Cardiovascular

Question 1

Define gangrene compared to nectrotising fasciitis.

What are the 3 types of gangrene.

What is the cause of gas gangrene

Answer 1

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

Question 2

Explain the aetiology / risk factors of gangrene & necrotising fasciitis. Include the bugs that cause them

Type 1 vs type 2 necrotising fasciitis

Answer 2

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). 

2. 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

Question 3

Summarise the epidemiology of gangrene

Answer 3

Gas:

- Severe penetrating trauma or crush injuries associated with interruption of the blood supply

Question 4

Recognise the presenting symptoms of gangrene

Answer 4

loss of sensation or severe pain in the affected area

sores or blisters that bleed or release a dirty-looking or foul-smelling discharge

Question 5

Recognise the signs of gangrene on physical examination

Answer 5

redness and swelling
foul smelling discharge
crepitus when pressed, caused by gas under the skin

Question 6

Identify appropriate investigations for gangrene and interpret the results

Answer 6

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

Question 7

Define peripheral vascular disease. (chronic and then acute)

Answer 7

….

Question 8

Explain aetiology/risk factors of PVD (chronic and then acute)

Answer 8

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.

Question 9

Summarise epidemiology of PVD (chronic and then acute)

Answer 9

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.

Question 10

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

Answer 10

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

Question 11

Recognise the signs of PVD on physical examination (chronic and then acute)

Answer 11

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.

Question 12

Identify appropriate invesitgations for PVD (chronic and then acute)

Imaging

Answer 12

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

Question 13

Explain the ankle/brachial pressure index

When might the ABPI be wrong

Answer 13

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

Question 14

Management of PVD (chronic and then acute)

Answer 14

Chronic:

Risk factor management- even if cholesterol is normal, reducing it still reduces mortality from cardiovascular disease

Question 15

What ABPI values might suggest PVD, what about critical limb ischaemia

Answer 15

PVD can be diagnosed using ABPI:

0.5-0.9 = peripheral vascular disease;

< 0.5 =
critical limb ischaemia.

Question 16

Define arterial ulcer

Answer 16

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/

Question 17

Explain aetiology/risk factors of arterial ulcers

Answer 17

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

Question 18

Recognise presenting symptoms of arterial ulcer/signs of arterial ulcer on physical examination

Answer 18

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)

Question 19

Identify appropriate invesitgations for arterial ulcer

Answer 19

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).

Question 20

Identify management of arterial ulcer

Answer 20

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.

Question 21

Define aortic dissection

Answer 21

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)

Question 22

Explain the aetiology / risk factors of aortic dissection

Standard classification of aortic dissection

Answer 22

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.

Question 23

Summarise the epidemiology of aortic dissection

Answer 23

Most common in males between 40-60

Question 24

Recognise the presenting symptoms of aortic dissection

Answer 24

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)

Question 25

Signs of aortic dissection on physical examination

Answer 25

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)

Question 26

Identify appropriate investigations for aortic dissection and interpret the results

Answer 26

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

Question 27

Define cardiac failure (acute and chronic)

Answer 27

Inability of the cardiac output to meet the body's demands despite normal venous pressures.

Question 28

Explain the aetiology / risk factors of cardiac failure (acute and chronic)

Answer 28

LOW OUTPUT (i.e. the cause is reduced cardiac output): 1. Left heart failure: ischaemic heart disease, HTN, cardiomyopathy, aortic valve disease, mitral regurg 2. R heart failure: Secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade. 3. Biventricular failure : Arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug toxicity HIGH OUTPUT (i.e. the cause is increased demand). Anaemia, beriberi, pregnancy, Paget's disease, hyperthyroidism, arteriovenous malformation.

Question 29

Summarise the epidemiology of cardiac failure (acute and chronic)

Answer 29

10% of > 65-year-olds.

Question 30

Recognise the presenting symptoms of cardiac failure (acute and chronic)

Answer 30

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.

Question 31

Recognise the signs of cardiac failure (acute and chronic) on physical examination (left and right)

Answer 31

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).

Question 32

Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results

Answer 32

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. 1. 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.

Question 33

Generate a management plan for cardiac failure (acute and chronic)

Answer 33

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!)

Question 34

Identify the possible complications of cardiac failure (acute and chronic) and its management

Answer 34

Respiratory failure, cardiogenic shock, death.

Question 35

Summarise the prognosis for patients with cardiac failure (acute and chronic)

Answer 35

Fifty per cent of patients with severe heart failure die within 2 years.

Question 36

``` 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 ```

Answer 36

see rapid medicine page

Question 37

# Define pericarditis Constrictive?

Answer 37

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

Question 38

Explain the aetiology / risk factors of pericarditis Overall categories

Answer 38

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 ```

Question 39

Summarise the epidemiology of pericarditis

Answer 39

Uncommon, <1 in 100 admissions. More common in males

Question 40

Recognise the presenting symptoms of pericarditis

Answer 40

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

Question 41

Recognise the signs of pericarditis on physical examination (how best heard) What about if it leads to: cardiac tamponade, what about constrictive pericarditis

Answer 41

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

Question 42

Identify appropriate investigations for pericarditis and interpret the results

Answer 42

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).

Question 43

Generate a management plan for pericarditis Extra considerations about physical activity?

Answer 43

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

Question 44

Identify the possible complications of pericarditis and its management

Answer 44

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.

Question 45

Summarise the prognosis for patients with pericarditis

Answer 45

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).

Question 46

Define pulmonary hypertension

Answer 46

A consistently increased pulmonary arterial pressure ( > 20 mmHg) under resting conditions.

Question 47

Explain the aetiology / risk factors of pulmonary hypertension

Answer 47

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).

Question 48

Summarise the epidemiology of pulmonary hypertension

Answer 48

Primary pulmonary hypertension is usually seen in young females.

Question 49

Recognise the presenting symptoms of pulmonary hypertension

Answer 49

Dyspnoea (on exertion), chest pain, syncope, tiredness, symptoms of the underlying cause (e.g. chronic cough)

Question 50

Recognise the signs of pulmonary hypertension on physical examination

Answer 50

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

Question 51

Identify appropriate investigations for pulmonary hypertension and interpret the results

Answer 51

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

Question 52

Why might an ASD cause pulmonary HTN

Answer 52

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

Question 53

Why might a left atrial myxoma cause pulmonary HTN?

Answer 53

When situated in the left side of the heart, they may cause symptoms of left atrial outflow obstruction such as pulmonary hypertension.

Question 54

Why does COPD cause pulmonary HTN

Answer 54

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.

Question 55

CTPA vs V/Q scan for assessment of PE

Answer 55

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.

Question 56

# Define mitral regurgitation Explain the aetiology / risk factors of mitral regurgitation

Answer 56

Retrograde flow of blood from the left ventricle back into the left atrium during systole Aetiology: 1. 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) 2. Functional mitral regurgitation may be secondary to left ventricular dilation. 3. 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)

Question 57

Summarise the epidemiology of mitral regurgitation

Answer 57

Affects 5% of adults. Mitral valve prolapse is more common in young females

Question 58

Recognise the presenting symptoms of mitral regurgitation In acute MR, chronic MR and mitral valve proplapse? A complication related to MR?

Answer 58

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

Question 59

Recognise the signs of mitral regurgitation on physical examination

Answer 59

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.

Question 60

Identify appropriate investigations for mitral regurgitation and interpret the results

Answer 60

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.

Question 61

Define rheumatic fever

Answer 61

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)

Question 62

Explain the aetiology / risk factors for rheumatic fever

Answer 62

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)

Question 63

Summarise the epidemiology of rheumatic fever

Answer 63

Occurs in children and young adults (first attack usually between 5 and 15 years old) Incidence in developed countries has decreased dramatically since 1920

Question 64

Recognise the presenting symptoms of rheumatic fever

Answer 64

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

Question 65

Recognise the signs of rheumatic fever on physical examination What is the skin manifestation

Answer 65

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

Question 66

Identify appropriate investigations for rheumatic fever and interpret the results

Answer 66

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.

Question 67

Define pulmonary embolism

Answer 67

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site.

Question 68

Explain the aetiology / risk factors of pulmonary embolism

Answer 68

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. ```

Question 69

Summarise the epidemiology of pulmonary embolism

Answer 69

Relatively common, especially in hospitalized patients, they occur in 10– 20% of those with a confirmed proximal DVT.

Question 70

Recognise the presenting symptoms of pulmonary embolism Small?Moderate?Large (or proximal)?Multiple small recurrent?

Answer 70

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.,

Question 71

Recognise the signs of pulmonary embolism on physical examination

Answer 71

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

Question 72

Identify appropriate investigations for pulmonary embolism and interpret the results What are the x ray and ecg signs

Answer 72

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)

Question 73

Generate a management plan for pulmonary embolism

Answer 73

..

Question 74

Identify the possible complications of pulmonary embolism and its management

Answer 74

Death, pulmonary infarction, pulmonary hypertension, right heart

Question 75

Summarise the prognosis for patients with pulmonary embolism

Answer 75

Thirty percent untreated mortality, 8% with treatment (due to recurrent emboli or underlying disease). Patients have " risk of future thromboembolic disease.

Question 76

Comment on the sensitivity and specificity of d-dimer

Answer 76

Highly sensitive but not very specific

Question 77

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

Answer 77

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

Question 78

How is streptococcus viridans differentiated from streptococcus pneumonia

Answer 78

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

Question 79

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

Answer 79

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.

Question 80

What causes damage to heart and valves in rheumatic fever

Answer 80

A type II hypersensitivity reaction to the M protein damages the heart and valves. M protein binds with factor H to decrease complement activation.

Question 81

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

Answer 81

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.

Question 82

What condition is associated with mitral valve prolapse

Answer 82

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

Question 83

Patent ductus arteriosus is associated with which murmur

Answer 83

Can cause a continuous "machine-like" murmur which is accentuated in systole. Gibson.

Question 84

Define cardiomyopathy

Answer 84

Primary disease of the myocardium. 1) Dilated 2) Hypertrophic 3) Restrictive

Question 85

Explain the aetiology / risk factors of cardiomyopathy

Answer 85

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.

Question 86

Summarise the epidemiology of cardiomyopathy

Answer 86

Restrictive rare

Question 87

Recognise the presenting symptoms of cardiomyopathy

Answer 87

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

Question 88

Recognise the signs of cardiomyopathy on physical examination

Answer 88

.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

Question 89

Identify appropriate investigations for cardiomyopathy and interpret the results

Answer 89

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.

Question 90

# Define aortic regurgitation What is acute AR

Answer 90

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.

Question 91

Explain the aetiology / risk factors of aortic regurgitation

Answer 91

1. Aortic valve leaflet abnormalities or damage: - Bicuspid aortic valve, IE, rheumatic fever, trauma 2. 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.

Question 92

Summarise the epidemiology of aortic regurgitation

Answer 92

Often begins in late 50s, documented most frequently in patients >80yo

Question 93

Recognise the presenting symptoms of aortic regurgitation

Answer 93

Chronic AR: Initially asymptomatic. Later, HF symptoms: exertional dyspnoea, orthopnea, fatigue. Occasionally angina Sever acute AR: sudden cardiovascular collapse

Question 94

Recognise the signs of aortic regurgitation on physical examination

Answer 94

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)

Question 95

Identify appropriate investigations for aortic regurgitation and interpret the results

Answer 95

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

Question 96

What might explain the collapsing pulse and wide pulse pressure in aortic regurgitation

Answer 96

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.

Question 97

Differentiate the type of hypertrophy in aortic stenosis vs regurgitation

Answer 97

Stenosis= concentric (new sarcomeres deposited in parallel) Regurg: eccentric (new sarcomeres deposited side by side)

Question 98

Which condition gives you canon waves

Answer 98

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

Question 99

What is fibrinoid necrosis and when can it occur

Answer 99

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.

Question 100

T/F A split S2 in aortic stenosis can rule out severe aortic stenosis

Answer 100

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.

Question 101

Describe the carotid pulse in aortic stenosis

Answer 101

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

Question 102

Rheumatic heart disease has a strong assocation with which murmurs?

Answer 102

Rheumatic heart disease has a strong association with mitral stenosis and aortic regurgitation murmurs.

Question 103

Major cause of aortic stenosis, and when it manifests

Answer 103

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

Question 104

What are the classic findigns on ecg in left ventricular hypertrophy

Answer 104

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)

Question 105

How does diabetes cause atherosclerosis

Answer 105

The mechanism by which diabetes is thought to induce atherosclerotic disease is through hyperglycemic damage to the intimal layer of arteries.

Question 106

Define infective endocarditis

Answer 106

Infection of intracardiac endocardial structures (mainly heart valves).

Question 107

Explain the aetiology of infective endocarditis Most common cause in IVDU? Talk about the effect of the bacteria on the valves

Answer 107

Can be colonised by virtually any organism. Commonest: 1. Streptococci (mainly alpha haemolytic strep viridans or group D beta haemolytic strep bovis) 2. Staphylococcus: mainly staph aureus and occasionally staph epidermidis (in IVDU, BUT it is not most common causative organism in this group) 3. 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.

Question 108

Summarise the epidemiology of infective endocarditis

Answer 108

.

Question 109

Recognise the presenting symptoms of infective endocarditis

Answer 109

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.

Question 110

Recognise the signs of infective endocarditis on physical examination Frequency of valves affected by IE

Answer 110

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)

Question 111

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

Answer 111

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

Question 112

Generate a management plan for infective endocarditis What should you give to a patient with history of IE if undergoing dental procedure

Answer 112

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.

Question 113

Identify the possible complications of infective endocarditis and its management

Answer 113

Valve incompetence, intracardiac fistulae or abscesses, aneurysm formation, heart failure. Renal failure, glomerulonephritis. Arterial emboli from the vegetations (brain, kidneys, lungs, spleen)

Question 114

Summarise the prognosis for patients with infective endocarditis

Answer 114

Fatal if untreated. Even when treated, 15– 30% mortality.

Question 115

List the risk factors for infective endocarditis S bovis is associated with which condition

Answer 115

- 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.

Question 116

What is the Duke's classification of diagnosis of endocarditis

Answer 116

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

Question 117

What is the normal QT interval

Answer 117

<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

Question 118

Outline the normal ventricular cardiac cycle

Answer 118

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

Question 119

What does a prolonged QT interval indicate. Causes of long QT syndrome.

Answer 119

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) 2. 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)

Question 120

What arrythmia is associated with long QT syndrome and why

Answer 120

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

Question 121

What range of heart beat associated with torsade de pointes What are the consequences

Answer 121

150-250bpm It can revert spontaneously, or it can have symptoms like palpitations, dizziness and syncome, and it can lead to sudden cardiac death

Question 122

What is the treatment for drug induced LQTS

Answer 122

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

Question 123

What to think if a young person comes in with symptoms of MI but no risk factors?

Answer 123

Prinzmetal (variant) angina should be suspected in a young patient without cardiovascular risk factors,

Question 124

What increases risk of Prinzmetal (variant) angina

Answer 124

Medications can increase the risk of vasospasm (e.g. triptans, cocaine, amphetamines).

Question 125

Treatment of variant angina

Answer 125

Treatment is different to that of traditional atherosclerotic STEMI or NSTEMI and involves the use of a calcium channel blocker to decreased vasospasm.

Question 126

Why not give aspirin in variant angina

Answer 126

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.

Question 127

What criteria are used to test for rheumatic fever. What are the major and minor features

Answer 127

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.

Question 128

Mitral stenosis most common cause

Answer 128

Scarring due to rheumatic fever

Question 129

What kind of murmur does mitral stenosis cuase

Answer 129

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.

Question 130

What could happen to the p waves in somebody with mitral stenosis

Answer 130

Bifid P waves (because of left atrial enlargement) No P waves (because mitral stenosis predisposes you to AF!)

Question 131

``` 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 ```

Answer 131

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

Question 132

Define deep vein thrombosis (DVT)

Answer 132

Formation of thrombus in the deep veins, commonly of calf or thigh

Question 133

Explain the aetiology / risk factors of deep vein thrombosis (DVT)

Answer 133

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.

Question 134

Summarise the epidemiology of deep vein thrombosis (DVT)

Answer 134

Common, especially in hospitalised patients; exact incidence unknown.

Question 135

Recognise the symptoms and signs of deep vein thrombosis (DVT) on physical examination

Answer 135

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

Question 136

Identify appropriate investigations for deep vein thrombosis (DVT) and interpret the results

Answer 136

.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.

Question 137

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

Answer 137

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.

Question 138

Identify the possible complications of deep vein thrombosis (DVT) and its management

Answer 138

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.

Question 139

Summarise the prognosis for patients with deep vein thrombosis (DVT) Having a clot where is worse, above or below knee?

Answer 139

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.

Question 140

What must you check before giving somebody heparin and why

Answer 140

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.

Question 141

What do you do to the warfarin dose when you put someone on Abx? Why

Answer 141

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.

Question 142

How long does warfarin take to work?

Answer 142

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)

Question 143

What is sinus arrhythmia and what causes it

Answer 143

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.

Question 144

What are the following heart rhythms related to: 1) Ventricular tachycardia 2) Multifocal atrial tachycardia

Answer 144

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

Question 145

Which condition in cardiology can be identified using PET scanning

Answer 145

In the context of cardiology, PET can be used to identify hibernating myocardium

Question 146

What indicates severe aortic stenosis

Answer 146

late-peaking murmur, paradoxically split S2 (pulmonary valve shuts before aortic) or inaudible A2, small and delayed carotid pulses (pulsus parvus et tardes), a LV heave, and an audible (and occasionally palpable) S4.

Question 147

What would increase and reduce an aortic stenosis murmur

Answer 147

Typically the intensity of an AS murmur will increase with passive leg raise (because of increased blood volume in the left ventricle) and decrease with standing or Valsalva (because of decreased blood volume in the left ventricle).

Question 148

Which 2 conditions lead to the heart becoming "preload dependent" Which drug should be avoided as a result

Answer 148

Aortic stenosis and inferior myocardial infarctions can cause the heart to become preload dependent. Preload dependence means the heart chamber essentially becomes a conduit through which blood flows. When this occurs, the patient becomes highly dependent on central venous pressure to maintain adequate cardiac output. Reducing preload in these patients can lead to decreased cardiac output, heart failure exacerbation, and hypotension. Because of this, nitrates should be avoided in these patients. Nitrates are commonly used in the treatment of heart failure. As venodilators, they lead to venous pooling of the blood and therefore a reduction in preload.

Question 149

Should dihydropyridines be avoided in AS? Why/why not?

Answer 149

Dihydropyridine calcium channel blockers such as amlodipine and nicardipine are arterial vasodilators. They primarily reduce afterload and may help promote forward cardiac output in patients with aortic stenosis.

Question 150

Are beta blockers contraindicated in aortic stenosis?

Answer 150

-blockers should be avoided in patients in cardiogenic shock and severe aortic stenosis (e.g. if the murmur was "late-peaking").

Question 151

What happens to the QRS complexes in LBBB. What about ST segments

Answer 151

Broad QRS. ST segments NOT interpreterable

Question 152

Causes of AF

Answer 152

ATRIAL FIB ``` Alcohol Abuse Thyroid Disease Rheumatic Heart Disease Ischemic Heart Disease Atrial Myxoma Lung (Pulmonary Embolism, Emphysema) Pheochromocytoma Idiopathic Blood Pressure (Hypertension) ``` Most commonly associated with longer term HTN. Ischaemic heart disease most common cause according to prof meeran

Question 153

3rd degree heart block, what would you find in the neck and why

Answer 153

When the atria and ventricles contract simultaneously (as occurs when the atria and ventricles don't have coordinated depolarisation due to complete heart block), the blood will be pushed against the AV valve, and a very large pressure wave runs up the vein. It is associated with heart block, in particular third-degree (complete) heart block. It is also seen in pulmonary hypertension.

Question 154

Define supraventricular tachycardia

Answer 154

A regular, narrow-complex tachycardia with no p waves and a supraventricular origin.

Question 155

Explain the aetiology / risk factors of supraventricular tachycardia

Answer 155

2 types: AVRT. Accessory pathway, so that the depolarisation continues from purkinje fibres back into the atria (in WPW syndrome, this is called the bundle of Kent) AVNRT. Local circuit within the AV node, which can lead to atria and ventricles contracting at the same time

Question 156

Summarise the epidemiology of supraventricular tachycardia

Answer 156

.

Question 157

Recognise the presenting symptoms of supraventricular tachycardia

Answer 157

palpitations, syncope, dyspnoea, chest discomfort

Question 158

Identify appropriate investigations for supraventricular tachycardia and interpret the results -What does it show during tachycardia episode, what about after the SVT has terminated

Answer 158

During the SVT: -Regular, narrow complex tachycardia WITHOUT p waves After termination: - AVNRT: normal - AVRT: ’Delta wave’ (slurred upstroke on QRS) Presence of an accessory pathway resulting in a delta wave on ECG: Wolff-Parkinson-White Syndromecomplex)

Question 159

Generate a management plan for supraventricular tachycardia What if the main drug is contraindiacted

Answer 159

Haemodynamically stable? YES--> vagal manoeuvres NO--> Synchronised DC cardioversion Vagal manoevres, did it work? YES--> great NO--> IV adenosine 6mg (UNLESS CONTRAINDICATED-->USE VERAPAMIL) IV adenosine 6mg, did it work? YES--> great NO--> IV adenosine (12mg). If it works, great, if not, give another 12mg adenosine. If all the adenosine doesn't work, choose from: IV beta blocker IV amiodarone IV digoxin Synchronised DC cardioversion Definitive treatment: radiofrquency catheter ablation AVRT--> destroy accessory pathway AVNRT--> destroy slow (alpha pathway) (one of the AV node pathways, don't worry about it it's not worth learning)

Question 160

Identify the possible complications of supraventricular tachycardia and its management

Answer 160

Haemodynamic collapse can occur. ... Deep vein thrombosis. Systemic embolism. Cardiac tamponade.

Question 161

What are vagal manoeuvres. What is their effect

Answer 161

The following all STIMULATE the VAGUS nerve. This SLOWS conduction at the AV node, and thus may teriminate reentrant arrhythmias using the AV node as part of the circuit Carotid sinus massage Valsalva manoevre (forced exhalation against closed glottis) Sticking fingers down throat Putting face in cold water (diving reflex) Pressing hard on eyeballs Swallowing crushed ice/cold drink

Question 162

Define Wolff–Parkinson–White syndrome

Answer 162

Short PR interval and Delta wave on ECG predisposing to supraventricular tachycardias (SVT). A specific type of AVRT. The accessory pathway is called bundle of Kent

Question 163

Explain the aetiology / risk factors of Wolff–Parkinson–White syndrome Can you classify it

Answer 163

Accessory pathway (bundle of Kent) bypasses the atrioventricular node causing ventricular pre-excitation. Type A: left sided Bundle of Kent (most common) Type B: bundle of kent on right side

Question 164

Recognise the presenting symptoms of Wolff–Parkinson–White syndrome What is a WPW pattern, and what is WPW syndrome Why is it an issue

Answer 164

A WPW PATTERN generally causes no symptoms and is benign. So why is it an issue? But in WPW SYNDROME it's an issue because it can facilitate certain arrhythmia, or make certain arrhythmias worse, or cause sudden cardiac death E.g.: 1. In atrial arrhthmia. Usually atrial arrhythmia won't lead to seriously fast ventricular rate because the signals are delayed at the AV node. But with WPW syndrome, the bundle of kent conducts all the atrial signals to the ventricles, and this can cause cardiogenic shock because the ventricles don't have time to fill with blood 2. If the Bundle of Kent conducts retrograde, instead of anterograde (which is what causes the pre-excitation and the delta wave, see below), then the depolarisation moves back up the accessory pathway, and you can then you can go into a SVT due to the re-entry circuit, so it will be an AVRT (with orthodromic conduction) (note, most Bundles of Kent are bi-directional!) It's congenital and present at birth.

Question 165

Recognise the signs of Wolff–Parkinson–White syndrome on physical examination

Answer 165

.

Question 166

Identify appropriate investigations for Wolff–Parkinson–White syndrome and interpret the results

Answer 166

ECG: short PR interval, delta wave, QRS prolongation (note, it's only when there is tachycardia that the QRS becomes narrow complex) Usually PR interval <120ms and QRS complex >100ms T wave may be oppoiste to QRS

Question 167

Explain when there is a delta wave in wolff parkinson white, vs when there is a narrow complex regular tachycardia

Answer 167

There is pre-excitation when there isn't tachycardia. This happens when there is antegrade depolarisation. Because the depolarisation travels prematurely from the atria into the ventricles (bypassing the AV node), so you get some depolarisation before the AV node fires (so a slanted delta wave upstroke). When there is retrograde depolarisation from the ventricles back to the atria, then a circuit can form, and you can get the tachycardia, as the AV node is stimulated independently of SA node firing.

Question 168

Treatment of WPW

Answer 168

If it's just WPW pattern, you don't need to do anything But it it's WPW SYNDROME, and they develop dangerous arrhythmias, then you may need pharmacologic treatment (see above), and the definitive treatment is radiofrequency catheter ablation of the Bundle of Kent

Question 169

# Define vasovagal syncope Firstly, what is syncope, then what are the differentials for syncope

Answer 169

Syncope is a form of loss of consciousness caused by HYPOPERFUSION OF TEH BRAIN Ddx: - Vasovagal (=Reflex bradycardia) - Arrhythmia (palpitations?) - Outlflow obstruction (e.g. HOCM, aortic stenosis) - Postural hypotension (e.g. medication and dehydration)

Question 170

Explain the aetiology / risk factors of vasovagal syncope

Answer 170

Increased vagal discharge leading to drop in BP and HR Can be precipitated by different situations: Prolonged standing especially in warm surroundings. Emotion, micturition, cough, carotid sinus hypersensitivity (e.g. shaving neck or head turning) Metabolic: hypoglycaemia

Question 171

Recognise the presenting symptoms of vasovagal syncope

Answer 171

May feel sweaty/pale before collapse

Question 172

Clinical features of HOCM

Answer 172

``` • Jerky carotid pulse • Double apex beat • Ejection systolic murmur • Family history of sudden death at a relatively young age (< 65 yrs) ```

Question 173

What are the following risk scores for: ``` CHA2DS2- VASc QRISK 2 ABCD2 GRACE CURB ```

Answer 173

The CHA2DS2-VASc score is used to assess the risk of stroke in patients with atrial fibrillation, and, hence, determine the benefit of long-term anticoagulation. QRISK2 is used to predict the risk of cardiovascular disease based on traditional risk factors such as blood pressure and smoking status. It is used to decide whether to give primary prevention (e.g. statins). ABCD2 predicts a patient’s risk of stroke in the days following a TIA. GRACE score is used for risk assessment and triaging of patients with ACS. CURB-65 is used to assess severity of community-acquired pneumonia.

Question 174

What would a score of 2 on CURB-65 tell you

Answer 174

A score of 2 warrants hospital admission. A score of 3 or more is considered ‘severe’ pneumonia and should be considered for ITU admission.

Question 175

What would a score of 1 on CHADS-VASc tell you

Answer 175

Guidelines recommend that patients with a score of 2 or more should be offered anticoagulation with warfarin or a NOAC (novel oral anticoagulant).`

Question 176

Normal diameter of aorta

Answer 176

2cm

Question 177

What is the management of AAAs?

Answer 177

AAAs diameter <5.5cm have rupture risk <1% per year. Regular surveilance recommended with AAA diameter: 3-4.5cm (every year) and 4.5-5.5 cm (every 3 months). In patients with an AAA diameter > 5.5 cm or a rapidly expanding AAA (> 1 cm per year), surgical intervention: 1) Open repair 2) Endovascular aneurysm repair (EVAR). -EVAR has a lower morbidity and mortality but a higher rate of graft complications, therefore, it is usually used in elderly patients.

Question 178

Inflammation of heart muscle 2 days after MI is dresslers syndrome T/F

Answer 178

f Dressler’s should not be confused with a simple post-MI pericarditis which occurs within 2-4 days of an MI. With dresslers t is thought that injury to the myocardium during an MI stimulates the production of autoantibodies against heart muscle. These autoantibodies cause pericardial inflammation many weeks later.

Question 179

What is intermittent claudication vs critical limb ischaemia

Answer 179

Intermittent claudication is a cramping pain in the lower limb muscles that occurs on exercise and is relieved by rest. Critical limb ischaemia is a more severe form of PVD characterised by rest pain, night pain and tissue loss (e.g. arterial ulcers, gangrene).

Question 180

What is Leriche syndrome

Answer 180

Leriche syndrome is a type of intermittent claudication resulting in buttock claudication, erectile dysfunction and weak distal pulses, due to aortoiliac stenosis.

Question 181

When do the following murmurs occur ``` Austin-Flint Graham-Steell Gibson Carey-Coombs Barlow ```

Answer 181

Austin-Flint: in severe aoritc regurg, a phsiological mitral stenosis is caused causing a low grade, rumbing mid-diastolic murmur Graham-Steell: high pitched early diastolic murmur. Pulmonary regurg Gibson: Continuous machine murmur associated with patient ductus arteriosus Carey-Coombs: A Carey-Coombs murmur is a mid-diastolic murmur caused by turbulent blood flow over a thickened mitral valve. It is associated with acute rheumatic fever. Barlow: a mid-systolic click and an end-systolic murmur heard best at the apex and is associated with mitral valve prolapse.

Question 182

What is the Framingham criteria for?

Answer 182

The Framingham criteria for congestive cardiac failure (CCF) states that the diagnosis of CCF requires the simultaneous presence of at least 2 major criteria OR 1 major criterion + 2 minor criteria.

Question 183

What are some features of heart failure

Answer 183

``` Major Criteria • Paroxysmal nocturnal dyspnea • Crepitations • S3 gallop • Cardiomegaly • Increased central venous pressure • Weight loss > 4.5 kg in 5 days in response to treatment • Neck vein distention • Acute pulmonary oedema • Hepatojugular reflex ``` ``` Minor Criteria • Bilateral ankle oedema • Dyspnoea on ordinary exertion • Tachycardia (> 120 bpm) • Decrease in vital capacity by 1/3 from maximum recorded • Nocturnal cough • Hepatomegaly • Pleural effusion ```

Question 184

# Define hypertension What about malignant HTN?

Answer 184

Defined as systolic BP >140mmHg and/or diastolic BP >85mmHg measured on three separate occasions. Malignant hypertension is defined as BP >200/ 130mmHg.

Question 185

Explain the aetiology / risk factors of hypertension Resistant hypertension in young?

Answer 185

Primary: essential or idiopathic hypertension (commonest, >90% cases) Secondary: - Renal: renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, PKD, CKD - Endocrine: Diabetes mellitus, hyperthyroidism, cushing's syndrome, conn's syndrome, hyperparathyroidism, phaeochromocytoma, congenitaladrenalhyperplasia, acromegaly. - Cardiovascular: Aortic coarctation, raised intravascular volume. - Drugs: Sympathomimetics, corticosteroids, oral contraceptive pill. - Pregnancy: Pre-eclampsia. Risk factors: -old age, obesity, family history, a salt-heavy diet, a sedentary lifestyle, heavy alcohol consumption, smoking, and race An important causes of renal artery stenosis is fibromuscular dysplasia in the young- can cause HTN

Question 186

Summarise the epidemiology of hypertension

Answer 186

Very common. 10–20% of adults in the Western world. In general the younger the patient, the more likely it’s secondary hypertension.

Question 187

Recognise the presenting symptoms of hypertension Symptoms of malignant HTN?

Answer 187

Primary is commonly asymptomatic Symptoms of complications/cause Malignant: Scotomas (visual field loss), blurred vision, headache, seizures, nausea, vomiting, acute heart failure

Question 188

Recognise the signs of hypertension on physical examination

Answer 188

Loud 2nd heart sound, 4th heart sound. Radiofemoral delay --> aortic coarctation Renal artery bruit --> renal artery stenosis End organ damage --> fundoscopy for retinopathy (SEE BELOW)

Question 189

Identify appropriate investigations for hypertension and interpret the results

Answer 189

Bloods: U&Es, glucose, lipids Urine dipstick: Blood and protein ECG: May show left ventricular hypertrophy (deep S wave in V1-2, tall R wave in V5-6, inverted T waves in I, AVL, V5-6, left acis deviation) or ischaemia The best test is ambulatory blood pressure monitoring (avoid white coat HTN), also allows treatmnet monitoring

Question 190

Generate a management plan for hypertension (incl. hypertensive emergencies)

Answer 190

Conservative: Stop smoking, lose weight, reduce alcohol, reduce dietary Na+ Investigate for secondary causes (in young patients, malignant HTN, or persistent) Medical: 1) Patients <55: ACEi/ARB. Patients >55 or afro-caribbean: CCB (amlodipine), or thiazide-like diuretic (IF evidence of HF) 2) ACEi/ARB + CCB (or thiazide if heart failure) 3) Combination of ACEi/ARB + CCB + thiazide like diuretic 4) "Resistant hypertension". Expert help, 4th antihypertensive like spironalactone may be added

Question 191

Identify the possible complications of hypertension and its management

Answer 191

Heart failure, coronaryarterydisease and MI, CVA, peripheral vascular disease, emboli, retinopathy, renal failure, hypertensive encephalopathy, posterior reversible encephalopathy syndrome (PRES), malignant hypertension.

Question 192

Summarise the prognosis for patients with hypertension

Answer 192

Good, if BP controlled. Uncontrolled hypertension linked with increased mortality (6 X stroke risk and 3 X cardiac death risk). Treatment reduces incidence of renal damage, stroke and heart failure.

Question 193

Which drugs could cause HTN

Answer 193

Sympathomimetic agents like decongestants or even cocaine, Cyclosporine or tacrolimus, Sodium-containing antacids, Stimulants like amphetamines, Atypical antipsychotics like clozapine, Antidepressants, Oral contraceptives, Erythropoietin, and even NSAIDS and liquorice

Question 194

Outline the Keith-Wagner classification of retinopathy

Answer 194

1- silver wiring 2- as above, plus arteriovenous nipping 3- as above, plus flame haemorrhages and cotton wool exudates 4- as above, plus papilloedema.

Question 195

What is the target blood pressure in non-diabetics, diabetics without proteinuria, and diabetics with proteunuria

Answer 195

Target BP: <140/85mmHg (non-diabetic); <130/80mmHg (diabetes without proteinuria); <125/75mmHg (diabetes with proteinuria).

Question 196

What is the management of acute malignant hypertension

Answer 196

IVb-blocker, labetolol or hydralazine sodium nitroprusside. Avoid very rapid lowering which can cause cerebral infarction.

Question 197

What would be the difference between chest x-ray with pericardial effusion vs heart failure

Answer 197

Both will have a large looking heart. The enlarged heart but in the absence of pulmonary vascular congestion indicates the pericardial effusion rather that congestive failure.

Question 198

What differentiates a pericardial effusion from cardiac tamponade

Answer 198

If there is any degree of pericardial tamponade the JVP will be elevated.

Question 199

T/F the ECG findings are never normal in pericarditis

Answer 199

F. The ECG findings are normal in 10% of patients with acute pericarditis

Question 200

What is the most common cause of BLOODY pericardial effusion

Answer 200

Malignant disease

Question 201

Where is the needle inserted in pericardiocentesis

Answer 201

In pericardiocentesis, the needle is inserted subcostally in the midline aiming towards the left shoulder.

Question 202

What dose of diamorphine should be given for MI Initial investigations and management of MI

Answer 202

THIS MUST BE TITRATED TO WEIGHT So bit of a trick question. Most crucial initial management of MI is ECG & o2 monitoring Oral 300mg aspirin Sublingual GTN IV opiates IV metaclopramide 10mg

Question 203

Breathlessness after treatment for a heart attack

Answer 203

Acute pulmonary oedema secondary to myocardial infarction Extensive pulmonary airspace opacity extending out from the hila. Bibasal pleural effusions and enlarged heart (may be associated with substantial cardial enlargement, or none!)`.

Question 204

What are the hyperkaelamia signs on ECG

Answer 204

Tall tented T waves Widened QRS complex Absent p waves A "sine wave" appearance

Question 205

What medications should an MI patient be sent home with

Answer 205

Clopidogrel 75mg OD, Atenolol 50mg OD, Ramipril 10mg OD, Aspirin 75mg OD, Simvastatin 40mg OD

Question 206

Define ventricular tachycardia

Answer 206

When there are more than 3 consecutive beats in a row that arise from the ventricles (these are known as premature ventricular contractions, or PVC) It is NOT a sinus tachycardia, because the beats do not start from the SAN

Question 207

Explain the aetiology / risk factors of ventricular tachycardia

Answer 207

Split into those which cause MONOMORPHIC QRS tachycardia and POLYMORPHIC QRS tachycardia on ECG. MONOMORPHIC: -Caused by increased automaticity and re-entry circuits (which can be post MI, which causes an area of poor conduction around a scar) e.g due to ischaemia. Can also be due to aortic stenosis POLYMORPHIC VT: - Caused by abnormal ventricular repolarisation: - E.g. long QT syndrome (--> Torsades de pointes), drug toxicity, electrolyte abnormalities. Whatever the cause, the increased ventricular rate leads leads to reduced blood flow into the ventricle during diastole, and reduced CO. This can cause haemodynamic compromise ischaemia, electrolyte abnormality, long QT syndrome

Question 208

Recognise the presenting symptoms and signs of ventricular tachycardia

Answer 208

Often asymptomatic, particuarly when nonsustained. Common symptoms of sustained VT: -Palpitations, hypotension, syncope In more severe case (when there is reduced CO): - chest pain (often in conjunction with an MI!) - Cardiogenic shock - fainting - dizziness - SoB Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death.

Question 209

Identify appropriate investigations for ventricular tachycardia and interpret the results

Answer 209

ECG: 3 or more consecutive premature ventricular beats ( BROAD QRS COMPLEXES (>120ms) and TACHYCARDIA (>120bpm) Sustained means >30s Monomorphic: all QRS complexes look similar (identical origin) Polymorphic: QRS complexes are different (multiple origins) Other ECG findings: AV-dissociation (no relationship between P waves and QRS complexes, in VT, ventricular rhythm is often faster than atrial rhythm) -Fusion complex (atrial and ventricular impulses occur simultaneously) "Polymorphic ventricular tachycardia with QRS complexes that appear to twist around the isoelectric line"= Torsades de pointes Holter monitor: useful for diagnosing intermittent VT which may not be present on a single ECG ECHO: provides information about possible etiologies of VT (e.g. structural heart disease, prior MI) and is thus a useful tool for evaluation of VT

Question 210

Generate a management plan for ventricular tachycardia Specifically how is torsades de pointes treated

Answer 210

INITIAL THERAPY: VT WITHOUT pulse--> defibrillate VT WITH pulse--> cardioversion with drug or electrical cardioversion: - Drug cardioversion with IV AMIODARONE (class III anti-arrhythmic) - Failing that, DC cardioversion LONG TERM THERAPY: -IMPLANTABLE CARDIOVERTER DEFIBRILLATOR - RADIOFREQUENCY CATHETER ABLATION - Radiowaves destroy tissue responsible for irregular heart beat (can cure some types, presumably re-entrant types) -ANTIARRHYTHMICS (class I or III) ---------------------------- Torsades de pointes: If haemodynamically unstable--> defibrillate If haemodynamically unstable--> IV magnesium sulfate

Question 211

Identify the possible complications of ventricular tachycardia and its management

Answer 211

The issue is that it can lead to really fast tachycardias, as high as 250bpm, which means that the ventricles don't fill fast enough, so there is hypoperfusion and it can lead to sudden cardiac death It can also lead to ventricular fibrillation

Question 212

Summarise the prognosis for patients with ventricular tachycardia

Answer 212

.

Question 213

What is sinus tachycardia

Answer 213

Appropriate increase in heart rate, e.g. due to exercise/anxiety/sepsis The increase in HR is due to increased frequency of SINOATRIAL node firing

Question 214

Explain what increased automaticity means (cause of monomorphic centricular tachy)

Answer 214

- Certain area of the ventricle has abnormal automaticity, the ventricular pace maker cells (i.e NOT cardiomyocytes) - Normal automacity of the ventricular pacemaker cells is 30bpm (so the ventricles never initiate the beat because the SAN automaticity is 60-100bpm, so ventricle pace maker cells never get a chance to) - In focal ventricular tachycardia, some stress to ventricular pacemaker cells can increase its automaticity, so it switches roles with the SAN and actually initiates the contractions and thus determines the heart rate - This can be caused by: - drugs (e.g. cocaine, amphetamine) - electrolyte imbalance - ischaemia

Question 215

What is ventricular re-entry (cause of monomorphic ventricular tachy)

Answer 215

REENTRANT (MORE COMMON) - Where a bit of the heart becomes fibrotic, e.g. due to ischaemia - There are cardiomyctes around the fibrotic region with differing characeristics - On one side, there are cardiomyocytes that have rapid conduction but long refractory period, and on the other side there is cardiomyocytes with slower conduction but shorter refractory period - When the normal depolarisation from SAN comes down, these characteristics can lead to re-entrant circuit WITHIN the ventricle, that can lead to ventricular beats.

Question 216

How would you differentiate VT for SVT Why does it matter to differentiate them

Answer 216

Signs and symptoms suggestive of VT: - Age >35 - Hx of structural heart defects of past MI - AV dissocation, fusion beats Signs and symptoms suggestive of SVT: - Bundle branch block on prior ECG - Hx of SVT - Evidence of WPW (delta wave) It is important to make the distinction between SVT with aberrancy and VT because treatment of the two conditions differs and sometimes the wrong treatment can lead to hemodynamic instability (e.g., using AV-nodal blocking drugs in patient with VT).

Question 217

What is Kussmaul's sign When might it occur

Answer 217

Kussmaul sign is a paradoxical rise in JVP on inspiration, which occurs in patients with impaired right ventricular filling (e.g. constrictive pericarditis, restrictive cardiomyopathy).

Question 218

What electrolyte imbalance could cause VT

Answer 218

Low magnesium

Question 219

What are the following medications used for: - Adenosine - Atropine - Amiodarone

Answer 219

Adeonsine: terminate SVT Atropine: treat acute heart blocl Amiodarone: haemodynamically stable ventricular tachycardia

Question 220

What are the signs of mitral stenosis

Answer 220

Mid diastolic murmur Malar flush (red cheecks) Irregularly irregular pulse (mitral stenosis) Parasternal heave Loud S1

Question 221

What do each of the following waves on ECG correspond to: - A wave - C wave - X descent - V wave - Y descent

Answer 221

- A wave. Atrial contraction pushes some blood back up to the SVC - C wave. The ventricular contraction pushes the tricuspid valve into the right atrium, which pincreases the pressure in the SVC - X descent. The right atrium is relaxed and filling - V wave. There's increased venous return to the right atrium in late systole - Y descent. Tricuspid valve opens causing blood to flow into the right ventricle.

Question 222

When does a cannon A wave occur

Answer 222

Cannon A waves occur when the atria and ventricles contract simultaneously. This results in the right atrium contracting against a closed tricuspid valve and causing a column of blood to shoot up the superior vena cava into the jugular vein. This happens in complete heart block!

Question 223

When is large V wave seen

Answer 223

Large V waves are seen in tricuspid regurgitation. Ventricular contraction causes blood to surge through an incompetent tricuspid valve, through the right atrium and into the jugular vein.

Question 224

What causes a raised JVP with absent pulsation

Answer 224

Raised JVP with absent pulsation occurs in superior vena cava obstruction.

Question 225

What causes slow Y descent

Answer 225

Slow Y | descent is associated with tricuspid stenosis.

Question 226

Difference between aneurysm and dissectioin

Answer 226

A true aneurysm involves all three vessel layers; the tunica intima, media and adventitia. A dissection occurs when there is a tear in the tunica intima, allowing blood to literally “dissect” into the vessel wall.

Question 227

Where is the most common site for AAA and why

Answer 227

Abdominal aortic aneurysms, or AAAs, are most common below the origin of the renal arteries, which corresponds to the L2 vertebral level. This is because below this level, the abdominal aorta lacks “vasa vasorum”, small blood vessels in the adventitial layer that provide nutrients to the aorta itself. Therefore, the absence of vasa vasorum in this part of the aorta makes the tunica media particularly susceptible to ischemia, when blood within the artery can no longer oxygenate the artery wall due to atherosclerosis

Question 228

AAA rupture triad

Answer 228

Sudden onset flank/lower back pain | hypotension from blood loss, and a pulsatile abdominal mass.

Question 229

When is this JVP waveform seen: Raised JVP, normal waveform

Answer 229

Fluid overload and right ventricular failure

Question 230

When is this JVP waveform seen: Large A wave

Answer 230

This is the first wave. Usually seen when the right atrium is stronger, during pulmonary HTN and pulmonary stenosis

Question 231

When is this JVP waveform seen: Canon A wave

Answer 231

3rd degree heart block, single chamber ventricular pacing, | ventricular arrhythmias and ventricular ectopics.

Question 232

When is this JVP waveform seen: Large V wave

Answer 232

Tricuspid regurgitation

Question 233

When is this JVP waveform seen: Absent A waves

Answer 233

In atrial fibrillation, the ‘a waves’ are absent (D) due to dysfunctional atrial systole.

Question 234

What are is the cause of right parasternal heave in mitral stenosis

Answer 234

Pulmonary HTN leading to right ventricular hypertrophy

Question 235

Define ventricular fibrillation

Answer 235

Quivering of the ventricles due to uncoordinated contraction of the myocardium Very dangerous. Leads to death within minutes of onset due to hypoperfusion (sudden cardiac death)

Question 236

Explain the aetiology / risk factors of ventricular fibrillation

Answer 236

Heart cells become stressed such that the tissue is structurally or electrically changed to have different properties Known as tissue heterogeneity. So they don't depolarise and contract at the same time. This is the same pathology basically as VT. When there is some damage, but clusters care cells are acting coordinately, the depolarisation from the ventricle spreads out and causes a premature ventricular contraction (i.e. in VT, where there are >3 PVCs) But when there is more damage, and all the cells are acting differently, the depolarisation isn't conducted across the ventricles, and instead you get individual depolarising areas and causing functional re-rentry and fibrillation -------------------------- Medications and illicit durgs (metamphetamine and cocaine), electrolyte imbalances ischaemia external electrical stimulation (if the heart is stimulated on the upstroke to the T wave it can induce fibrillation)

Question 237

Generate a management plan for ventricular fibrillation

Answer 237

SEE DPD lecture (Advanced life support) You defibrillate with a electrical external simulation. It depolarises the whole heart at once, to then allow the SAN to take control again ICD to monitor patient's ECG and shock if in V fib

Question 238

Define varicose veins

Answer 238

Veins that have become elongated, dilated and tortuous, most commonly the SUPERFICIAL veins of the lower limb Thread veins, spider veins of reticular veins refer to smaller superficial venous telangetcasias and varicosities

Question 239

Explain the aetiology / risk factors of varicose veins

Answer 239

PRIMARY: -Genetic or developmental weakness of the vein wall, leading to reduced elasticity, dilation over time and valvular incompetence SECONDARY: -Venous outflow obstruction: pregnancy, pelvic malignancy, ovarian cysts, ascites, lymphadenopathy, retroperitoneal fibrosis VALVE DAMAGE: -Following DVT. High flow: arteriovenous fistula

Question 240

Summarise the epidemiology of varicose veins

Answer 240

Increase with age. 10-15% adult men, 20-25% adult women

Question 241

Recognise the presenting symptoms of varicose veins

Answer 241

Cosmetic appearance complaints Aching in legs, worse towards end of day of after standing for long periods Swelling, itching or complications, like bleeding, infection or ulceration. Previous history of DVT, predisposing factors and vascular risk factors

Question 242

Recognise the signs of varicose veins on physical examination

Answer 242

Inspection: Patient standing. Vein distribution. Varicose eczema, lipodermatosclerosis, oedema, atrophie blanche or ulceration Palpation: - Fascial defects along dilated veins - Cough impulse felt over saphenofemoral junction - Tap test: impulse felt distally along the veins after tapping over the SFJ. - Presence of foot pulses should be documented Trendelenburg test: -Patient supine. Leg elevated and veins emptied. Hand used to compress SFJ. Leg is placed in the dependent position and filling of veins observed before or after the hand is released Hand-held doppler: can demonatrate valvular incompetence sites Rectal or pelvic examination if secondary causes are suspected

Question 243

Identify appropriate investigations for varicose veins and interpret the results

Answer 243

DUPLEX ULTRASOUND locates sites of incompetence of reflux AND can exclude DVT. MRI venography for complex cases

Question 244

Generate a management plan for varicose veins

Answer 244

Conservative: -Exercise (improve calf muscle pump), elevate legs at rest. Support stockings to aid venous return and reduce swelling - Surgical: SFJ ligation, long saphenous vein stripping to the knee and avulsion of varicosities via small stab incisions - Short saphenous vein not stripped, just ligated to avoid damage to sural nerve -Endovenous procedures: increasingly popular, performed under LA. Endovenous laser treatment (EVLT) used to ablate long saphenous vein with ultrasound guidance. After all treatments, legs are bandaged and early mobilisation is envouraged. Venous telangiectasia and reticular veins: microinjeciton or laser sclerotherapy

Question 245

Identify the possible complications of varicose veins and its management

Answer 245

Venous pigmentation, eczema, lipodermatosclerosis, venous ulceration, superficial thrombophlebitis Of treatment: recurrence Endovenous treatment complications: skin burns, nerve injury, bruising embolsim, DVT. Surigcal treatment complications: haemorrhage, infection, paraesthesia or nerve injury

Question 246

Summarise the prognosis for patients with varicose veins

Answer 246

In general, slowly progressive

Question 247

What are the ECG findings in complete heart block

Answer 247

Complete heart block causes bradycardia, broad | QRS complexes and complete dissociation between p waves and QRS complexes.

Question 248

What is the proportion of HOCM that is inherited, and what is the inheritance pattern

Answer 248

Up to 50% of cases are genetic (autosomal dominant) with mutations in b -myosin, troponin T or a -tropomyosin

Question 249

T/F IV contrast is contraindicated if you think someone has an AAA

Answer 249

FALSE!!!!!! The contast CT abdomen is required to identify the leak!! An USS will visualise an aneurysm but it cannot distinguish between an intact aneurysm and one that is leaking or ruptured

Question 250

Heart valve complication of SLE?

Answer 250

Libman-Sacks endocarditis is a non-bacterial thrombotic endocarditis that is characterized by sterile vegetations located in the mitral valve surface and chordae. If left untreated, can progress to develop mitral valve regurgitation Leads to signs of HF.

Question 251

Define myocarditis

Answer 251

Inflammation of cardiac MUSCLE

Question 252

Aetiology/RF for myocarditis

Answer 252

``` INFECTIOUS Viral infection (Cocksackie B virus) trigger lymphocytic myocarditis, Chagas, Lyme disease (Borrelia burgdorferi) ``` In immunovompormised: Toxoplasma gondii (harboured by cats) SLE Polymyositis Drug reactions (--> hypersensitivity myocarditis), eosinophils in the blood vessels of the myocardium. Chemo agents. Giant cell myocarditis

Question 253

Hx for myocarditis

Answer 253

Sharp chest pain (suggesting associated pericarditis) Arrythmias if inflammation affcts pacemaker cells Fatigue, fever, SoB Severe cases can develop heart failure (oedema)

Question 254

Signs of myocarditis

Answer 254

Signs of complications (HF, arrhythmias)

Question 255

Investigations for myocarditis

Answer 255

Bloods. Individuals with myocarditis suffer heart muscle damage, which causes troponin and creatine kinase levels to rise on blood tests. ECG. An electrocardiogram can show sinus tachycardia, a fast heart rate, as well as T-wave inversions and “saddle-shaped” ST-segment elevations because it looks a bit like a horse saddle. Chest x ray. Enlarged heart with inflamed muscle walls. Pericardial fluid drainage. Echo. GOLD STANDARD: biopsy of cardiac muscle

Question 256

Most common cause of tricuspid regurge

Answer 256

Infective endocarditis

Question 257

Management of ACS

Answer 257

``` Morphine O2, aim for >94% Nitrates Antiplatelet: aspirin/clopi Betablockers to reduce myocardial O2 demand (CI in asthma, heart block or acute HF) ACEi Statins Heparin (LMWH) ```

Question 258

ECG findings in PE

Answer 258

Sinus tachycardia Right heart strain: RBBB, right axis deviation LONG TERM: right ventricular hypertrophy: D - Deep S wave in lead 1 - Pathological Q wave lead 3 - Inverted T wave lead 3

Question 259

Reverse tick sign?

Answer 259

Feature of digoxin toxicity

Question 260

Cardiac causes of finger clubbing

Answer 260

Congenital cyanotic heart disease (most common), atrial myxoma (benign tumour of the heart), subacute bacterial endocarditis and tetralogy of Fallot (a combination of four congenital heart defects: ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy and an overriding aorta)

Question 261

Infective endocarditis causative organism with: 1) IV drug use 2) Recent dental surgery

Answer 261

1) IVDU- S. Aureus | 2) Recent dental surgery- S Viridans

Question 262

Immediate management of PE

Answer 262

``` The immediate management of PE involves delivering high-flow oxygen and subcutaneous LMWH (e.g. enoxaparin). Once this measure has been taken, a Wells score can be calculated and, dependent on the score, appropriate investigations (either a CTPA or D-dimer) can be performed. ``` So the first management is to give LMWH, even before you've done a CTPA!

Question 263

Pulmonary hypertension can lead to which valve defect

Answer 263

Pulmonary regurgitation

Question 264

You've given acute HF patient IV diamorphone, IV furesomide, sat them up and given GTN. They are still struggling for breath. What next

Answer 264

CPAP

Question 265

Cause of superior vena cava syndrome

Answer 265

Superior vena cava syndrome (SVCS) is caused by compression of the superior vena cava, most commonly by lung tumours. Rarer causes include mediastinal lymphadenopathy and thymomas.

Question 266

Main features of SVCS

Answer 266

dyspnea, orthopnoea, swollen face and arms, plethora, cough and engorged neck and facial veins (raised and non-pulsatile JVP).

Question 267

What is pemberton test

Answer 267

the patient is asked to lift their arms over their head for approximately 1 minute, which leads to facial plethora, a raised non-pulsatile JVP and inspiratory stridor.

Question 268

What causes pulsus alternans in reduced ejection heart failure

Answer 268

In left ventricular systolic failure, the ejection fraction is low, which causes a reduced stroke volume and an increased end-diastolic volume. The high end-diastolic volume, following one weak contraction, stretches the ventricular muscle fibres which, by Starling’s law, leads to a stronger subsequent contraction. This pattern of alternating strong and weak pulses is described as pulsus alternans.

Question 269

Causes of pulsus paradoxus

Answer 269

Pulsus paradoxus refers to an abnormally large decrease in blood pressure and pulse amplitude during inspiration. Causes include constrictive pericarditis and cardiac tamponade.

Question 270

What is palsus parvus et tardus

Answer 270

Pulsus parvus et tardus is a slow-rising pulse | associated with aortic stenosis.

Question 271

What is pulsus bisferiens

Answer 271

Pulsus bisferiens refers to a biphasic pulse that has two peaks per cardiac cycle. It can be detected in HOCM and in patients with coexisting aortic regurgitation and aortic stenosis.

Question 272

Causes of central sleep apnoea

Answer 272

Stroke and heart failure among others

Question 273

Long QT syndrome is caused by which electircal abnormalities

Answer 273

Long QT syndrome is a dangerous heart condition that increases the risk of potentially fatal arrhythmias such as torsades de pointes and ventricular fibrillation. The main acquired causes of long QT syndrome are hypokalaemia and hypomagnesaemia. Inherited causes include Romano-Ward syndrome and Jervell and Lange-Nielsen syndrome.

Question 274

What can aortic dissection cause

Answer 274

If the tear spreads along the branches of the aorta it can lead to serious complications, depending on the arteries involved, such as strokes (carotid artery), MI (coronary arteries) and renal failure (renal artery).

Question 275

What heart murmur can aortic dissection cause

Answer 275

A dissection that spreads towards the heart can cause aortic regurgitation (giving rise to the early diastolic murmur heard in this patient).

Question 276

What abnormlaity of the aorta is a cause of secondary hypertension

Answer 276

Coarctation of the aorta is a congenital narrowing of the aorta – a cause of secondary hypertension.

Question 277

What are the ECG features of hypokalaemia

Answer 277

The main ECG features of hypokalaemia are U waves, ST depression, flattened T waves and prolonged PR interval.

Question 278

What are the reversible causes of cardiac arrest

Answer 278

``` Hypothermia Hyperkalaemia/hypokalaemia Hypovolaemia Hypoxia Tension pneumothorax Tamponade Thromboembolic Toxic ```

Question 279

What is S3

Answer 279

The protodiastolic gallop - a.k.a an S3, or a third- heart sound - is a sign of vascular congestion and fluid overload

Question 280

Best diagnostic test for aortic dissection

Answer 280

CT with arterial contrast enhancement is the test of choice for diagnosis as well as classifying the dissection and evaluating distal complications.

Question 281

pleuritic chest pain and muffled heart sounds

Answer 281

Uremic ``` pericarditis is one of the signs of renal failure and is characterized by pleuritic chest pain and muffled heart sounds . Dialysis is indicated. ```

Question 282

Causes of right bundle branch block

Answer 282

``` right ventricular hypertrophy , pulmonary embolism , ischaemic heart disease , rheumatic heart disease , myocarditis , cardiomyopathy or hypertension . ```

Question 283

What are the diagnostic criteria for RBBB

Answer 283

widened QRS- interval , a terminal R-wave in lead V1 (e.g. R, rR', rsR', rSR' or qR) and a slurred S-wave in leads I and V6 on ECG.

Question 284

What are the causes of aortic regurgitation

Answer 284

bicuspid aortic valve, infective endocarditis and rheumatic fever.

Question 285

What is a potential complication of AR

Answer 285

AR can lead to heart failure, and, hence, presents with symptoms such as dyspnoea, orthopnoea and a cough productive of pink, frothy sputum.

Question 286

Main signs of AR

Answer 286

Early diastolic murmur, water hammer pulse, wide pulse pressure.

Question 287

Other signs of AR?

Answer 287

Pulsation of nail bed (Quincke’s Sign) Head nodding in time with pulse (De Musset's sign) Pistol shot (loud systolic and diastolic sounds) over femoral artery (traube's sign) VIsible pulsation in the neck (Corrigan's) Visible pulsation of teh pupils and retinal arteries (Becker's)

Question 288

What is the investigations if you suspect someone has an aortic bleed but you're not sure?

Answer 288

CT is the technique of choice to evaluate the aorta and retroperitoneum acutely, but is only indicated in haemodynamically stable patients in whom the diagnosis is in doubt. Patients who are bleeding actively need to go straight to theatre for repair of the aneurysm. (e.g. if someone had acute back pain but were haemodynamically stable)

Question 289

Elderly man, loin to groin pain. No Hx renal calculi

Answer 289

Remember that an elderly male with loin to groin pain who has never had kidney stones before is much more likely to have a AAA than renal calculi!!!!! It’s really important to remember that a AAA can cause pain virtually anywhere in the abdomen even mimicking other pathologies such as renal calculi.

Question 290

Expansile mass felt below the umbilicus

Answer 290

Don’t forget, therefore, that a AAA is palpated above the umbilicus and if an expansile mass is felt below, it is most likely an iliac aneurysm.

Question 291

Fixed skin motting is a good or bad prognostic indicator in acute limb ischaemia

Answer 291

Fixed skin mottling indicates irreversible limb ischaemia.

Question 292

T/F limb rewarming may help in acute limb ischaemia

Answer 292

F | The limb should never be re-warmed as this enhances tissue damage.

Question 293

Acute limb ischaemia what is the best management

Answer 293

Either embolectomy or thrombolysis can be performed. There is no overall difference in limb salvage or 1 year survival between the two treatments. The increased risks of surgery are balanced by the increased risk of thrombolytic complications. The decision should be made on case-by-case basis.

Question 294

When would you use IV heparin in acute limb ischaemia

Answer 294

Intra-venous heparin can be used as sole treatment if the limb is viable or whilst awaiting transfer to a vascular centre. Heparin minimises clot propagation and improvement may occur through natural clot lysis and opening of collaterals.

Question 295

Lower limb purpura with epigastric pain radiating to the back

Answer 295

The presence of lower limb purpura is also concerning and would be explained by small emboli from the aneurysm if this was correct diagnosis

Question 296

T/F aggressive fluid resuscitation is needed in shocked patients with ruptured aortic aneursym

Answer 296

F Fluid resuscitation is needed, but should not be aggressive as this may cause re-bleeding if initial leak has sealed – aim for a systolic BP of < 100mmHg.

Question 297

Contraindications for beta blockers

Answer 297

Contraindications for the use of beta blockers include: asthma, cardiogenic shock, marked bradycardia, hypotension, second and third degree AV block, severe peripheral arterial disease. Prinzmetals angina Uncompensated or uncontrolled heart failure is only a contraindication for the older non-selective beta blockers.

Question 298

T/F sublingual nifedipine is indicated in hypertensive emergency

Answer 298

F. Sub-lingual nifedipine is fast acting and may precipitate a sudden drop in blood pressure leading to a stroke. The aim is for a gradual decrease in blood pressure to prevent cerebral hypoperfusion.

Question 299

Management of hypertensive emergency

Answer 299

Most patients do not need to be admitted and can be treated with oral medication, except in certain circumstances such as encephalopathy. But if they have had a seizure for example, Admit to hospital bed IV sodium nitroprusside CT head

Question 300

What is the threshold for isolated systolic pressure for treatment

Answer 300

Isolated systolic pressure ≥ 160mmHg

Question 301

Target BP in diabetics

Answer 301

The target blood pressure in diabetes is: systolic <140 mmHg and diastolic <90 mmHg.

Question 302

Target BP in renal impairment or persistent proteinuria

Answer 302

The target blood pressure for these patients should be systolic <130 mmHg and diastolic <80 mmHg. In patients with significant proteinuria (>1g/day) the target is lower

Question 303

What are the acute symptoms that cardiomyopathy can cause

Answer 303

Syncope (these individuals have higher risk of MI) And arrhtyhmias (due to pacemaker cells being affected), e.g. AF, ventricular ectopic beats, ventricular tachycardia/fibrillation of AV block

Question 304

Auscultation of hypertrophic cardiomyopathy

Answer 304

Crescendo-decrescendo murmur during systole

Question 305

What is heard on auscultation of dilated cardiomyopathy

Answer 305

S3 heart sound (blood slamming into the DILATED ventricular wall during diastole)

Question 306

What is heard on auscultation of restricted cardiomyopathy

Answer 306

S4 (due to reduced ventricular compliance)

Question 307

ECG findings in cardiomyopathy

Answer 307

Usually abnormal as there is remodelling of cardiac muscle: -AF, ST-T abnormalities, premature atrial and ventricular beats, AV block and intraventricular conduction delays

Question 308

Investigation for cardiomyopahty

Answer 308

Echocardiography (can look at wall thickness dimensions)

Question 309

What is the normal cardiac wall thickness and what value allows for diagnosis of hypertrophic cardiomyopathy

Answer 309

Normal: Men-12mm, women- 11mm If >15mm, you can diagnose with HYPERTROPHIC cardiomyopathy (between 12-15mm there is a grey area, and you can diagnose it only if there is a family member with cardiomyopathy) )

Question 310

What happens to cardiac wall thickness in each type of cardiomyopathy

Answer 310

Hypertrophic it increases, dilated it reduces, restrictive it is unremarkable

Question 311

What happens to contractility in dilated and hypertropohic cardiomyopathy

Answer 311

Hypertrophic it increases, dilated it reduces

Question 312

What is seen on echo with restrictive cardiomyopathy

Answer 312

Non-dilated ventrucles but with impaired ventricular filling (due to reduced compliance) Normal ejection fraction There might be increased wall thickness in left ventricle if it's due to infiltration disease

Question 313

Which additional investigations can be performed for restrictive cardiomyopathy

Answer 313

MRI/CT (to look for fat, iron or amyloid in the myocardium or inflammation of fibrosis) You may also wish to do endomyocardiac biopsy to look for those deposits

Question 314

Most common cause of sudden death in young athletes

Answer 314

Hypertrophic cardiomyopathy

Question 315

Which part of the heart is disproportionately involved in hypertrophic cardiomyopathy

Answer 315

disproportionate septal involvement

Question 316

Granular or "sparking" appearance of heart on echo

Answer 316

granular or ‘sparkling’ appearance of myocardium in amyloidosis. (restrictive cardiomyopathy)

Question 317

What is abdominal aortic aneurysm

Answer 317

Abdominal aortic aneurysm (AAA) is a focal dilatation of the abdominal aorta to more than 1.5 times its normal diameter.

Question 318

RFs for AAA

Answer 318

``` Men of advanced age are at increased risk for their formation; smoking (MOST IMPORTANT RISK FACTOR) hypertension Atherosclerosis Hypercholesterolaemia ```

Question 319

t/f abdominal aortic aneurysm is associated with increased risk of peripheral thromboembolsim

Answer 319

T | Possible formation of thrombi in the aneurysm → peripheral thromboembolism

Question 320

Investigations for AAA

Answer 320

The diagnosis of AAA is confirmed by imaging showing aortic diameter > 3 cm. Unstable patients should be taken directly to the OR for emergency surgery if ruptured AAA is suspected (see ruptured AAA). There are no laboratory findings specific to AAA. Imaging with duplex ultrasound CT angiogram of abdo and pelvis with IV contrast- More detailed evaluation of the location, size, and extent of the aneurysm, involvement of branch vessels, and presence of thrombus or rupture (to see if it's leaking!)

Question 321

What is concentric hypertrophy and when does it occur

Answer 321

Concentric hypertrophy can occur as a result of chronic hypertension . It occurs because the heart adds additional sarcomere units in parallel to increase strength, and attempt to overcome the additional afterload created by hypertension .

Question 322

What is eccentric hypertrophy and when does it occur

Answer 322

``` Eccentric hypertrophy can also be described as hypertrophy in series and occurs as sarcomeres are added in series. This results from volume overload and can be seen in dilated cardiomyopathy . ```

Question 323

What is asymmetric hypertrophy and when does it occur

Answer 323

``` Asymmetric hypertrophy is most often seen in hypertrophic cardiomyopathy as this pathology causes hypertrophy, but predominantly in the intraventricular septum. This condition can cause sudden cardiac death and is associated with a systolic ``` murmur that is louder with Valsalva maneuver .

Question 324

What can digoxin toxicity cause

Answer 324

``` paroxysmal atrial tachycardia with a 2:1 block, accelerated junctional rhythm , or bidirectional ventricular tachycardia . ```

Question 325

Eletrical alternans

Answer 325

Can't miss this, alternating different QRS complex! Look it up It's a sign of cardiac tamponade! ``` Electrical alternans with sinus tachycardia is a specific sign for tamponade . It is due to the swinging motion of the heart in the pericardial cavity causing a beat-to-beat variation in QRS-axis and amplitude . ```

Question 326

Why does constrictive pericarditis develop

Answer 326

Chronic pericarditis may either be constrictive or effusive-constrictive. Constrictive pericarditis is characterized by thickening and rigidity of the pericardium, resulting in both backward and forward failure

Question 327

What ausculation finding characterises constrictive pericarditis

Answer 327

pericardial knock on auscultation, which is caused by a sudden stop in ventricular diastolic filling (when the ventricle expands but is then stopped due to the fibrotic pericardium)

Question 328

Symptoms/sign of constrictve pericarditis

Answer 328

Patients typically present with fatigue, jugular vein distention, peripheral edema, and a characteristic pericardial knock on auscultation

Question 329

T/F constrictive pericarditis that is always caused by chronic pericarditis

Answer 329

F You can get transient constrictive pericarditis too, which lasts less htan 3 months

Question 330

What finding in acute pericarditis Where is it best heard and what is it caused by

Answer 330

Pericardial friction rub: high-pitched scratching on auscultation Indicates friction between the visceral and parietal pericardial tissue Best heard over the left sternal border during expiration while the patient is sitting up and leaning forward

Question 331

Pericarditis due to what cause typically does not have the characteristic ECG changes

Answer 331

Uraemia

Question 332

Constrictive pericarditis investigations

Answer 332

ECG ECHO (main): increased pericardial thickness... suffen halt of ventricular filling during early diatole MRI/CT pericardial thickening and calcifications Cardiac catheterisation if a def. diagnosis not reached. Square root sign

Question 333

Stroke involving ischaemia of SUPERIOR vs INFERIOR division of the left middle cerebral artery

Answer 333

SUPERIOR DIVISION: ``` produce Broca aphasia , which is an expressive type of aphasia that involves non-fluent ``` ``` speech , poor repetition, and the inability to write. Deficits in this area also cause hemiparesis and paresthesia in the right half of the body and face. ``` INFERIOR: ``` a sudden onset of right-sided hemiparesis and sensory deficits as well as Wernicke aphasia . ```

Question 334

What's heart block

Answer 334

Impairment of the atrioventricular (AV) node impulse conduction, as represented by the interval between P wave and QRS complex.

Question 335

1st vs 2nd vs 3rd degree block

Answer 335

1st=delayed conduction through AV node 2nd: Mobitz 1: progressive prolongation of AV node conduction resulting in one atrial impulse failing to be conducted through the AV node. The cycle then begins again. Mobitz 2: Intermittent or regular failure of conduction through AV node. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1). 3rd: No relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to a ventricular contraction generated by a focus of depolarization within the ventricle (ventricular escape).

Question 336

Causes of heart block

Answer 336

MI ischaemic heart disease (most common cause) Infection (rheumatic fever, infective endocarditis) Drugs: digoxin, b blockers, Ca2+ antag) Metabolic (hyperkalaemia, cholestatic jaundice, hypothermia) Infiltration (sarcoid, amyloid, neoplasms) Degeneration of conducting systems

Question 337

Hx of 1st, 2nd, 3rd degree block

Answer 337

First degree: Asymptomatic. Wenckebach: Usually asymptomatic Mobitz type II and third-degree block: -May cause Stokes–Adams attacks (syncope caused by ventricular asystole). Other presentations include dizziness, palpitations, chest pain and heart failure.

Question 338

Examination of 1st, 2nd, 3rd degree block

Answer 338

Often normal. Examine for signs of the cause. Complete heart block: Slow large volume pulse; JVP may show ‘cannon waves’. Mobitz type II and third-degree block: Signs of a reduced cardiac output (e.g. hypotension, heart failure).

Question 339

Investigation of heart block

Answer 339

ECG. CXR: Cardiac enlargement, pulmonary oedema. Blood: TFT, digoxin level, cardiac enzymes, troponin. Echocardiogram: Wall motion abnormalities, aortic valve disease, vegetations.

Question 340

Management of chronic block

Answer 340

Permanent pacemaker (PPM) insertion is recommended in patients with third-degree heart block, advanced Mobitz type II and symptomatic Mobitz type I.

Question 341

Management of acute block

Answer 341

IV atropine and consider temporary external pacemaker

Question 342

Complications of heart block

Answer 342

Asystole. Cardiac arrest. Heart failure. Complications of any pacemaker inserted.

Question 343

What is the mechanism of death in HOCM

Answer 343

ARRHYTHMIA! | NOT OUTFLOW OBSTRUCTION

Question 344

What causes arrhtyhmiasin HOCM

Answer 344

Arrhythmias occur in this condition because the severe thickening of the left ventricle increases the metabolic demand of the muscle whilst moving the subendocardial region further away from the coronary arterial blood supply on the epicardial surface of the heart. There is often also obstruction to aortic outflow by the thickened ventricular septum. The subendocardial region being at the “end of the line” of the blood supply becomes prone to ischaemia.

Question 345

Commnon symptoms of HOCM prior to death

Answer 345

Although there may be no symptoms prior to death, angina dyspnoea and syncopal attacks are fairly common

Question 346

Why are limbs that have been paralysed for a number of hours NOT revascularised?

Answer 346

If it's been paralysed for 4 hours and then you revascularise, then the toxins that have built up will be released into the systemic circulation. All the potassium that has built up will go to the heart following removal of the clot in the limb, and will cause the patient to go into cardiac arrest.

Question 347

When does the murmur associated with HOCM increase

Answer 347

``` Hypertrophic cardiomyopathy is a genetic condition characterized by a systolic ``` murmur which increases in intensity with decreased preload .

Question 348

What causes outflow obstruction in HOCM

Answer 348

``` Hypertrophic cardiomyopathy leads to enlargement of the interventricular septum . This can lead to left ventricular outflow obstruction during systole due to the motion of the anterior leaflet of the mitral valve . ``` This also causes the systolic murmur

Question 349

Why does reduced pre-load make the murmur louder in HOCM

Answer 349

``` A decrease in cardiac preload reduces the diameter of the outflow tract and thus increases obstruction which leads to an increased intensity of the murmur . Standing from a squatting position and the Valsalva maneuver are two methods to reduce preload by decreasing venous return. ```

Question 350

Stokes Adams attack?

Answer 350

Stokes-Adams attacks are episodes of transient LOC due to sudden decreased cardiac output. Pallor prior to the attack and facial flushing due to reactive hyperemia after the attack is characteristic of a Stokes-Adams attack. The underlying cause is a cardiac arrhythmia such as complete heart block.

Question 351

Most common cause of hypovolvaemia hypovolaemia

Answer 351

Thiazide diuretics are the most common cause of a hypovolaemic hyponatraemia

Question 352

Pseudohyponatraemia?

Answer 352

Additionally, isotonic hyponatraemia is an artefact due to high levels of lipid or protein and is referred to as pseudohyponatraemia.

Question 353

Best option for hypocalcaemia>?

Answer 353

If urgent replacement is necessary, calcium gluconate can be given IV. It is preferred over calcium chloride as it causes less tissue necrosis if it leaks out

Question 354

Which drug may not work properly if there is hypocalcaemia

Answer 354

It is worth noting that digoxin may be ineffective until serum calcium is restored to normal.

Question 355

Most common peripheral aneurysm

Answer 355

Popliteal

Question 356

What is the most common complication of a popliteal vs femoral aneurysm

Answer 356

A femoral aneurysm may occasionally spontaneously rupture; whereas a popliteal aneurysm may thrombose and present as an acutely ischaemic leg.

Question 357

What is a false femoral aneurysm (pseudoaneurysm)

Answer 357

False femoral aneurysms (or pseudoaneurysms), unlike true aneurysms, do not involve the vessel wall. Rather, they represent an accumulation of blood (haematoma) in a cavity that is held around the vessel by connective tissue. They are a major complication arising from arterial surgery and can occur following cannulation for angiography, or incorrect placement of needles by IVDUs as this leads to breach in the vessel wall and the extravasation of blood. They usually present as a pulsatile (not necessarily expansile) mass in the groin with a history of a surgical procedure/trauma to the region.

Question 358

Most common peripheral aneurysm

Answer 358

Popliteal

Question 359

What is the most common complication of a popliteal vs femoral aneurysm

Answer 359

A femoral aneurysm may occasionally spontaneously rupture; whereas a popliteal aneurysm may thrombose and present as an acutely ischaemic leg.

Question 360

What is a false femoral aneurysm (pseudoaneurysm)

Answer 360

False femoral aneurysms (or pseudoaneurysms), unlike true aneurysms, do not involve the vessel wall. Rather, they represent an accumulation of blood (haematoma) in a cavity that is held around the vessel by connective tissue. They are a major complication arising from arterial surgery and can occur following cannulation for angiography, or incorrect placement of needles by IVDUs as this leads to breach in the vessel wall and the extravasation of blood. They usually present as a pulsatile (not necessarily expansile) mass in the groin with a history of a surgical procedure/trauma to the region.