tissue death as a result of immune reactions in vessels. Immune complexes combine with fibrin to cause vessel wall damage.
It is seen in a number of vasculitis diseases and is often a result of malignant hypertension.
T/F A split S2 in aortic stenosis can rule out severe aortic stenosis
In patients with severe stenosis, but not so severe as to lose the sound of the closing aortic valve (A2), the S2 sound may be paradoxically split as the stenotic valve is delayed and closes after the pulmonary one (P2).
If there was severe aortic stenosis, it would lose the closing sound such that there would be no split S2 (just S2 coming from pulmonary)
The presence of a normal split S2 is sensitive enough to rule out severe aortic stenosis in adults.
Describe the carotid pulse in aortic stenosis
The stiff aortic valve leaflets impede outgoing blood flow and are slow to close.
PARVUS ET TARDUS
In this way, the amplitude of carotid pulse is characteristically diminished (parvus) and delayed from the contraction of the heart (tardus), which can be detected with simultaneous palpation of the point of maximal impulse
Rheumatic heart disease has a strong assocation with which murmurs?
Rheumatic heart disease has a strong association with mitral stenosis and aortic regurgitation murmurs.
Major cause of aortic stenosis, and when it manifests
Aortic stenosis is related to age related calcification.
It usually doesn’t cause symptoms until ages 70 or 80, but would be earlier if there was a bicuspid aortic valve
What are the classic findigns on ecg in left ventricular hypertrophy
The classic findings in LVH are an increased R-wave amplitude in the left-sided ECG leads (I, aVL, V4-V6) and increased S-wave depth in the right-sided leads (III, aVR, V1-V3)
How does diabetes cause atherosclerosis
The mechanism by which diabetes is thought to induce atherosclerotic disease is through hyperglycemic damage to the intimal layer of arteries.
Define infective endocarditis
Infection of intracardiac endocardial structures (mainly heart valves).
Explain the aetiology of infective endocarditis
Most common cause in IVDU?
Talk about the effect of the bacteria on the valves
Can be colonised by virtually any organism. Commonest:
- Streptococci (mainly alpha haemolytic strep viridans or group D beta haemolytic strep bovis)
- Staphylococcus: mainly staph aureus and occasionally staph epidermidis (in IVDU, BUT it is not most common causative organism in this group)
- Enterococci : usually enterococcus faecalis.
4. Other organisms: Haemophilus/Histoplasma Actinobacillus Cardiobacterium/Coxiella burnetii Eikenella Kingella
Most common in IVDU is staph aureas
Vegetations form as a result of lodging of the organisms on the heart valves during a period of bacteraemia. These vegetations are made up of platelets, fibrin and infective organisms and are poorly penetrated by the cellular or humoral immune system. Vegetations proceed to destroy the valve leaflets, invade the myocardium or aortic wall leading to abscess cavities.
Activation of the immune system also causes formation of immune complexes leading to cutaneous vasculitis, glomerulonephritis or arthritis.
Summarise the epidemiology of infective endocarditis
.
Recognise the presenting symptoms of infective endocarditis
Fever with sweats/chills/rigors (may be relapsing and remitting).
Persisting fever despite Abx treatment
Malaise, arthralgia, myalgia, confusion (particularly in elderly). Skin lesions.
Inquire about recent dental surgery or IV drug abuse.
Recognise the signs of infective endocarditis on physical examination
Frequency of valves affected by IE
Pyrexia, tachycardia, signs of anaemia
Clubbing (if long standing)
New regurgitant murmur or muffled heart sounds (right sided lesions may imply IV drug use)
Frequency: Mitral > aortic > tricuspid > pulmonary.
Splenomegaly
Vasculitic lesions: Ptechiae particularly on retinae (Roth’s spots), pharyngeal and conjunctival mucosa
Janeway lesions (PANLESS palmar macules, blanch on pressure)
Osler’s nodes (tender nodules on finger/toe pads);
Splinter haemorrhages (nail bed)
Identify appropriate investigations for infective endocarditis and interpret the results
When MIGHT an ECG be useful
Why might you want to do a CXR, and in which valve IE in particular
BLOOD:
FBC (raised neutrophils, normocytic anaemia; raised ESR and CRP, U&Es, rheum factor +ve!)
URINALYSIS:
Microscopic haematuria, proteinuria
BLOOD CULTURE:
At least three sets 1 h apart (ensure aseptic technique). Culture and sensitivity is vital, but empirical treatment should be started first. Cultures remain negative in 2– 5%.
ECHOCARDIOGRAPHY: Transthoracic. Transoesophageal echocardiography is much more sensitive for the detection of endocarditis; especially useful for the detection of vegetations and valve abscess, diagnosis of prosthetic valve endocarditis and assessment of embolic risk.
Other investigations: ECG (abscesses can cause conduction changes); CXR (septic pulmonary emboli: focal lung infiltrates +/- central vacitation, particularly in tricuspid valve endocarditis
Generate a management plan for infective endocarditis
What should you give to a patient with history of IE if undergoing dental procedure
Abx for 4-6 weeks, or at least 6 weeks if prosthetic valve endocarditis
On clinical suspicion (empirical treatment): benzylpenicillin + gentamicin (adjust dose for peak serum level of 3-4micrograms/mL and trough less than 1 micrograms/ml)
If found to be:
Strep–> continue with the benzyl + gent
Staph–> flucloxacillin/vanc + gent (for prosthetic valves, vancomycin + gentamicin + rifampin)
Enterococci: ampicillin or ceftriaxone + gent
Culture neg: vancomycin + gentamicin
Surgery
If poor response of deterioration, urgent valve replacement indicated. Surgical replacement of prostheses. In kissing mitral valve vegetations, mitral valve may be salvageable
Prophylactin Abx
Patients with a history of infective endocarditis undergoing high risk procedures: Dental, incision or biopsy of respiratory mucosa, procedures in patients with GI/GU tract infection, procedures on infected skin or musculoskeletal tissue, prosthetic heart valve placement. For patients undergoing a dental procedure: 2 g oral amoxicillin 30– 60 min before the procedure.
Identify the possible complications of infective endocarditis and its management
Valve incompetence,
intracardiac fistulae or abscesses,
aneurysm formation,
heart failure.
Renal failure,
glomerulonephritis.
Arterial emboli from the vegetations (brain, kidneys, lungs, spleen)
Summarise the prognosis for patients with infective endocarditis
Fatal if untreated. Even when treated, 15– 30% mortality.
List the risk factors for infective endocarditis
S bovis is associated with which condition
- Abnormal valves (e.g. congenital, post-rheumatic, calcification/degeneration)
- Recent dental work
- Prosthetic valves
- Turbulent flow (PDA or VSD)
- S. bovis may be associated with GI malignancy.
What is the Duke’s classification of diagnosis of endocarditis
2 major, 1 major and 3 minor, or all minor is diagnostic of andocarditis
Major criteria: Positive blood culture in 2 separate samples. Positive echocardiogram (vegetation, abscess, prosthetic valve dehiscence, new valve regurg)
Minor criteria: high grade pyrexia (>38 degrees). Risk factors (abnormal valves, IV drug use, dental surgery. Positive blood culture, but not major criteria. Positive echocardiogram but not major criteria. Vascular signs
What is the normal QT interval
<1/2 of the cardiac cycle
OR
<440mS for men, or <460mS for women, at 60bpm
The QT interval changes depending on the HR, which is why the corrected QT interval (QTc) is used
Outline the normal ventricular cardiac cycle
Phase 4- Baseline
-K+ channels main determinant of resting potential as membrane mroe permeable to K+ than any other ion. They are open at rest.
Phase 0-Fast depolarisation
- Voltage gated Na+ channels open (positive feedback, which influx of Na+ causing more Na+ channels to open). Na channels inactivate immediately after opening.
Phase 1- Notch
-Transient opening K+ channels rapidly repolarise the cell, before the plateau phase.
Phase 2- Plateau
- L-type calcium channels open, allowing calcium to bind to RyR on SR, causing CICR.
- K+ channels are open allowing K+ to travel out which is why the membrane remains stable
Phase 3- Repolsarisation
-Ca2+ channels close, so K+ channels succeed in repolarising the cell. Na+ cells begin to recover from inactivation
What does a prolonged QT interval indicate.
Causes of long QT syndrome.
That some cells of the ventricle are taking longer to repolarise compared to neighbouring heart cells.
This is thought to be due to abnormaliites in the movements of ions into and out of cell.
Causes:
1. Congenital (genetic defects in ion channels. 10 defects, named LQT1-10)
- Some medications that interfere with ion channels (e.g. Class 1a antiarrhytmics, which block Na+ and K+ channels, and class III antiarrythmics that block K+ channels)
What arrythmia is associated with long QT syndrome and why
Ion channel dysfunction e.g. l-type calcium or Na+/K+ channels can cause EARLY AFTERDEPOLARISATION.
This means that during phase 2 there is another depolarisation that increases the membrane potential.
If the EAD is large enough it might depolarise the ventricles early, causing a premature ventricular contraction (PVC)
As some only some cells are affected by the ion channel problems, the early depolarisation will propogate through those cells that are ready. Then, when the cells that are not ready repolarise, the wave of depolarisation can double back, causing a reentrant tachycardia.
The specific type of reentrant tachycardia in long QT is called Torsade de Pointes
It’s a type of polymorphic VT because the QRS are of different shapes
What range of heart beat associated with torsade de pointes
What are the consequences
150-250bpm
It can revert spontaneously,
or it can have symptoms like palpitations, dizziness and syncome,
and it can lead to sudden cardiac death
What is the treatment for drug induced LQTS
Stop causative medication (if just long QT syndrome)
BUT, once torsades de pointes develops:
- treat immediately with magnesium sulfate, to suppress EAD or
- Use electrical pacing, or medications that increase the HR to reduce the QT interval
What to think if a young person comes in with symptoms of MI but no risk factors?
Prinzmetal (variant) angina should be suspected in a young patient without cardiovascular risk factors,
What increases risk of Prinzmetal (variant) angina
Medications can increase the risk of vasospasm (e.g. triptans, cocaine, amphetamines).
Treatment of variant angina
Treatment is different to that of traditional atherosclerotic STEMI or NSTEMI and involves the use of a calcium channel blocker to decreased vasospasm.
Why not give aspirin in variant angina
Aspirin in high doses inhibits prostacyclin production, thereby potentially worsening vasospasm.
However, low dose aspirin could be started in a patient with a high atherosclerotic risk profile.
What criteria are used to test for rheumatic fever. What are the major and minor features
Jones’ criteria:
Major criteria – carditis, cardiac murmur, subcutaneous nodule, arthritis (migratory large joints), erythema marginatum (red geographical rash), chorea (Sydenham’s, St Vitus dance);
Minor: fever, raised ESR/CRP, long PR interval, arthralgia
There must be recent evidence of streptococcal infection plus 2 major or 1 major and 2 minor manifestations to diagnose an acute primary episode of rheumatic fever.
Mitral stenosis most common cause
Scarring due to rheumatic fever
What kind of murmur does mitral stenosis cuase
There is a low rumbling diastolic murmur best heard at the apex with the bell of the stethoscope. Often preceded by an opening snap.
The opening snap may be soft or absent if the mitral valve is calcified; the snap moves closer to S2 (increasing duration of the murmur) as mitral stenosis becomes more severe and LA pressure increases.
What could happen to the p waves in somebody with mitral stenosis
Bifid P waves (because of left atrial enlargement)
No P waves (because mitral stenosis predisposes you to AF!)
The following types of waves are seen in which conditions: Peaked P waves (p pulmonale) Bifid p waves (p mitrale) U waves delta waves no p waves
Peaked P waves (p pulmonale)–> R atrial enlargement
Bifid p waves (p mitrale)–> L atrial enlargement
U waves–> hypokalaemia
delta waves–> Wolff parkinson white syndrome
no p waves–> AF
Define deep vein thrombosis (DVT)
Formation of thrombus in the deep veins, commonly of calf or thigh
Explain the aetiology / risk factors of deep vein thrombosis (DVT)
Oral contraceptive pill, surgery,
prolonged immobility,
long bone fractures,
obesity,
pregnancy,
dehydration,
smoking,
polycythaemia,
anti-phospholipid syndrome,
thrombophilia disorders (e.g. protein C deficiency),
active malignancy.
Summarise the epidemiology of deep vein thrombosis (DVT)
Common, especially in hospitalised patients; exact incidence unknown.
Recognise the symptoms and signs of deep vein thrombosis (DVT) on physical examination
Well’s score
Entire calf swollen
Paralysis/immobile leg
Calf circumference >3cm bigger than other leg at 10cm below tibial tuberosity
Tenderness along deep veins
Visible superficial collateral veins
Recent bed rest (>3 days) or surgery (within 12 weeks)
Other diagnosis more likely (minus two from score)
Pitting oedema
Active cancer
Identify appropriate investigations for deep vein thrombosis (DVT) and interpret the results
.You use the well’s score:
High > 3 Moderate 1– 2 Low < 1.
See ‘leg tenderness’ for more comprehensive information about when each of the following are done.
Doppler ultrasound: Gold standard. Good sensitivity for femoral veins; less sensitive for calf veins.
Bloods: D-dimers (fibrinogen degradation products) are sensitive but very non-specific and only useful as a negative predictor in low-risk patients.
If indicated (e.g. recurrent episodes), a thrombophilia screen should be sent, prior to starting anticoagulation.
FBC (platelet SEE WHY), U&E and clotting. ECG, CXR and ABG: If there is suggestion that there might be PE.
Generate a management plan for deep vein thrombosis (DVT)
How long should the patient be on anticoagulants if the clot is above vs below the knee
What if anticoagulants are contraindicated? When else would you do the same thing
Anticoagulation:
Patients should be treated with heparin while awaiting therapeutic INR from warfarin anticoagulation.
DVTs not extending above the knee treated with anticoagulation for 3 months, while those extending beyond the knee require anticoagulation for 6 months.
Recurrent DVTs may require long-term warfarin. If active anticoagulation is contraindicated and/or high risk of embolisation, placement of an IVC filter, e.g. Greenfield filter, by interventional radiology is indicated to prevent embolus to the lungs.
Prevention: Use of graduated compression stockings. Mobilisation if possible. At-risk groups (immobilised hospital patients) should have prophylactic heparin, e.g. low-molecularweight heparin if no contraindications.
Identify the possible complications of deep vein thrombosis (DVT) and its management
Venous insufficiency, ulceration
Of the disease: Pulmonary embolus, damage to vein valves and chronic venous insufficiency of the lower limb (post-thrombotic syndrome).
Rare: Venous infarction (phlegmasia cerulea dolens).
Of the treatment: Heparin-induced thrombocytopaenia, bleeding.
Summarise the prognosis for patients with deep vein thrombosis (DVT)
Having a clot where is worse, above or below knee?
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.
What must you check before giving somebody heparin and why
Thrombocytopenia has been associated with the use of intravenous heparin, but the effect of low-dose, subcutaneously administered heparin on the platelet count is not known.
What do you do to the warfarin dose when you put someone on Abx? Why
You reduce the dose
When a patient is placed on antibiotics, these medications may eliminate gut flora that produce vitamin K. The normal synthesis of the clotting factors thus may be reduced, thus increasing the PT.
How long does warfarin take to work?
Warfarin interferes with the normal synthesis of clotting factors in the liver, a process that depends on vitamin K. The appropriate course of action would be to decrease the dose of warfarin in this scenario. Vitamin K-dependent factors include factors II, VII, IX, and X.
Because these factors have half-lives of 8 to 60 hours in the plasma, an anticoagulant effect is observed only after sufficient time has passed for the preformed factors to be eliminated (i.e. >60hrs)
What is sinus arrhythmia and what causes it
Respiratory sinus arrhythmia is a normal physiological phenomenon, most commonly seen in young, healthy people. It is defined as sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P-waves), producing an irregular ventricular rate. It is caused by changes in vagal tone during the respiratory cycle.
The heart rate increases with inspiration, due to the Bainbridge reflex, and decreases with expiration.
What are the following heart rhythms related to:
1) Ventricular tachycardia
2) Multifocal atrial tachycardia
1) Related to ischaemia (seen in cardiac arrest)
2) Rapid irrefular atrial rhythm arising from multiple ectopic foci within the atria.
In seriously ill patients with resp failure. HR >100bpm, irregularly irregular rhythm, and at least 3 distinct P-wave morphologies in the same lead
