Cardiovascular 2 Flashcards

1
Q

what is the pathophysiology of aortic dissection?

A
  • aortic dissection begins with a tear in the intimal lining of the aorta
  • the tear allows a column of blood under pressure to enter the aortic wall, forming a haemotoma which separates the intima from the adventitia and creates a false lumen
  • the false lumen extends for a variable distance in either direction; anterograde (towards bifurcations) and retrograde (towards the aortic root)
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2
Q

what is the clinical presentation of aortic dissection?

A
  • sudden onset of severe, tearing and central chest pain that radiates to the back and down the arms
  • pain described as tearing in nature and may be migratory
  • hypertension
  • unequal BP in the arms
  • pain is maximal from the time of onset, unlike in MI where the pain gains in intensity
  • patients may be shocked and may have neurological symptoms secondary to loss of blood supply to the spinal cord
  • peripheral pulses may be absent
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3
Q

what can aortic dissection develop into?

A
  • may develop aortic regurgitation, coronary ischaemia and cardiac tamponade
  • distal extension may produce acute kidney failure, acute lower limb ischaemia or visceral ischaemia
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4
Q

what are differential diagnoses of aortic dissection?

A
  • acute coronary syndrome
  • MI
  • aortic regurgitation without dissection
  • MSK pain
  • pericarditis
  • cholecystitis
  • atherosclerotic embolism
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5
Q

how is aortic dissection diagnosed?

A

CXR:
• widened mediastinum

urgent CT scan, transoesophageal echocardiography or MRI will confirm diagnosis

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6
Q

what is the treatment of aortic dissection?

A
  • at least 50% are hypertensive and may require urgent antihypertensive medication to reduce blood pressure to less than 120mmHg - give IV beta-blockers or vasodilators
  • adequate analgesia
  • surgery to replace aortic arch
  • endovascular intervention with stents
  • patients require long term follow-up with CT or MRI
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7
Q

what is peripheral vascular disease? what is its epidemiology?

A
  • partial blockage of leg or peripheral vessels by an atherosclerotic plaque/resulting thrombus resulting in insufficient perfusion of the lower limb resulting in lower limb ischaemia
  • commonly caused by atherosclerosis and usually affects the aorta-iliac and infra-inguinal arteries
  • more common in men than women
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8
Q

what are risk factors for peripheral vascular disease?

A
  • smoking
  • diabetes
  • hypercholesterolaemia
  • hypertension
  • physical inactivity
  • obesity
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9
Q

what are features of intermittent claudication?

A
  • this is a cramping pain that is induced by exercise and relieved by rest
  • pain is distal to site of atheroma
  • occurs when anaerobic metabolism comes into effect when O2 demand outstrips supply
  • pain is the result of lactic acid production
  • caused by inadequate blood supply to the affected muscles resulting in moderate ischaemia
  • most commonly seen in the calf and leg muscles as a result of atheroma of the leg arteries
  • leg pulses are often absent and the feet may be cold
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10
Q

what are features of critical limb ischaemia in moderate ischaemia/PVD?

A

• blood supply is barely adequate to allow basal
metabolism
• no reserve available for increased demand
• rest pain that is typically nocturnal
• risk of gangrene and/or infection
• chronic condition and the most severe clinical manifestation of peripheral vascular disease

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11
Q

what are general symptoms of chronic lower limb ischaemia?

A
  • absent femoral, popliteal or foot pulses

* cold, white legs

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12
Q

what are differential diagnoses of chronic lower limb ischaemia?

A
  • osteoarthritis of hip/knee due to knee pain at rest

* peripheral neuropathy

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13
Q

how is chronic lower limb ischaemia diagnosed?

A
  • exclude arteritis by looking at ESR/CRP; they would be raised in arteritis
  • FBC: looking particularly at haemoglobin to exclude anaemia or polycthaemia
  • ECG to look for cardiac ischaemia
  • severity of disease is indicated by the ankle/brachial pressure index (ABPI)
  • colour duplex ultrasound; first line test
  • MR/CT angiography to assess extent and location of stenoses and quality of distal vessels if considering intervention
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14
Q

what is the ankle/brachial pressure index (ABPI)? what are the values of intermittend claudication and critical leg ischaemia?

A
  • measurement of the cuff pressure at which blood flow is detectable by Doppler in the posterior tibial or anterior tibial arteries compared to the brachial artery
  • intermittent claudication associated with an ABPI of 0.5-0.9
  • values less than 0.5 are associated with critical leg ischaemia
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15
Q

what are the symptoms of acute lower limb ischaemia?

A
  • Pain
  • Pallor
  • Perishing cold
  • Pulseless
  • Paralysis
  • Paraesthesia - abnormal tingling or prickling
  • the more P’s present the more sudden and the more complete
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16
Q

what is done for risk factor modification for peripheral vascular disease?

A
  • smoking cessation - since every time you smoke, small vessels in the muscles near to ischaemia that provide ‘back up supply’ contract in response to nicotine and tobacco resulting in a reduction in blood flow
  • treat hypertension, hyperlipidaemia and diabetes
  • antiplatelet agent such as P2Y12 inhibitor to prevent progression and minimise risk
  • exercise and weight loss
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17
Q

how is revascularisation done for peripheral vascular disease?

A
  • percutaneous transluminal angioplasty: essentially squash plaque and thus increase perfusion and reduce ischaemia
  • bypass procedure
  • amputation if severe
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18
Q

what is the treatment of acute ischaemia in peripheral vascular disease?

A
  • surgical emergency requiring revascularisation within 4-6hrs to save limb
  • this is an emergency and requires urgent surgery and angioplasty
  • intra-arterial thrombolysis
  • surgical removal of embolus if present
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19
Q

what are clinical symptoms and sings linked to diagnosis of critical/acute ischaemia?

A
  • severe nocturnal pain in all toes of the left foot only relieved by hanging foot over the edge of bed (using gravity to perfuse) = critical ischaemia
  • acute MI = acute ischaemia
  • loss of the use of right side of body and fast irregular pulse = acute ischaemia
  • non-healing painful ulcer on big toe with no trauma = critical ischaemia
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20
Q

what is the definition of shock?

A

term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion (inadequate substrate for aerobic cellular respiration), resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen

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21
Q

what is clinical presentation of shock?

A
  • skin is pale, cold, sweaty and vasoconstricted
  • pulse is weak and rapid
  • pulse pressure reduced
  • mean arterial pressure may be maintained
  • arterial BP is not a good indicator of shock since it will be maintained until a very large amount of blood loss occurs
  • reduced urine output
  • confusion, weakness, collapse and coma
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22
Q

what is the earliest and most accurate sign of shock?

A

capillary refill time taking more than 3 seconds to turn pink after 5 seconds of compression

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23
Q

what are causes of shock?

A
  • hypovolaemic shock
  • cardiogenic shock
  • distributive shock:
    • septic shock
    • anaphylactic shock
    • neurogenic shock
  • anaemic shock
  • cytotoxic shock
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24
Q

what are types of distributive shock?

A

septic, anaphylactic and neurogenic shock

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25
Q

what can cause loss of blood in hypovolaemic shock?

A
  • acute GI bleeding
  • trauma
  • peri/post-operative
  • splenic rupture
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26
Q

what can cause loss of fluid in hypovolaemic shock?

A
  • dehydration - diarrhoea and vomiting
  • burns - heat damage increases the permeability of capillaries so plasma leaks
  • pancreatitis
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27
Q

what are causes of cardiogenic shock?

A

heart doesn’t pump
• cardiac tamponade - blood in pericardial sack placing pressure on heart thereby limiting cardiac output
• pulmonary embolism - flow of blood to lungs is blocked
• acute MI
• fluid overload
• myocarditis

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28
Q

what are causes of septic shock?

A

shock when an infection becomes out of control
• referred to as a distributive shock
• sepsis exists when a systemic inflammatory response is associated with an infection
• septic shock exists when sepsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation

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29
Q

what are causes of anaphylactic shock?

A

release of IgE due to allergic response
• intense allergic reaction
• massive release of histamine and other vasoactive mediators causing haemodynamic collapse
• accompanied by breathlessness and wheeze (due to bronchospasm)

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30
Q

what is used to classify haemorrhagic shock?

A

Tennis score

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31
Q

what are features of class I haemorrhagic shock (Tennis score)?

A
  • 15% blood loss
  • pulse below 100 bpm
  • BP normal
  • pulse pressure normal
  • resp rate; 14-20
  • urine output greater than 30ml/hr
  • slightly anxious
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32
Q

what are features of class II haemorrhagic shock (Tennis score)?

A
  • 15-30% blood loss
  • tachycardia
  • BP normal due to autonomic response (increased sympathetic activity)
  • pulse pressure decreased
  • resp rate; 20-30
  • urine output: 20-30ml/hr
  • mental status: mildly anxious
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33
Q

what are features of class III haemorrhagic shock (Tennis score)?

A
  • 30-40% blood loss
  • pulse above 120 bpm
  • BP decreased
  • pulse pressure decreased
  • resp rate; 30-40
  • urine output: 5-15ml/hr
  • mental status: confused
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34
Q

what is the pathophysiology of haemorrhagic shock?

A
  • reduction in ventricular filling -> fall in BP and SV -> hypotension
  • leads to reduced stimulation of baroreceptors -> increased sympathetic activity with release of noradrenaline and adrenaline
  • vasoconstriction and increased contractility and heart rate helps restore BP and CO
  • reduced capillary BP -> greater level of net movement of fluid into vascular compartment
  • renin release -> Na and water retention
  • angiotensin II causes thirst
  • ADH release
  • release of cortisol causes fluid retention
  • release of glucagon raises blood sugar levels
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35
Q

what is the clinical presentation of hypovolaemic shock?

A
• inadequate tissue perfusion:
- skin: cold, pale, clammy, slate-grey,
- brain: drowsiness and confusion
• increased sympathetic tone
• tachycardia - narrow pulse pressure and weak pulse
• sweating
• BP may be maintained initially but later hypotension
• bradycardia
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36
Q

what is the clinical presentation of cardiogenic shock?

A
  • signs of myocardial failure
  • raised jugular venous pressure (JVP)
  • gallop rhythm
  • basal crackles and pulmonary oedema
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37
Q

what is the clinical presentation of septic shock?

A
  • pyrexia and rigors
  • nausea and vomiting
  • vasodilation with warm peripheries
  • bounding pulse
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38
Q

what is the clinical presentation of anaphylactic shock?

A
  • signs of profound vasodilation
  • warm peripheries
  • low BP
  • tachycardia
  • bronchospasm
  • pulmonary oedema
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39
Q

what are organ systems at risk of shock? how are they affected?

A
  • kidneys; acute tubular necrosis
  • lung; Acute Respiratory Distress Syndrome (ARDs)
  • heart; myocardial ischaemia and infarction
  • brain; confusion, irritability and coma
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40
Q

what is treatment of shock?

A

A: airway (ensure patency)

B: breathing (give 100% O2) and correct immediately life threatening problems such as:

  • congestive cardiac failure
  • bronchospasm
  • tension pneumothorax

C: circulation

  • establish secure IV access
  • give fluid quickly and blood if acute blood loss
  • ensure haemostasis i.e. stop bleeding
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41
Q

what is acute respiratory distress syndrome?

A
  • Impaired oxygenation
  • bilateral pulmonary infiltrates
  • no cardiac failure
  • normal pulmonary arterial pressure (PAOP)
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42
Q

what are extrapulmonary causes of acute respiratory distress syndrome?

A
  • shock of any cause
  • head injury
  • drug reaction
  • sepsis
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43
Q

what are pulmonary causes of acute respiratory distress syndrome?

A
  • pneumonia
  • chemical pneumonitis
  • smoke inhalation
  • near drowning
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44
Q

what is the pathophysiology of acute respiratory distress syndrome?

A
  • alveolar capillary membrane injury results in leakage of fluid into the alveolar spaces
  • there is resulting neutrophil invasion which attracts more neutrophils (exudative phase)
  • eventually fibroblasts come in and initiate healing (proliferative phase)
  • and make scar tissue (fibrotic phase)
  • results in severely stiff lungs and thus severe difficulty in ventilation and thus reduced O2 blood perfusion
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45
Q

what is the clinical presentation of acute respiratory distress syndrome?

A
  • cyanosis
  • tachypnoea
  • tachycardia
  • peripheral vasodilation
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46
Q

what is mitral stenosis?

A
  • obstruction and narrowing of left ventricle inflow that prevents proper filling during diastole
  • mitral valve has 2 cusps
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47
Q

what are the causes/epidemiology of mitral valve stenosis?

A
  • normal mitral valve area is 4-6cm2, symptoms begin at areas less than 2cm2
  • most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever
  • the condition is more common in men than women
  • prevalence and incidence is decreasing due to a reduction of rheumatic heart disease
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48
Q

what is the most common cause of mitral valve stenosis?

A

most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever due to infection with group A beta-haemolytic streptococcus e.g. Streptococcus pyogenes

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49
Q

how does rheumatic fever cause mitral valve stenosis? how does the condition progress?

A
  • inflammation due to rheumatic fever leads to commissural fusion and a reduction in mitral valve orifice area, causing the characteristic doming
    pattern seen on echocardiography
  • over many years, the condition progresses to valve thickening, cusp fusion, calcium deposition, a severely narrowed (stenotic) valve orifice and progressive immobility of the valve cusps
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50
Q

what are causes of mitral valve stenosis other than rheumatic fever/disease?

A
  • infective endocarditis (3.3%)
  • mitral annular calcification (2.7%) - rarely leads to mitral stenosis if extensive, particularly in elderly patients and those with end-stage renal disease
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51
Q

what are risk factors for mitral valve stenosis?

A
  • history of rheumatic fever

- untreated streptococcus infections

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52
Q

what is the pathophysiology of mitral valve stenosis?

A
  • thickening and immobility of the valve leads to obstruction of blood flow from the left atrium to the left ventricle
  • for cardiac output to be maintained, the left atrial pressure increases and left atrial hypertrophy and dilatation occur
  • pulmonary venous, pulmonary arterial and right heart pressures increase
  • the increase in pulmonary capillary pressure leads to development of pulmonary oedema; seen particularly when atrial fibrillation occurs, due to the elevation of left atrial pressure and dilatation, with tachycardia and loss of coordinated atrial contraction
  • partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction
  • pulmonary vasoconstriction leads to pulmonary hypertension and eventually right ventricular hypertrophy, dilatation and failure with subsequent tricuspid regurgitation
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53
Q

what is the clinical presentation of mitral valve stenosis?

A
  • no symptoms until the valve orifice is moderately stenosed i.e. area is less than 2cm2
  • usually doesn’t occur until several decades after the first attack of rheumatic fever
  • progressive exertional dyspnoea
  • haemoptysis
  • atrial fibrillation leading to PE and abrupt deterioration
  • pulmonary hypertension leading to right heart failure with fatigue and lower limb oedema
  • systemic emboli
  • prominent “a” wave in jugular venous pulsations
  • mitral facies/malar flush
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54
Q

why does progressive dyspnoea occur in mitral valve stenosis?

A

due to left atrial dilation resulting in pulmonary

congestion (reduced emptying), which is worse with exercise, fever, tachycardia and pregnancy

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55
Q

why does haemoptysis occur in mitral valve stenosis?

A

due to rupture of bronchial vessels due to the elevated

pulmonary pressure

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56
Q

why does right heart failure occur in mitral valve stenosis?

A

due to the development of pulmonary hypertension with symptoms of weakness, fatigue and abdominal or lower limb swelling

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57
Q

why does atrial fibrillation occur in mitral valve stenosis?

A

due to left atrium dilation giving rise to palpitations

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58
Q

why do systemic emboli occur in mitral valve stenosis?

A

due to atrial fibrillation, most commonly in the cerebral

vessels

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59
Q

why does the prominent a wave in jugular venous pulsations occur in mitral valve stenosis?

A

due to pulmonary hypertension and right ventricular hypertrophy

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60
Q

why does mitral facies/malar flush occur in mitral valve stenosis?

A

bilateral, cyanotic or dusky pink discolouration over the upper cheeks; pinkish-purple patches on the cheeks due to vasoconstriction in response to diminished cardiac output

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61
Q

what heart sounds are heard in mitral valve stenosis on auscultation?

A
  • diastolic murmur
  • loud opening S1 snap
  • the apex beat is ‘tapping’ in quality due to combination of a palpable first heart sound and left ventricular backward displacement produced by an enlarging right ventricle.
  • auscultation at the apex reveals a loud first heart sound, an opening snap (when the mitral valve opens) in early diastole, followed by a rumbling mid-diastolic murmur. If the patient is in sinus rhythm the murmur becomes louder when atrial systole occurs (presystolic accentuation), as a result of increased flow across the narrowed valve.
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62
Q

when is the mitral valve stenosis murmur heard?

A
  • heard when blood flows over a valve
  • low-pitched diastolic rumble most prominent at the apex
  • heard best with patient lying on the left side in held expiration
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63
Q

when is a loud opening S1 snap heard in mitral valve stenosis?

A
  • heard at apex when leaflets are still mobile
  • due to the abrupt halt in leaflet motion in early diastole, after a rapid initial opening, due to fusion at the leaflet tips
  • as the valve cusps become more immobile, the loud first heart sound softens and the opening snap disappears
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64
Q

how is mitral valve stenosis diagnosed by CXR, ECG and echocardiogram?

A
CXR:
• left atrial enlargement
• pulmonary venous hypertension
• pulmonary oedema/congestion in severe disease
• occasionally calcified mitral valve

ECG:
• atrial fibrillation
• left atrial hypertrophy -> bifid P wave (P mitrale)
• features of right ventricular hypertrophy in progressive disease

Echocardiogram:
• gold standard for diagnosis, assesses severity
• assess mitral valve mobility, gradient and mitral valve area
• valve area of <2cm2 indicates moderate stenosis, <1cm2 severe

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65
Q

what is the treatment of mitral valve stenosis?

A
  • mitral stenosis is a mechanical problem and medical therapy does not prevent progression
  • beta-blockers and digoxin which control heart rate (for AF) and thus prolong diastole for improved diastolic filling
  • diuretics for fluid overload
  • anticoagulation in patients with AF to prevent clot formation and embolisation
  • percutaneous mitral balloon valvotomy
  • mitral valve replacement
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66
Q

what is done in percutaneous mitral balloon valvotomy as treatment for mitral valve stenosis?

A
  • catheter is inserted into the right atrium via the femoral vein under local anaesthesia
  • the interatrial septum is punctured and the catheter advanced into the left atrium and across the mitral valve
  • the balloon is inflated and puts pressure on valve thereby separating the leaflets and increasing the size of the mitral valve opening, enabling more blood to flow from left atrium into left ventricle
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67
Q

what is mitral regurgitation? why does it occur?

A

• backflow of blood from the left ventricle to the left atrium during systole
• mild physiological mitral regurgitation (MR) is seen in 80% of normal individuals
- occurs due to abnormalities of the valve leaflets, chordae tendinae, papillary muscles or left ventricle

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68
Q

what is the most frequent cause of mitral regurgitation?

A

most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) resulting in a floppy mitral valve that prolapses

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69
Q

what are other causes of mitral regurgitation?

A
  • ischaemic mitral valve
  • rheumatic heart disease
  • infective endocarditis
  • papillary muscle dysfunction/rupture
  • dilated cardiomyopathy
  • ruptured chordae tendineae
  • dilating left ventricle disease causing functional mitral regurgitation
  • hypertrophic cardiomyopathy
  • rarely: systemic lupus erythematosus, Marfan’s syndrome
  • Ehlers-Danlos syndrome
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70
Q

what are risk factors for mitral regurgitation?

A
  • associated with females
  • lower BMI
  • advanced age
  • renal dysfunction
  • prior MI
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71
Q

what is the pathophysiology of mitral regurgitation?

A
  • regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is longstanding, since the regurgitant flow is compensated for by the large left atrium
  • pure volume overload due to leakage of blood into left atrium during systole
  • circulatory changes depend on the speed of onset and severity of regurgitation
  • with acute mitral regurgitation there is a rise in left atrial pressure, resulting in an increase in pulmonary venous pressure and pulmonary oedema
  • left ventricle dilates, but more so with chronic regurgitation
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72
Q

what are compensatory mechanisms for mitral valve regurgitation? what do they lead to?

A

left arterial enlargement, left ventricle hypertrophy (since left ventricle must put in same effort to pump less blood due to regurgitation so needs to pump harder to maintain cardiac output and thus hypertrophy occurs to increase stroke volume) and increases contractility:

  • progressive left atrial dilatation and right ventricular dysfunction due to pulmonary hypertension
  • progressive left ventricular volume overload leads to dilatation and progressive heart failure
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73
Q

what is the clinical presentation of mitral valve regurgitation on auscultation?

A
  • soft S1 and a pansystolic murmur (palpated as a thrill) loudest at the apex radiating over the precordium and into the axilla
  • prominent third extra heart sound (S3) in congestive heart failure/left atrium overload, caused by rapid filling of the dilated left ventricle in early diastole
  • in chronic mitral regurgitation, the intensity of the murmur does not correlate with the severity
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74
Q

what is the clinical presentation of mitral valve regurgitation?

A
  • exertion dysponea i.e. exercise intolerant
  • dysponea develops because of pulmonary venous hypertension that arises as a direct result of the mitral regurgitation and secondarily as a consequence of left ventricular failure
  • fatigue and lethargy due to reduced cardiac output
  • increased stroke volume is felt as a palpitation
  • symptoms of right heart failure and eventually lead to congestive cardiac failure
  • heart failure may coincide with increased haemodynamic burden e.g in pregnancy, infection or atrial fibrillation
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75
Q

what is the prognosis of mitral valve regurgitation?

A
  • compensatory phase: 10-15 years
  • once patients ejection fraction becomes less than 60% and/or becomes symptomatic then mortality rises sharply
  • severe mitral regurgitation has a 5%/year mortality rate
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76
Q

how is mitral valve regurgitation diagnosed?

A

ECG
• may show left atrial enlargement, atrial fibrillation and left ventricle hypertrophy in severe MR (seen late in course of disease)
• but not diagnostic

CXR:
• left atrial enlargement and central pulmonary artery enlargement

Echocardiogram:
• estimation of left atrium and left ventricle size and function
• also gives valve structure assessment
• transoesophageal is very helpful
• can establish the aetiology and haemodynamic consequences of mitral regurgitation

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77
Q

what medication is given for mitral valve regurgitation?

A
  • vasodilators such as ACE-inhibitors
  • heart rate control for atrial fibrillation with beta blockers, calcium channel blockers and digoxin
  • anticoagulation in atrial fibrillation and flutter
  • diuretics for fluid overload
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78
Q

what are indications for surgery for mitral valve regurgitation?

A

• symptomatic severe mitral regurgitation
- left ventricular fraction >30% and end-diastolic dimension of under 55mm
• asymptomatic:
- if ejection fraction is less than 60%
- left ventricular dysfunction (end systolic dimension >45mm and/or ejection fraction of under 60%)
- if new onset, atrial fibrillation, pulmonary hypertension

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79
Q

what is aortic stenosis?

A

narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue

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80
Q

what is the epidemiology of aortic stenosis?

A
  • normal aortic valve area is 3-4cm2
  • symptoms occur when valve area is 1/4th of normal area
  • primarily a disease of ageing
  • congenital is the second most common cause
  • the most common type of valvular disease in the western world
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81
Q

what are the types of aortic stenosis?

A
  • supravalvular e.g congenital fibrous diaphragm above the aortic valve
  • subvalvular e.g congenital condition in which a fibrous ridge or diaphragm is situated immediately below the aortic valve
  • valvular; most common
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82
Q

what are the 3 main causes of aortic stenosis?

A
  • calcific aortic valvular disease (CAVD) - essentially calcification and degeneration of the aortic valve resulting in stenosis, most commonly seen in elderly
  • calcification of a congenital bicuspid aortic valve (BAV) (valve has 2 leaflets instead of 3 due to genetic disease; this is the most common congenital heart disease) resulting in stenosis
  • rheumatic heart disease; rare now due to eradication
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83
Q

what are risk factors for aortic stenosis?

A
  • congenital bicuspid aortic valve (BAV) predisposes to stenosis and regurgitation
  • congenital BAV is predominant in males
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84
Q

what is the pathophysiology of aortic stenosis?

A
  • due to narrowing there is obstructed left ventricular emptying and a pressure gradient develops between the left ventricle and the aorta resulting in increased afterload
  • results in increased left ventricular pressure and compensatory left ventricular hypertrophy
  • this results in relative ischaemia of the left ventricular myocardium (since hypertrophy results in increased blood demand), and consequent angina, arrhythmias and left ventricular failure
  • left ventricular systolic function is typically preserved in aortic stenosis
  • the obstruction to left ventricular emptying is relatively more severe on exercise; since exercise causes a many-fold increase in cardiac output, however due to severe narrowing of the aortic valve, the cardiac output can hardly increase; thus, the blood pressure falls, coronary ischaemia worsens, the myocardium fails and cardiac arrhythmias develop
  • when this compensatory mechanism is exhausted left ventricular function declines rapidly
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85
Q

what is the clinical presentation of aortic stenosis?

A
  • think aortic stenosis in any elderly person with chest pain, exertional dysponea or syncope
  • classic triad
  • sudden death
  • slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus)
  • heart sounds
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86
Q

what is the classic triad of aortic stenosis?

A
  • syncope - usually exertional
  • angina (increases myocardial oxygen demand; with resulting demand/supply mismatch)
  • heart failure (usually after 60)
  • dysponea on exertion due to heart failure
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87
Q

what heart sounds are heard in aortic stenosis?

A
  • soft or absent second heart sound when the valve becomes immobile
  • carotid pulse is slow rising (plateau pulse) and the apex beat thrusting
  • harsh systolic ejection murmur (palpated as a thrill) at the right upper sternal border and radiating to the carotids
  • prominent 4th (S4) heart sound due to left ventricular hypertrophy
  • ejection systolic murmur crescendo-decrescendo character
  • loudness does not tell you anything about severity
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88
Q

what are differential diagnoses are there for aortic stenosis?

A
  • aortic regurgitation

- subacute bacterial endocarditis

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89
Q

how is aortic stenosis diagnosed through echocardiogram, ECG and CXR?

A

Echocardiogram:
• two measurements obtained are:
- left ventricular size and function; left ventricular hypertrophy, dilation and ejection fraction
- doppler derived gradient and valve area (AVA), allows for the assessment of the pressure gradient across the valve during systole

ECG:
• left ventricular hypertrophy
• left atrial delay
• left ventricular ‘strain’ pattern due to ‘pressure overload’ - depressed ST segments and T-wave inversion in leads orientated towards left ventricle i.e. I, AVL, V5 and 6 when disease is severe

CXR:
• left ventricular hypertrophy
• calcified aortic valve
• normal heart size, prominence of the ascending aorta

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90
Q

what is treatment of aortic stenosis?

A
  • rigorous dental hygiene/care due to the increased risk of infective endocarditis (IE) in anyone with valvular heart disease; consider IE prophylaxis in dental procedures
  • limited role for medication due to the fact that aortic stenosis is a mechanical problem
  • vasodilators are contraindicated in severe aortic stenosis because they may trigger hypotension and thus syncope
  • surgical aortic valve replacement (definitive treatment)
  • TAVI
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91
Q

what is the definitive treatment for aortic stenosis?

A

surgical aortic valve replacement

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92
Q

what are indications for surgical aortic valve replacement for aortic stenosis?

A
  • any symptomatic patients with severe aortic stenosis
  • any patient with decreasing ejection fraction
  • any patent undergoing CABG with moderate or severe aortic stenosis
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93
Q

what is involved in TAVI for aortic stenosis?

A

Transcutaneous Aortic Valve Implantation
• minimally invasive
• pass catheter up the aorta then inflate balloon across the narrowed valve which will crack the calcification
• then pass another catheter which leaves a stent with a valve = new aortic valve

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94
Q

what is aortic regurgitation?

A
  • leakage of blood into the left ventricle from the aorta during diastole due to ineffective coaptation (bringing together) of the aortic cusps
  • reflux of blood from the aorta through the aortic valve into the left ventricle during diastole
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95
Q

what is the epidemiology of aortic regurgitation? what are the main causes of it?

A
  • can be associated with aortic stenosis
  • main causes:
    • congenital bicuspid aortic valve (BAV)
    • rheumatic fever
    • infective endocarditis
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96
Q

what are risk factors for aortic regurgitation?

A
  • SLE
  • Marfan’s and Ehlers-Danlos syndrome; connective tissue disorders
  • aortic dilatation
  • infective endocarditis or aortic dissection
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97
Q

what is the pathophysiology of aortic regurgitation?

A
  • if net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase and the left ventricular size must enlarge -> left ventricle dilatation and hypertrophy
  • progressive dilation leads to heart failure
  • the remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole; regurgitation causes diastolic blood pressure to fall and thus coronary perfusion decreases
  • the large left ventricular size is mechanically less efficient, so demand for oxygen is greater and cardiac ischaemia develops
  • stroke volume increases, leading to increased pulse pressure
  • contraction of the ventricle deteriorates -> left ventricular failure
  • adaptation to volume load entering left ventricle don’t occur with acute regurgitation, leading to pulmonary oedema and reduced stroke volume
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98
Q

what is the clinical presentation of aortic regurgitation?

A
  • in chronic regurgitation, patients remain asymptomatic for many years before symptoms develop
  • exertional dysponea
  • palpitations
  • angina
  • syncope
  • wide pulse pressure
  • apex beat displaced laterally
  • collapsing water hammer pulse (bounding and forceful, rapidly increasing and subsequently collapsing)
  • Quincke’s sign - capillary pulsation in the nail beds
  • de Musset’s sign - head nodding with each heart beat
  • pistol shot femoral - a sharp bang heard on auscultation
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99
Q

what heart sounds are heard in aortic regurgitation?

A
  • early diastolic blowing murmur at the left sternal border in the 4th intercostal space; accentuated when patient sits forward with breath held in expiration
  • ejection systolic murmur; due to increased stoke volume leading to turbulent flow across the aortic valve
  • Austin Flint murmur: mid-diastolic murmur over the cardiac apex produced due to aortic jet impinging on the mitral valve, producing premature closure of the valve and physiological stenosis
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100
Q

what is collapsing water hammer pulse?

A
  • bounding and forceful pulse rapidly increasing and subsequently collapsing
  • seen in aortic regurgitation
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101
Q

what is Quincke’s sign?

A
  • capillary perfusion in the nail beds

- seen in aortic regurgitation

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102
Q

what is de Musset’s sign?

A
  • head nodding with each heart beat

- seen in aortic regurgitation

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103
Q

what is pistol shot femoral?

A
  • a sharp bang heard on auscultation

- seen in aortic regurgitation

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104
Q

what are differential diagnoeses of aortic regurgitation?

A
  • heart failure
  • infective endocarditis
  • mitral regurgitation
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105
Q

how is aortic regurgitation diagnosed with CXR, echocardiogram and ECG?

A

echocardiogram:
• evaluation of the aortic valve and aortic root
• measurement of left ventricle dimensions and function
• cornerstone for decision making and follow up evaluation

CXR:
• enlarged cardiac silhouette and aortic root enlargement
• left ventricular enlargement

ECG:
• signs of left ventricular hypertrophy due to ‘volume overload’ - tall R waves and deeply inverted T waves in left-sided chest leads, and deep S waves in right-sided leads

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106
Q

what is treatment of aortic regurgitation?

A
  • in general consider infective endocarditis prophylaxis
  • vasodilators and diuretics e.g ACE-inhibitors e.g. Ramipril will improve stroke volume and reduce afterload and regurgitation but only if patient is symptomatic or has hypertension
  • serial echocardiograms to monitor progression
  • surgery for valve replacement:
    • if symptoms are increasing, enlarging heart on CXR/ECHO, ECG
    deterioration (T wave inversion in lateral leads)
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107
Q

what is infective endocarditis?

A
  • an infection of the endocardium or vascular endothelium of the heart
  • known as subacute bacterial endocarditis (SBE)
  • may occur as a fulminating or acute infection
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108
Q

where in the heart does infection of endocarditis occur on?

A
  • valves with congenital or acquired defects (usually on the left side of the heart)
  • right sided endocarditis more common in IV drug addicts
  • normal valves with virulent organisms
  • prosthetic valves and pacemakers
  • in association with a ventricular septal defect or persistent ductus arteriosus
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109
Q

what is the epidemiology of infective endocarditis?

A
  • more common in developing countries
  • disease of:
    • the elderly or those with prosthetic valves
    • the young IV drug user
    • the young with congenital heart disease
  • more common in males
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110
Q

what organisms cause infective endocarditis?

A
  • Staphylococcus aureus (IVDU, diabetes and surgery); most common cause
  • Pseudomonas aeruginosa
  • Streptococcus viridans (dental problems); gram positive, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri and strep. oralis)
  • enterococci
  • Coxiella burnetii, Chlamydia spp., Bartonella spp. and Legionella
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111
Q

what are risk factors for infective endocarditis?

A
  • IV drug use
  • poor dental hygiene
  • skin and soft tissue infection
  • dental treatment
  • IV cannula
  • cardiac surgery
  • pacemaker
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112
Q

what is the pathophysiology of infective endocaditis?

A
  • a mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valve
  • damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation
  • aortic and mitral valves are most commonly involved; IV drug users are the exception since right-sided lesions are more common in them
  • virulent organisms destroy the valve they are on, leading to regurgitation and worsening heart failure
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113
Q

what are things that would raise high clinical suspicion of infective endocarditis?

A

• new valve lesion/regurgitant murmur
• embolic events of unknown origin
• sepsis of unknown origin
• haematuria, glomerulonephritis and suspected renal infarction
• fever plus:
- prosthetic material inside the heart
- risk factor for infective endocarditis e.g. IV drug user
- newly developed ventricular arrhythmias or conduction disturbances

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114
Q

what are clinical presentations of infective endocarditis?

A
  • headache, fever, malaise, confusion, and night sweats
  • finger clubbing
  • if Staphylococcus aureus, then will develop very quickly; high fever and feel ill rapidly, with the other virulent ones you don’t feel as ill
  • embolisation of vegetations e.g. stroke, pulmonary embolus, bone infections, kidney dysfunction and myocardial infarction
  • valve dysfunction results in in arrhythmia and heart failure
  • endocarditis should be excluded in any patient with a heart murmur and fever
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115
Q

what are clinical manifestations of infective endocarditis?

A
  • splinter haemorrhages on nail beds of fingers
  • embolic skin lesions; black spots on skin (infarcts caused by bits of infective vegetation blocking small capillaries)
  • Osler nodes; tender nodules in the digits
  • Janeway lesions; haemorrhages and nodules in the fingers
  • Roth spots; retinal haemorrhages with white or clear centres seen on fundoscopy
  • Petechiae; small red/purple spots caused by bleeds in the skin
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116
Q

what are embolic skin lesions?

A

black spots on skin (infarcts caused by bits of infective vegetation blocking small capillaries)
- seen in infective endocarditis

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117
Q

what are Osler nodes?

A

painful, red, raised lesions found on the hands and feet

- seen in infective endocarditis

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118
Q

what are Janeway lesions?

A

rare, non-tender, small erythematous or haemorrhagic macular, papular or nodular lesions on the palms or soles only a few millimeters in diameter
- seen in infective endocarditis

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119
Q

what are Roth spots?

A

retinal haemorrhages with white or clear centres seen on fundoscopy
- seen in infective endocarditis

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120
Q

what are petechiae?

A

small red/purple spots caused by bleeds in the skin

- seen in infective endocarditis

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121
Q

how is infective endocarditis diagnosed?

A
  • use Dukes criteria
  • blood cultures and tests
  • urinalysis (look for haematuria)
  • CXR: cardiomegaly, heart failure or septic emboli in right-sided endocarditis
  • ECG: long PR interval at regular intervals (may show MI or conduction defects)
  • echocardiogram
  • serum immunoglobulins are increased and complement levels are decreased due to immune complex formation
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122
Q

what is looked for in blood cultures when diagnosing infective endocarditis?

A
  • 3 sets from different sites over 24 hours
  • take before starting antibiotics
  • identifies in 75% of cases
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123
Q

what is looked for in blood tests when diagnosing infective endocarditis?

A
  • CRP and ESR raised
  • normochromic, normocytic anaemia
  • neutrophilia
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124
Q

what types of echocardiogram are used in diagnosing infective endocarditis?

A
  • transthoracic echo (TTE)

- tranoesophageal echo (TOE)

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125
Q

how is transthorachic echo used to diagnose infective endocarditis?

A
  • safe, non invasive, no discomfort but often poor images so low sensitivity but can identify vegetations
    (if greater than 2mm); a negative TTE does not exclude the diagnosis of infective endocarditis
  • identifies vegetations and underlying valvular dysfunction
  • smaller vegetations may be missed
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126
Q

how is transoesophageal echo used to diagnose infective endocarditis?

A
  • more sensitive but very uncomfortable, is useful for visualising mitral lesions and possible development of aortic root abscess; better at diagnosing than TTE
  • used in cases of suspected prosthetic valve endocarditis
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127
Q

what is the treatment of infective endocarditis?

A
  • antibiotic treatment for 4-6 weeks
  • if not staphylococcus then use penicillin, benzylpenicillin and gentamycin
  • if staphylococcus then use vancomycin and rifampicin (if MRSA)
  • treat complications
  • surgery
  • recommend good oral health and inform patients of symptoms
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128
Q

what are the complications of infective endocarditis?

A

arrhythmia, heart failure, heart block, embolisation, stroke rehab and abscess

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129
Q

how is surgery used to treat infective endocarditis?

A
  • operate if the infection cannot be cured with antibiotics
  • operate to remove infected devices
  • operate to remove large vegetations before they embolise
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130
Q

what is the most common form of congenital heart disease?

A

bicuspid aortic valve (1-2% of live births)

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131
Q

what is the epidemiology of bicuspid aortic valve?

A
  • most common form of congenital heart disease, occurring in 1-2% of live births
  • more common in males than females
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132
Q

what occurs in bicuspid aortic valve?

A
  • bicuspid aortic valve only has 2 cusps
  • these can work well at birth and go undetected but can be severely stenotic in infancy or childhood
  • degenerate quicker than normal valves
  • become regurgitant earlier than normal valves
  • are associated with coarctation and dilation of the ascending aorta
  • may eventually develop aortic stenosis (requiring valve replacement) with or without aortic regurgitation thereby predisposing to infective endocarditis
  • intense exercise may accelerate complications so do yearly echocardiograms on affected athletes
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133
Q

what is the epidemiology of atrial septal defects?

A

• often first diagnosed in adulthood and represents
one third of congenital heart disease
• more common in women than men

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134
Q

what are features of atrial septal defects?

A

• abnormal connection between the two atria
• a probe can be passed through the layers of the
foramen ovale (called the primum and secundum)
so is sometimes known as “Probe patent foramen
ovale”
• slightly higher pressure in the left atrium than the
right atrium
• shunt is left-to-right
• thus not blue i.e. acyanotic
• increased flow into the right heart and lungs

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135
Q

what can happen to untreated atrial septal defects?

A

if left untreated develop right heart overload and dilatation; the right ventricle is compliant and easily dilates to accommodate the increased pulmonary flow. this can result in:

  • right ventricular hypertrophy
  • pulmonary hypertension - Eisenmenger’s reaction
  • increased risk of infective endocarditis
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136
Q

what is the clinical presentation of atrial septal defects?

A
  • dysponea
  • exercise intolerance
  • may develop atrial arrhythmias from right atrial dilatation
  • pulmonary flow murmur
  • fixed split second heart sound (delayed closure of the pulmonary valve because more blood has to get out)
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137
Q

how can atrial septal defects be diagnosed?

A

CXR:
• large pulmonary arteries
• large heart

ECG:
• right bundle branch block (RBBB) due to right ventricle dilatation

echocardiogram:
• hypertrophy and dilation of right side of heart and pulmonary arteries

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138
Q

what are features of ventricular septal defects?

A
  • abnormal connection between the two ventricles
  • many close spontaneously during childhood
  • common - 20% of all congenital heart defects
  • higher pressure in left ventricle than right ventricle
  • thus left-to-right shunt
  • thus does not go blue i.e. acyanotic
  • increased blood flow through the lung
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139
Q

what are some large defects in ventricular septal defects?

A
  • the large volumes of blood flowing through the pulmonary vasculature lead to pulmonary hypertension and eventual Eisenmenger’s complex, when right ventricular pressure becomes higher than the left, as a result blood starts to shunt right-to-left resulting in cyanosis
  • small breathless skinny baby
  • increased respiratory rate
  • tachycardia
  • CXR: big heart
  • murmur varies in intensity
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140
Q

what are some small defects in ventricular septal defects?

A
  • large systolic murmur
  • thrill (buzzing sensation)
  • well grown
  • normal heart rate
  • normal heart size
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141
Q

what is treatment for ventricular septal defects?

A
  • medical initially since many will spontaneously close
  • surgical closure
  • if small then no intervention is required
  • prophylactic antibiotics
  • if moderately sized lesion; furosemide, ACE inhibitor and digoxin may suffice
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142
Q

what are features of atrio-ventricular septal defects?

A

• associated with Downs syndrome
• basically a hole in the very centre of the heart
• involves the ventricular septum, the atrial septum,
the mitral and tricuspid valves
• can be complete or partial
• instead of two separate atrio-ventricular valves
there is just one big malformed one which usually leaks

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143
Q

what is the clinical presentation of a complete atrio-ventricular septal defect?

A
  • breathlessness as neonate
  • poor weight gain and feeding
  • torrential pulmonary flow which can result in Eisenmenger’s resulting in cyanosis over time
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144
Q

what is the clinical presentation of a partial atrio-ventricular septal defect?

A
  • can present in late adulthood

* presents similar to ventricular/atrial septal defect e.g. dysponea, tachycardia, exercise intolerance etc.

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145
Q

what is the treatment of atrio-ventricular septal defects?

A
  • pulmonary artery banding if large defect in infancy; band reduces blood flow to lungs thereby reducing pulmonary hypertension and Eisenmenger’s syndrome
  • surgical repair is challenging
  • a partial defect may be left alone if there is no right heart dilatation
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146
Q

what is the definition of patent ductus arteriosus? what is its epidemiology?

A

• affects girls more than boys
• ductus arteriosus is a persistent communication
between the proximal left pulmonary artery and the
descending aorta

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147
Q

what usually happens to the ductus arteriosus?

A

• in foetal life, pulmonary vascular resistance is high
(since bronchioles are filled with fluid and vessels are
vasoconstricted due to lack of O2) and the right heart
pressure exceeds that of left; consequently flow is
from right to left atrium through foramen ovale, and
from pulmonary artery to aorta via the ductus arteriosus
• normally, the ductus arteriosus closes within a few hours of birth in response to decreased pulmonary resistance; however in some cases e.g. in premature babies and in cases with maternal rubella, the ductus persists

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148
Q

why may a ductus arteriosus not close?

A
  • premature babies

- maternal rubella

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149
Q

what happens if the ductus arteriosus remains open?

A

• if it remains open, there is an abnormal left-to-right shunt (from aorta to pulmonary artery) and
eventually means that the lung circulation is overloaded with pulmonary hypertension (leading
to Eisenmenger syndrome) and right side cardiac
failure (due to right ventricular hypertrophy in
response to increased afterload)
• also increases risk of infective endocarditis

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150
Q

what is the clinical presentation of a patent ductus arteriosus?

A
  • continuous ‘machinery’ murmus
  • bounding pulse
  • if large then large heart and breathlessness
  • Eisenmenger’s syndrome with differential cyanosis that is clubbed and blue toes but pink and not clubbed fingers
  • tachycardia
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151
Q

how can a patent ductus arteriosus be diagnosed?

A

CXR: with large shunt the aorta and pulmonary arterial system may be prominent

ECG: may demonstrate left atrial abnormality and left ventricular hypertrophy

echocardiogram: may show dilated left atrium and left ventricle

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152
Q

what is the treatment of patent ductus arteriosus?

A
  • can be closed surgically or percutaneously
  • low risk of complications
  • venous approach may require an AV loop
  • Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure
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153
Q

what is the definition of coarctation of the aorta?

A

• a narrowing of the aorta at, or just distal to, the
insertion of the ductus arteriosus (distal to the origin of the left subclavian artery)
• the net result is a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body, thus stronger perfusion to upper body compared to lower

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154
Q

what are the consequences of coarctation of the aorta?

A

resultant decreased renal perfusion leads to systemic hypertension that persists even after surgical correction

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155
Q

what is the epidemiology of coarctation of the aorta?

A
  • more common in men than women

- associated with Turner syndrome, berry aneurysms and patent ductus arteriosus

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156
Q

what is the clinical presentation of coarctation of the aorta?

A
  • often asymptomatic for many years
  • right arm hypertension
  • bruits (buzzes) over the scapulae and back from collateral vessels
  • murmur
  • headaches and nose bleeds (due to hypertension)
  • hypertension in the upper limbs
  • discrepant blood pressure in the upper and lower body (will notice radial pulse before femoral pulse)
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157
Q

what are long term problems associated with coarctation of the aorta?

A

hypertension:

  • early coronary artery disease
  • early strokes
  • sub-arachnoid haemorrhage
158
Q

how can coarctation of the aorta be diagnosed?

A

CXR: dilated aorta indented at the site of the coarctation

ECG: left ventricular hypertrophy

CT: can accurately demonstrate the coarctation and quantify flow

159
Q

what is treatment of coarctation of the aorta?

A
  • surgery
  • balloon dilatation (preferred for re-coarctation) and stenting
  • risk of aneurysm formation at the site of repair
160
Q

what is the most common form of cyanotic congenital heart disease?

A

Tetralogy of Fallot

161
Q

what occurs in Tetralogy of Fallot?

A

• consists of:

  • a large, maligned Ventricular Septal Defect (VSD)
  • an overriding aorta
  • pulmonary valve stenosis
  • right ventricular hypertrophy
  • the stenosis of the right ventricle outflow leads to the right ventricle being at a higher pressure than the left
  • thus blue blood passes from the right ventricle to the left ventricle
  • the patients are blue/cyanotic
162
Q

what is clinical presentation of Tetralogy of Fallot?

A
  • central cyanosis
  • low birthweight and growth
  • dysponea on exertion
  • delayed puberty
  • systolic ejection murmurs
  • CXR: boot shaped heart
163
Q

what is the treatment of Tetralogy of Fallot?

A
  • full surgical treatment during first two years of life due to the progressive cardiac debility and cerebral thrombosis risk
  • often get pulmonary valve regurgitation in adulthood and require redo surgery
164
Q

what is pulmonary stenosis? what are the different types?

A
  • narrowing of the outflow of the right ventricle

- valvar, sub-valvar or supra-valvar

165
Q

what are features of severe pulmonary stenosis?

A
  • right ventricular failure as neonate
  • collapse
  • poor pulmonary blood flow
  • right ventricular hypertrophy
  • tricuspid regurgitation
166
Q

what are features of moderate/mild pulmonary stenosis?

A
  • well tolerated for many years

- right ventricular hypertrophy

167
Q

what is treatment of pulmonary stenosis?

A
  • balloon valvoplasty: place catheter with balloon through femoral vein then inflate balloon at stenosis to crush it but this can result in regurgitation
  • open valvotomy
  • shunt to bypass the blockage
168
Q

what are features of complete transposition of the great arteries?

A
  • involves the aorta coming off the right ventricle and the pulmonary trunk coming off the left ventricle
  • two closed circulations result
  • more common in men and associated with diabetes
169
Q

what is required for survival in complete transposition of the great arteries?

A

survival is only possible if there is communication between the two circuits and virtually all have some form of atrial septal defect with blood mixing

170
Q

what is treatment of complete transposition of the great arteries?

A

atrial switch operation, with good results

171
Q

what is dextrocardia?

A
  • heart points to the right side of the chest instead of to the left
  • associated with severe cardiovascular abnormalities
172
Q

what are some common symptoms of heart disease?

A

chest pain, breathlessness, palpitations, syncope, fatigue and peripheral oedema

173
Q

what does the NYHA grading classify?

A

cardiac status; severity of anginal pain, dyspnoea, palpitations or fatigue

174
Q

what the 4 grades of the NYHA grading of cardiac status?

A

Grade 1: uncompromised (no breathlessness)
Grade 2: slightly compromised (on severe exertion)
Grade 3: moderately compromised (on mild exertion)
Grade 4: severely compromised (breathless at rest)

175
Q

what is chest pain? what can point to its cause?

A
  • chest pain or discomfort is a common presenting symptom of cardiovascular disease and must be differentiated from non-cardiac causes
  • the site of pain, its character, radiation and associated symptoms will often point to the cause
176
Q

what are the common causes of central chest pain?

A
  • angina pectoris
  • ACS
  • pericarditis
  • aortic dissection
  • massive PE
  • MSK pain
  • GORD
177
Q

what are features of angina pectoris as a common cause of central chest pain?

A

crushing pain on exercise, relieved by rest. may radiate to jaw or arms

178
Q

what are features of ACS as a common cause of central chest pain?

A

similar in character to angina but more severe, occurs at rest, lasts longer

179
Q

what are features of pericarditis as a common cause of central chest pain?

A

sharp pain aggravated by movement, respiration and changes in posture

180
Q

what are features of aortic dissection as a common cause of central chest pain?

A

severe tearing chest pain radiating through to the back

181
Q

what are features of massive PE as a common cause of central chest pain?

A

with dyspnoea, tachycardia and hypotension

182
Q

what are features of MSK causes of central chest pain?

A

tender to palpate over affected area

183
Q

what are features of GORD as a common cause of central chest pain?

A

may be exacerbated by bending or lying down (at night). pain may radiate into the neck

184
Q

when is the normal heartbeat sensed?

A

when the patient is anxious, excited, exercising or lying on the left side

185
Q

what are abnormal causes of palpitations?

A

cardiac arrhythmia, commonly ectopic beats or a paroxysmal tachycardia

186
Q

what is syncope? what are features of an attack?

A

temporary impairment of consciousness due to inadequate cerebral blood flow

  • attacks occur suddenly and without warning
  • they last only 1 or 2 minutes, with complete recovery in seconds (compare with epilepsy, where complete recovery may be delayed for some hours)
187
Q

what are some common causes of altered consciousness and falls in adults?

A
  • syncope
  • underlying structural cardiopulmonary disease, e.g. aortic stenosis, PE
  • arrhythmias
  • reflex – vasovagal (simple faint)
  • carotid sinus hypersensitivity
  • situational: cough, micturition, postexertional
  • postural (orthostatic) hypotension: autonomic failure, volume depletion
  • epilepsy
  • hypoglycaemia
  • psychogenic
  • panic attacks
  • hyperventilation
  • narcolepsy and cataplexy
188
Q

what are the cardiac causes of syncope?

A
  • result of either very fast (e.g. ventricular tachycardia) or very slow heart rates (e.g. complete heart block) which are unable to maintain an adequate cardiac output
  • obstruction to ventricular outflow also causes syncope (e.g. aortic stenosis, hypertrophic cardiomyopathy), which occurs on exercise when the requirements for increased cardiac output cannot be met
189
Q

what is postural hypotension?

A

a drop in systolic blood pressure (BP) of 20mmHg or more on standing up from a sitting or lying position

190
Q

what are common causes of lateral/peripheral chest pain?

A
  • pulmonary infarct
  • pneumonia
  • pneumothorax
  • MSK
  • lung carcinoma
  • herpes zoster
191
Q

what are features of lung carcinoma as a common cause of lateral/peripheral chest pain?

A

constant dull pain

192
Q

what are features of herpes zoster as a common cause of lateral/peripheral chest pain?

A

burning unilateral pain corresponding to a dermatome that appears 2 to 3 days before the typical rash

193
Q

what is an abnormal cardiothoracic ratio in a chest X-ray? what can it indicate?

A

a cardiothoracic ratio of greater than 50% on a PA film is abnormal and normally indicates cardiac dilatation or pericardial effusion

194
Q

what does the main LBB divide into?

A

anterior superior division (anterior hemi-bundle) and a posterior inferior division (posterior hemi-bundle)

195
Q

what are features of an abnormal P wave?

A
  • broad and notched (> 0.12 s, i.e. three small squares) in left atrial enlargement (‘P mitrale’, e.g. mitral stenosis)
  • tall and peaked (> 2.5 mm) in right atrial enlargement (‘P pulmonale’, e.g. pulmonary hypertension)
  • replaced by flutter or fibrillation waves (p. 430)
  • absent in sinoatrial block
196
Q

what does ST elevation and ST depression indicate?

A
  • ST elevation (>1mm above isoelectric line) occurs in early stages of MI and with acute pericarditis
  • ST depression (>0.5mm below the isoelectric line) indicates myocardial ischaemia
197
Q

how is the corrected QT interval calculated?

A

QTc = QT/square root of (R-R)

198
Q

what is long QT syndrome associated with?

A

increased risk of torsades de pointes ventricular tachycardia and sudden death

199
Q

what is the cardiac axis?

A

overall direction of the wave of ventricular depolarisation in the vertical plane measured from a zero reference point

200
Q

what is the normal range for the cardiac axis?

A

the normal range for the cardiac axis is between −30° and +90. an axis more negative than −30° is termed left axis deviation and an axis more positive than +90° is termed right axis deviation

201
Q

what is left axis deviation? why does it occur?

A

an axis more negative than −30° is termed left axis deviation
- block of anterior bundle of the main LBB, inferior MI and WPW syndrome

202
Q

what is right axis deviation? why does it occur?

A

an axis more positive than +90° is termed right axis deviation

  • may be normal
  • right ventricular overload, dextrocardia, WPW and left posterior hemiblock
203
Q

how can cardiac axis be calculated?

A

a simple method to calculate the axis is by inspection of the QRS complex in leads I, II and III.

  • the axis is normal if leads I and II are positive
  • there is right axis deviation if lead I is negative and lead III positive
  • there is left axis deviation if lead I is positive and leads II and III negative
204
Q

what do the QRS complexes look like in a normal cardiac axis?

A

lead I: normal QRS complex
lead II: tall R wave
lead III: small equal QRS complex

205
Q

what are contraindications to exercise ECG?

A
  • unstable angina
  • severe hypertrophic cardiomyopathy
  • severe aortic stenosis
  • malignant hypertension
206
Q

what is a positive test and indications for stopping the exercise ECG?

A
  • chest pain
  • ST segment depression or elevation >1mm
  • fall in systolic BP >20mmHg
  • fall in HR despite and increase in workload
  • BP >240/110
  • significant arrhythmias or increased frequency of ventricular ectopics
207
Q

what is tilt testing used for?

A

tilt testing is performed to investigate suspected neurocardiogenic (vasovagal) syncope in which patients give a history of repeated episodes of syncope which occur without warning and are followed by a rapid recovery

208
Q

what are the two types of echocardiography of the heart?

A
  • transthoracic echo

- transoesophageal echo

209
Q

how is transthoracic echo performed?

A

transthoracic echo is the most common method and involves the placement of a handheld transducer on the chest wall. ultrasound pulses are emitted through various body tissues, and reflected waves are detected by the transducer as an echo

210
Q

how is left ventricular function assessed in a transthoracic echo?

A

left ventricular function is assessed by the ejection fraction (percentage of blood ejected from the left ventricle with each heartbeat) – normally > 55%

211
Q

how is transoesophageal echocardiography performed?

A

transoesophageal echo uses miniaturized transducers incorporated into special endoscopes. it allows better visualization of some structures and pathology, e.g. aortic dissection, endocarditis

212
Q

how is Doppler echocardiography performed? what does it assess?

A

doppler echocardiography uses the Doppler principle to identify and assess the severity of valve lesions, estimate cardiac output and assess coronary blood flow.

213
Q

what are general principles of management of arrhythmias?

A
  • patients with adverse symptoms and signs (low cardiac output, chest pain, hypotension, impaired consciousness or severe pulmonary oedema) require urgent treatment of their arrhythmia
  • oxygen is given to all patients, intravenous access established and serum electrolyte abnormalities (potassium, magnesium, calcium) are corrected
214
Q

what is sinus bradycardia?

A
  • fluctuations of autonomic tone result in phasic changes in the sinus discharge rate
  • normal during sleep and in well-trained athletes
215
Q

what are causes of sinus bradycardia that are extrinsic to the heart?

A
  • drug therapy (beta blockers, digitalis and other antiarrhythmic drugs)
  • hypothyroidism
  • hypothermia
  • cholestatic jaundice
  • raised intracranial pressure
216
Q

what are causes of sinus bradycardia that are intrinsic to the heart?

A
  • acute ischaemia and infarction of the sinus node (as a complication of MI)
  • chronic degenerative changes e.g. fibrosis of the atrium and sinus node (sick sinus syndrome) occurring in elderly people
217
Q

what is the treatment of persistent symptomatic bradycardia?

A
  • patients with persistent symptomatic bradycardia are treated with a permanent cardiac pacemaker.
  • first-line treatment in the acute situation with adverse signs is atropine
  • temporary pacing (transcutaneous, or transvenous) is an alternative.
218
Q

what is the pathophysiology of sick sinus syndrome?

A
  • bradycardia is caused by intermittent failure of sinus node depolarization (sinus arrest) or failure of the sinus impulse to propagate through the perinodal tissue to the atria (sinoatrial block)
  • the slow heart rate predisposes to ectopic pacemaker activity and tachyarrhythmias are common (tachy–brady syndrome)
219
Q

what is seen on the ECG in sick sinus syndrome?

A

the ECG shows severe sinus bradycardia or intermittent long pauses between consecutive P waves (> 2 s, dropped P waves)

220
Q

what is the treatment of sick sinus syndrome?

A
  • permanent pacemaker insertion
  • antiarrhythmic drugs are used to treat tachycardias.
  • thromboembolism is common in sinus node dysfunction and patients are anticoagulated unless there is a contraindication.
221
Q

when is ventricular tachycardia more likely than SVT?

A

ventricular tachycardia is more likely than SVT with:

  • history of ischaemic heart disease
  • QRS interval > 140 ms
  • atrioventricular dissociation – P waves have no relationship to the QRS complexes
  • capture complexes – intermittent normal QRS complex
  • RS interval > 100 ms
  • bifid, upright QRS complex with a taller first peak in V1
  • deep S wave in V6
  • concordant QRS direction in leads V1–V6, i.e. all positive or all negative complexes
222
Q

what drugs are used in AVRT and AVNRT?

A
  • adenosine (very short acting AV nodal blocking drug that will terminate most junctional tachycardias)
  • IV verapamil
  • beta blockers
223
Q

what are cardiac causes of atrial arrhythmias?

A
  • ischaemic heart disease, rheumatic heart disease, valvular heart disease
  • cardiomyopathy
  • lone atrial fibrillation (no cause identified)
  • Wolff–Parkinson–White syndrome
  • pericarditis, myocarditis
  • atrial septal defect, cardiac surgery
224
Q

what are pulmonary causes of atrial arrhythmias?

A
  • pneumonia
  • PE
  • carcinoma of the bronchus
  • COPD
225
Q

what are NOACs? what categories can they be classified into?

A

novel oral anticoagulants

  • direct thrombin inhibitors (e.g. Dabigatran)
  • oral direct factor Xa inhibitors (e.g. Rivaroxaban and Apixaban)
226
Q

how do NOACs compare to warfarin? what should be considered before prescribing them?

A
  • block a single step in the coagulation cascade (thrombin or factor Xa inhibitors)
  • warfarin blocks several vitamin K dependent factors (II, VII, IX, X)
  • unlike warfarin, the NOACs have rapid onset of action, shorter half-life, fewer food and drug interactions and do not require INR testing
  • however, these agents require dose reduction or avoidance in patients with renal impairment, elderly patients or those with low body weight
227
Q

what is cardiac arrest?

A
  • in cardiac arrest there is no effective cardiac output. the patient is unconscious and apnoeic with absent arterial pulses (best felt in the carotid artery in the neck)
  • irreversible brain damage occurs within 3 minutes if an adequate circulation is not established
228
Q

what is non-sustained ventricular tachycardia?

A
  • this is defined as VT ≥ 5 consecutive beats but lasting <30s
  • common in patients with heart disease (and in a few individuals with normal hearts)
229
Q

what is treatment of non-sustained ventricular tachycardia?

A

the treatments indicated are β-blockers in symptomatic patients or an ICD in patients with poor left ventricular function (ejection fraction < 30%) in whom it improves survival

230
Q

what are other causes of heart failure?

A

• valvular heart disease e.g. aortic stenosis, aortic and mitral regurgitation, tricuspid
• cardiomyopathy (hypertrophic, restrictive)
• congenital heart disease (atrial septal defect, ventricular septal defect)
• hyperdynamic circulation (anaemia, thyrotoxicosis, Paget’s disease)
• hypertension
• alcohol and chemotherapy (e.g. imatinib, doxorubicin)
• right heart failure (RV infarct, pulmonary hypertension, PE, cor pulmonale, COPD)
• pericardial disease (constrictive pericarditis, pericardial effusion)
• infections (Chagas’ disease)
• any factor that increases myocardial work e.g. anaemia, arrhythmias, hyperthyroidism, pregnancy and obesity
- endocardial/pericardial causes

231
Q

how are natriuretic peptides involved in heart failure?

A
  • ANP, BNP, C type pepide have diuretic, natiuretic and hypotensive properties
  • may lead to beneficial but inadequate compensatory response leading to reduced preload and afterload
  • N-terminal fragment released from pro-BNP and BNP itself correlate with severity of heart failure
232
Q

how is ventricular dilatation involved in heart failure?

A
  • myocardial failure leads to a reduction of volume of blood ejected with each heartbeat, thus an increase in the volume of blood remaining after systole
  • increased diastolic volume stretches the myocardial fibres and myocardial contraction is restored
  • once heart failure is established, the compensatory effects of dilatation are limited by flattened contour of Starling’s curve
  • increased venous pressure -> pulmonary and peripheral oedema
  • ventricular diameter increases and greater tension is needed to expel a given volume of blood, and oxygen requirements increase
233
Q

what is ventricular remodelling? how is it involved in heart failure? what happens in it?

A
  • hypertrophy, loss of myocytes and increased interstitial fibrosis
  • leads to progressive and irreversible pump (contractile failure)
  • process is multifactorial and includes apoptosis of myocytes and changes in cardiac contractile gene expression (e.g. myosin)
234
Q

what are the clinical syndromes of heart failure?

A
  • left ventricular systolic dysfunction (LVSD)
  • right ventricular systolic dysfunction (RVSD)
  • diastolic heart failure
235
Q

what is diastolic heart failure?

A
  • heart failure with normal ejection fraction
  • syndrome consisting of symptoms and sings of heart failure but with normal/near-normal left ventricular ejection fraction (above 45-50%) and evidence of diastolic dysfunction on echo
  • impairment of diastolic ventricular filling and decreased cardiac output
236
Q

what are other investigations of heart failure?

A
  • cardiac catheterisation
  • thallium perfusion imaging
  • PET scanning
  • MRI
  • dobutamine stress echocardiography
237
Q

what is hibernating myocardium?

A

a region of impaired myocardial contractility due to persistently impaired coronary blood flow

238
Q

what is the algorithm for diagnosis of heart failure?

A

heart failure suspected due to symptoms and signs -> assess presence of cardiac disease by ECG, CXR and natriuretic peptides (normal BNP <100pg/mL -> abnormal -> imaging by echocardiography -> abnormal: assess aetiology, degree, precipitating factors, types of cardiac dysfunction

239
Q

what is the pharmacological treatment of heart failure?

A
  • ACEi (or ARA)
  • beta blockers
  • diuretic
  • spironolactone/eplerenone
  • digoxin
  • vasodilators
  • inotropic agents
240
Q

what are non-pharmacological treatments of heart failure?

A
  • revascularisation
  • cardiac resynchronisation therapy (biventricular pacing)
  • implantable cardioverter-defibrillator
  • replacement of diseased valves
  • repair of congenital heart disease
  • cardiac transplantation
  • left ventricular assist device and artificial heart
241
Q

what is acute heart failure?

A
  • medical emergency, with left or right heart failure developing over minutes or hours
  • aetiology similar to chronic heart failure
  • initial investigations: ECG, CXR, blood tests, transthoracic echocardiogram
  • blood tests of serum troponin (for myocardial necrosis) and D-dimer (PE)
242
Q

what are clinical syndromes of acute heart failure?

A
  • acute decompensation of chronic heart failure
  • hypertensive heart failure – high BP, preserved left ventricular function, pulmonary oedema on chest X-ray
  • acute pulmonary oedema – acutely breathless, tachycardia, profuse sweating (sympathetic overactivity), wheezes and crackles throughout the chest, hypoxia, pulmonary oedema on chest X-ray
  • cardiogenic shock – hypotension, tachycardia, oliguria, cold extremities
  • high output cardiac failure – e.g. septic shock, warm peripheries, pulmonary congestion, BP may be low
  • right heart failure – low cardiac output, elevated jugular venous pressure, hepatomegaly, hypotension.
243
Q

what is the management of acute heart failure with systolic dysfunction?

A
  • high flow oxygen, CPAP sometimes indicated
  • furosemide IV 50mg
  • clinical evaluation of systolic blood pressure
244
Q

what is the management of acute heart failure with systolic BP >100mmHg?

A
  • vasodilator e.g. GTN, nitroprusside, BNP
  • no response: consider mechanical assist devices, e.g. right or left ventricular assist devices
  • good response: oral therapy; furosemide and ACEi
245
Q

what is the management of acute heart failure with systolic BP 85-100mmHg?

A
  • vasodilator and/or inotropic (dobutamine, PDE inhibitor)
  • no response: consider mechanical assist devices, e.g. right or left ventricular assist devices
  • good response: oral therapy; furosemide and ACEi
246
Q

what is the management of acute heart failure with systolic BP <85mmHg?

A
  • volume loading?
  • inotropic and/or dopamine and/or noradrenaline
  • no response: consider mechanical assist devices, e.g. right or left ventricular assist devices
  • good response: oral therapy; furosemide and ACEi
247
Q

what is immediate management of a STEMI?

A
  • immediate investigations and treatment
  • reperfusion therapy or thrombolysis
  • metoprolol (5mg slow IV injection) if heart rate >100bpm (contraindicated if hypotension, heart failure, bradycardia, asthma)
  • insulin infusion
  • treat complications
248
Q

what is subsequent management of uncomplicated STEMI?

A
  • repeat ECG, serum cardiac markers and electrolytes at 24 and 48 hours after admission.
  • initiate secondary prevention therapy: aspirin, clopidogrel, statin, metoprolol, ACEI and modification of CAD risk factors (as for ACS).
  • transfer from CCU to medical ward after 48 hours.
  • mobilize gradually and discharge from hospital after 5 days.
  • submaximal exercise ECG test prior to discharge if primary angioplasty not performed.
  • refer to cardiac rehabilitation programme.
  • no driving for 1 month; special assessment is required for heavy goods or public service licence holder before driving. Usually return to work in 2 months.
249
Q

what is post-ACS drug therapy?

A
  • aspirin
  • a second anti-platelet agent
  • an oral β-blocker to maintain heart rate < 60 beats/min
  • ACEIs or angiotensin receptor blockers, particularly if left ventricular ejection fraction is below 40%
  • high-intensity statins with target low-density lipoprotein (LDL) cholesterol < 1.8 mmol/L
  • aldosterone antagonist – post-MI with clinical evidence of heart failure and left ventricular ejection fraction ≤ 40% if the serum creatinine is < 221 μmol/L (men) or < 177 μmol/L (women) and the serum potassium < 5.0 mEq/L.
250
Q

what is rheumatic fever? why does it develop? when is the first onset?

A
  • an inflammatory disease that usually has its first onset between 5 and 15 years of age as a result of infection with group A streptococci
  • It is a complication of less than 1% of streptococcal pharyngitis, developing 2–3 weeks after the onset of sore throat.
  • it is thought to develop because of an autoimmune reaction triggered by the streptococci rather than direct infection of the heart
251
Q

what are the clinical features of rheumatic fever?

A
  • presents suddenly with fever, joint pains and loss of appetite
  • changing heart murmurs, mitral and aortic regurgitation, heart failure and chest pain, caused by carditis affecting all three layers of the heart
  • polyarthritis – fleeting and affecting the large joints, e.g. knees, ankles and elbows
  • skin manifestations – erythema marginatum (transient pink coalescent rings develop on the trunk) and small non-tender subcutaneous nodules which occur over tendons, joints and bony prominences
  • Sydenham’s chorea indicates involvement of the central nervous system and presents with ‘fidgety’ and spasmodic, unintentional movements.
252
Q

what are skin manifestations of rheumatic fever?

A

erythema marginatum (transient pink coalescent rings develop on the trunk) and small non-tender subcutaneous nodules which occur over tendons, joints and bony prominences

253
Q

what is seen on a blood count in rheumatic fever?

A

leucocytosis and a raised ESR

254
Q

what is treatment of rheumatic fever?

A
  • complete bed rest and high dose aspirin
  • penicillin to eradicate residual streptococcal infection
  • long term to patients with persistent cardiac damage
255
Q

what indicates that pulmonary hypertension producing right ventricular overload has occurred in mitral stenosis?

A
  • loud second heart sound
  • parasternal heave
  • elevated JVP
  • peripheral oedema
256
Q

what are rare causes of mitral regurgitation?

A

systemic lupus erythematosus, Marfan’s syndrome

257
Q

what is the pathophysiology of acute mitral regurgitation?

A

rise in left atrial pressure, resulting in an increase in pulmonary venous pressure and pulmonary oedema

258
Q

what causes the third heart sound in mitral regurgitation?

A

caused by rapid filling of the dilated left ventricle in early diastole

259
Q

what is prolapsing mitral valve?

A
  • common condition that occurs mainly in young women
  • one or more of the mitral valve leaflets prolapses back into the left atrium during ventricular systole, producing mitral regurgitation in a few cases
260
Q

what are the causes of prolapsing mitral valve?

A

the cause is unknown, but it is associated with Marfan’s syndrome, hyperthyroidism and rheumatic or ischaemic heart disease

261
Q

what are the clinical features of prolapsing mitral valve?

A
  • most patients are asymptomatic
  • atypical chest pain is the most common symptom
  • some patients complain of palpitations caused by atrial and ventricular arrhythmias
  • the typical finding on examination is a mid-systolic click, which may be followed by a murmur
  • occasionally, there are features of mitral regurgitation
262
Q

what is the management of prolapsing mitral valve?

A
  • chest pain and palpitations are treated with β-blockers
  • anticoagulation to prevent thromboembolism is indicated if there is significant mitral regurgitation and atrial fibrillation
263
Q

what are the causes and associations of acute aortic regurgitation?

A
  • infective endocarditis
  • acute rheumatic fever
  • dissection of the aorta
  • ruptured sinus of Valsalva aneurysm
  • failure of prosthetic heart valve
264
Q

what are the causes and associations of chronic aortic regurgitation?

A
  • chronic rheumatic heart disease
  • bicuspid aortic valve
  • aortic endocarditis
  • arthritides: Reiter’s syndrome, ankylosing spondylitis, rheumatoid arthritis
  • severe hypertension
  • Marfan’s syndrome
  • syphilis
  • osteogenesis imperfecta
265
Q

what is the usual cause of tricuspid stenosis?

A

tricuspid stenosis is almost always the result of rheumatic fever and is frequently associated with mitral and aortic valve disease, which tends to dominate the clinical picture

266
Q

what are causes, clinical presentations, investigations and treatment of tricuspid regurgitation?

A
  • tricuspid regurgitation is usually functional and secondary to dilatation of the right ventricle (and hence tricuspid valve ring) in severe right ventricular failure
  • much less commonly it is caused by rheumatic heart disease, infective endocarditis or carcinoid syndrome
  • on examination there is a pansystolic murmur heard at the lower left sternal edge, the jugular venous pressure is elevated, with giant ‘v’ waves (produced by the regurgitant jet through the tricuspid valve in systole), and the liver is enlarged and pulsates in systole
  • there may be severe peripheral oedema and ascites
  • in functional tricuspid regurgitation these signs improve with diuretic therapy
267
Q

what are causes, clinical presentations, investigations and treatment of pulmonary regurgitation?

A
  • pulmonary regurgitation results from pulmonary hypertension and dilatation of the valve ring
  • occasionally it is the result of endocarditis (usually in intravenous drug abusers)
  • auscultation reveals an early diastolic murmur heard at the upper left sternal edge (Graham Steell murmur), similar to that of aortic regurgitation
  • usually there are no symptoms and treatment is rarely required
  • pulmonary stenosis is usually a congenital lesion but may present in adult life with fatigue, syncope and right ventricular failure
268
Q

what is a Graham Steell murmur?

A

early diastolic murmur heard at the upper left sternal edge

- heard in pulmonary regurgitation

269
Q

what are the major Duke criteria for the diagnosis of infective endocarditis?

A
  • positive blood cultures for infective endocarditis
  • typical microorganism for infective endocarditis from two separate blood cultures in the absence of a primary focus
  • persistently positive blood cultures, defined as recovery of a microorganism consistent with infective endocarditis from blood cultures drawn more than 12 hours apart or all of three or the majority of four or more separate blood cultures, with first and last drawn at least 1 hour apart
  • single positive blood culture for Coxiella burnetii or antiphase IgG antibody titre
  • evidence for endocardial involvement
  • TTE (TOE in prosthetic valve) showing oscillating intracardiac mass on a valve or supporting structures, in the path of regurgitant jet or on implanted material, in the absence of an alternative anatomic explanation, or
  • abscess
  • new partial dehiscence of prosthetic valve
  • new valvular regurgitation
270
Q

what are minor Duke criteria for diagnosis of infective endocarditis?

A
  • predisposition, e.g. prosthetic valve, intravenous drug use
  • fever – 38°C
  • vascular phenomena (e.g. major arterial emboli, septic pulmonary infarcts)
  • immunological phenomena (e.g. Osler’s nodes, glomerulonephritis)
  • echocardiogram – findings consistent with infective endocarditis but not meeting major criteria
  • microbiological evidence – positive blood culture but not meeting major criteria
271
Q

what do symptoms and signs of infective endocarditis result from?

A
  • systemic features of infection, such as malaise, fever, night sweats, weight loss and anaemia. slight splenomegaly is common. clubbing is rare and occurs late.
  • valve destruction, leading to heart failure and new or changing heart murmurs (in 90% of cases).
  • vascular phenomena due to embolization of vegetations and metastatic abscess formation in the brain, spleen and kidney. embolization from right-sided endocarditis causes pulmonary infarction and pneumonia.
  • immune complex deposition in blood vessels producing a vasculitis and petechial haemorrhages in the skin, under the nails (splinter haemorrhages) and in the retinae (Roth’s spots). Osler’s nodes (tender subcutaneous nodules in the fingers) and Janeway lesions (painless erythematous macules on the palms) are uncommon.
  • immune complex deposition in the joints causes arthralgia and, in the kidney, acute glomerulonephritis. microscopic haematuria occurs in 70% of cases but acute kidney injury is uncommon.
272
Q

when should surgery be used to treat infective endocarditis?

A

surgery to replace the valve should be considered when there is severe heart failure, early infection of prosthetic material, worsening renal failure and extensive damage to the valve.

273
Q

what is required for a definite diagnosis of endocarditis?

A

one of the following:

  • direct evidence of infective endocarditis by histology or culture of organism, e.g. from a vegetation
  • two major (Dukes) criteria
  • one major and any three minor criteria
  • five minor criteria
274
Q

what is a requirement for possible endocarditis diagnosis?

A

if there is one major and one minor criterion or three minor (Dukes)

275
Q

what is pulmonary hypertension? why does it occur?

A
  • the lung circulation offers a low resistance to flow compared to the systemic circulation and the normal mean pulmonary artery pressure (PAP) at rest is 10–14 mmHg (compared to mean systemic arterial pressure of about 90 mmHg)
  • pulmonary hypertension is characterized by an elevated PAP (> 25 mmHg at rest) and secondary right ventricular failure
  • occurs due to an increase in pulmonary vascular resistance or an increase in pulmonary blood flow
276
Q

what are causes of pulmonary arterial hypertension?

A
  • idiopathic (no cause identified)
  • autoimmune rheumatic diseases, e.g. systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis
  • congenital heart disease with systemic-to-pulmonary communication (atrial septal defect, ventricular septal defect)
  • portal hypertension (portopulmonary hypertension)
  • drugs: long-term use of cocaine and amphetamines, dexfenfluramine
  • HIV infection
  • Hereditary
  • schistosomiasis
  • chronic haemolytic anaemia
  • pulmonary veno-occlusive disease
277
Q

what can pulmonary hypertension occur secondary to?

A
  • left heart disease: valvular, systolic dysfunction, diastolic dysfunction
  • lung disease and/or hypoxia, e.g. chronic obstructive pulmonary disease, obstructive sleep apnoea, lung fibrosis
  • thromboembolic occlusion of proximal or distal pulmonary vasculature
  • multifactorial mechanisms: myeloproliferative disorders, sarcoidosis, glycogen storage disease
278
Q

what are clinical features of pulmonary hypertension?

A
  • exertional dyspnoea, lethargy and fatigue are the initial symptoms due to an inability to increase cardiac output with exercise.
  • as right ventricular failure develops there is peripheral oedema and abdominal pain from hepatic congestion.
  • on examination there is a loud pulmonary second sound, and a right parasternal heave (caused by right ventricular hypertrophy). - in advanced disease there are features of right heart failure (cor pulmonale): elevated jugular venous pressure with a prominent V wave if tricuspid regurgitation is present, hepatomegaly, a pulsatile liver, peripheral oedema, ascites and a pleural effusion. there are also features of the underlying disease.
279
Q

what is seen on CXR in pulmonary hypertension?

A

chest X-ray shows enlarged proximal pulmonary arteries which taper distally. it may also reveal the underlying cause (e.g. emphysema, calcified mitral valve).

280
Q

what is seen on ECG in pulmonary hypertension?

A

ventricular hypertrophy and P pulmonale

281
Q

what is seen on echocardiography in pulmonary hypertension?

A

echocardiography shows right ventricular dilatation and/or hypertrophy and may also reveal the cause of pulmonary hypertension

282
Q

how can catheterisation used to diagnose pulmonary hypertension?

A

right heart catheterization may be indicated to confirm the diagnosis (elevated PAP), to determine the pulmonary wedge pressure (PWP), to calculate the cardiac output and to assess for pulmonary vascular resistance and reactivity.

283
Q

what is the initial management of pulmonary hypertension?

A
  • oxygen
  • warfarin (due to higher risk of intrapulmonary thrombosis)
  • diuretics for oedema
  • oral calcium-channel blockers as pulmonary vasodilators
  • treatment of underlying cause
284
Q

what is the treatment of more advanced pulmonary hypertension?

A
  • aimed at decreasing pulmonary vascular resistance
  • oral endothelin receptor antagonists (bosentan, sitaxentan)
  • prostanoid analogues (inhaled iloprost, treprostinil, beraprost)
  • IV epoprostenol and oral sildenafil or tadalafil

in primary pulmonary hypertension there is a progressive downhill course and many patients ultimately require heart and lung transplantation

285
Q

what is the pathophysiology of a PE?

A
  • a massive embolism obstructs the right ventricular outflow tract and therefore suddenly increases pulmonary vascular resistance, causing acute right heart failure.
  • a small embolus impacts in a terminal, peripheral pulmonary vessel and may be clinically silent unless it causes pulmonary infarction.
  • lung tissue is ventilated but not perfused, resulting in impaired gas exchange.
  • it is important to consider PE in the differential diagnosis of chest pain with elevated troponin. the rise in troponin reflects right ventricular ischaemia and is associated with adverse outcomes.
286
Q

what are clinical presentations of small/medium PE?

A
  • small/medium PEs present with breathlessness, pleuritic chest pain, and haemoptysis if there is pulmonary infarction.
  • on examination the patient may be tachypnoeic and have a pleural rub and an exudative (occasionally bloodstained) pleural effusion can develop.
287
Q

what are clinical presentations of massive PE?

A
  • massive PE presents as a medical emergency: the patient has severe central chest pain and suddenly becomes shocked, pale and sweaty, with marked tachypnoea and tachycardia.
  • syncope and death may follow rapidly.
  • on examination the patient is shocked, with central cyanosis.
  • there is elevation of the jugular venous pressure, a right ventricular heave, accentuation of the second heart sound and a gallop rhythm (acute right heart failure).
288
Q

how can CXRs, ECG and ABGs be used to diagnose PE?

A
  • chest X-ray, ECG and blood gases may all be normal with small/medium emboli and any abnormalities with massive emboli are non-specific.
  • chest X-ray and ECG are useful to exclude other conditions that may present similarly.
  • CXR show decreased vascular markings and a raised hemidiaphragm (caused by loss of lung volume). with pulmonary infarction, a late feature is the development of a wedge-shaped opacity adjacent to the pleural edge, sometimes with a pleural effusion.
  • the most common ECG finding is sinus tachycardia or there may be new-onset atrial fibrillation. features of acute right heart strain may be seen: tall peaked P waves in lead II, right axis deviation and right bundle branch block.
  • ABGs show hypoxaemia and hypocapnia with massive emboli.
289
Q

how are plasma D-dimers used to diagnose PE?

A
  • plasma D-dimers are a subset of fibrinogen degradation products released into the circulation when a clot begins to dissolve.
  • D-dimers are, however, elevated in many other conditions (e.g. cancer, pregnancy, post-operatively) and a positive result is not diagnostic of thromboembolic disease.
  • the value of D-dimer testing is in patients with a low pre-test clinical probability score
290
Q

what are plasma D-dimers?

A

subset of fibrinogen degradation products released into the circulation when a clot begins to dissolve

291
Q

how is spiral CT used to diagnose PE?

A
  • spiral CT with intravenous contrast (CT pulmonary angiography, CTPA) images the pulmonary vessels directly and is highly sensitive for the detection of large proximal pulmonary emboli.
  • increasingly being used as the diagnostic test of choice for patients with suspected PE.
  • subsegmental emboli may be missed and occasionally patients may need further imaging
292
Q

how are ultrasounds, MRI and echo used to diagnose PE?

A
  • ultrasound will detect clots in the pelvic or iliofemoral veins.
  • MRI gives similar results and is used if CT is contraindicated
  • Echocardiography is diagnostic in massive PE and can be performed at the bedside. it demonstrates proximal thrombus and right ventricular dilatation.
293
Q

what are risk factors on the revised Geneva score for the clinical prediction of a PE?

A
  • age >65yrs (+1 point)
  • previous DVT or PE (+3)
  • surgery or fracture within 1 month (+2)
  • active malignancy (+2)
294
Q

what are symptoms on the revised Geneva score for the clinical prediction of a PE?

A
  • unilateral leg pain (+3)

- haemoptysis (+2)

295
Q

what are clinical signs on the revised Geneva score for the clinical prediction of a PE?

A
  • HR 75-94 (+3 points)
  • HR >95 (+5 points)
  • pain on leg deep vein palpation and unilateral oedema (+4 points)
296
Q

what are the categories for clinical probability of a PE in the Geneva score?

A

low: 0-3
intermediate: 4-10
high: >11

297
Q

what is the emergency assessment of suspected and confirmed PE?

A
  • determine pre test clinical probability of PE (Geneva)
  • low -> D-dimer
  • intermediate/high -> start LMWH -> CT pulmonary angiogram
  • positive D-dimer test -> CT pulmonary angiogram
  • PE present on CT pulmonary angiogram -> start warfarin
298
Q

what is the long term management of PE?

A
  • only definitive indication for thrombolysis in acute massive embolism is persistent arterial hypotension
  • surgical embolectomy done if thrombolysis is contraindicated or ineffective
  • patients who are stable and with no other pathology can be treated at home
  • anticoagulation continued for 6 weeks to 6 months
  • lifelong treatment for recurrent emboli
  • insertion of a vena caval filter used to prevent further emboli
299
Q

what is the investigation, clinical features and treatment of PE in pregnancy?

A
  • occurs more frequently in pregnancy
  • leading cause of maternal death in the developed world
  • compression ultrasonography of legs is initial investigation
  • CT pulmonary angiography required if ultrasound is normal; delivers lower dose of radiation to fetus than other scans
  • warfarin is teratogenic
  • treated with LMWH
300
Q

what are causes of myocarditis?

A
  • the most common cause in the UK is viral, particularly Coxsackie virus infection
  • it may also occur with diphtheria, rheumatic fever, radiation injury and some drugs.
  • myocarditis in association with human immunodeficiency virus (HIV) infection is seen at postmortem in up to 20% of cases but causes clinical problems in less than 10% of cases.
301
Q

what are clinical features of myocarditis?

A
  • acute illness characterised by fever and varying degrees of biventricular failure
  • cardiac arrhythmias and pericarditis may also occur
302
Q

what are investigations used to diagnose myocarditis?

A
  • CXR may show cardiac enlargement
  • ECG shows non-specific T wave and ST changes and arrhythmias
  • the diagnosis is supported by demonstration of an increase in serum viral titres. cardiac biopsy is not usually performed as the findings rarely influence management.
  • cardiac enzymes are elevated.
303
Q

why does an ejection systolic murmur occur in hypertrophic cardiomyopathy?

A

due to left ventricular outflow obstruction

304
Q

when may invasive tests be required to establish the cause of pleural effusion?

A
  • persistent effusion
  • purulent, tuberculous or malignant effusion is suspected
  • if effusion is not known to be secondary to an underlying illness
305
Q

what invasive tests can be used to diagnose pleural effusion?

A
  • pericardiocentesis (aspiration of fluid under echo guidance)
  • pericardial biopsy for culture
  • cytology/histology
  • PCR
306
Q

what are the causes of essential hypertension?

A
  • genetic component
  • low birthweight
  • obesity
  • excess alcohol intake
  • high salt intake
  • the metabolic syndrome
307
Q

what are causes of secondary hypertension?

A
  • renal disease
  • endocrine disease
  • pre-eclampsia
  • drugs
308
Q

what types of renal disease can cause hypertension/

A
  • diabetic nephropathy
  • chronic glomerulonephritis
  • adult polycystic kidneys
  • chronic tubulointerstital nephritis
  • renovascular disease
309
Q

what is coarctation of the aorta?

A

a congenital narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus

310
Q

how are retinal abnormalities in hypertension graded?

A

grade 1: increased tortuosity and reflectiveness of the retinal arteries (silver wiring)

grade 2: grade 1 plus arteriovenous nipping

grade 3: grade 2 plus flame shaped haemorrhages and soft cotton wool exudates

grade 4: grade 3 plus papilloedema

311
Q

what is the action of ACE inhibitors?

A

block the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor, and block degradation of bradykinin, which is a vasodilator

312
Q

what is the action of diuretics?

A

increase renal sodium and water excretion and directly dilate arterioles

313
Q

when are beta-adrenergic blocking patients used for hypertension?

A
  • younger patients
  • intolerance or contraindication to ACEi and angiotensin-II receptor blockers
  • women of child bearing potential
  • patients with evidence of increased sympathetic drive
314
Q

what is the action of beta blockers?

A
  • the β-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas and liver are blocked.
  • they decrease heart rate, reduce the force of cardiac contraction and lower BP.
  • these effects reduce myocardial oxygen demand and give more time for coronary perfusion. β-Blockers improve functional status and reduce cardiovascular morbidity and mortality in patients with heart failure.
315
Q

what other drugs are used for hypertension?

A
  • alpha blocking agents e.g. doxazosin
  • hydralazine
  • aldosterone antagonist (spironolactone)
  • centrally acting agents (clonidine, moxonidine)
316
Q

what is the intervention for those with stage 1 hypertension?

A

offer treatment to everyone under 80yrs old with at least one of the following risk factors:

  • target organ damage
  • cardiovascular disease
  • renal disease
  • diabetes
  • 10 year cardiovascular risk >20%
317
Q

what is the management of severe hypertension?

A
  • oral antihypertensives, e.g. atenolol or amlodipine
  • sublingual and IV hypertensives not recommended because they may produce a precipitous fall in BP, leading to cerebral infarction
  • when rapid control of BP is required, the agent of choice is sodium nitroprusside (starting dose 0.3 μg/kg/min, i.e. 100 mg nitroprusside in 250 mL saline at 2–5 mL/h) or labetalol
318
Q

what is Raynaud’s phenomenon? what are symptoms?

A
  • consists of intermittent spasm in the arteries supplying the fingers and toes
  • usually precipitated by cold and relieved by heat
  • initial pallor (resulting from vasoconstriction) followed by cyanosis and finally, redness from hyperaemia
319
Q

what is Raynaud’s disease?

A

no underlying disorder causing Raynaud’s phenomenon

320
Q

what is treatment of Raynaud’s disease/phenomenon?

A
  • keeping hands and feet warm
  • stopping smoking
  • stopping beta blockers
  • oral Nifedipine
  • occasionally prostacyclin infusions
  • lumbar sympathectomy may help lower limb symptoms
321
Q

what is superficial thrombophlebitis? what is its treatment?

A
  • inflammation of a vein near the surface of the skin (usually a varicose vein) caused by a blood clot
  • vein is painful, tender adn hard, with overlying redness
  • treatment with simple analgesia, e.g. NSAIDs
  • anticoagulation with fondaparinux can limit the extension of superficial thrombosis
  • thromboembolic events are uncommon
322
Q

what are the main complications of DVT?

A
  • PE
  • post-thrombotic syndrome (permanent pain, swelling, oedema and sometimes venous eczema may result from destruction of deep-vein valves)
  • recurrence of thrombosis
323
Q

how can DVT be prevented?

A
  • hospital-acquired venous thromboembolism is largely preventable.
  • all patients should be assessed on admission to hospital and those at risk should be considered for pharmacological prophylaxis (fondaparinux, LMWH or unfractionated heparin if renal impairment) unless they have a risk factor for bleeding.
324
Q

what is the Wells score for clinical probability of a DVT for signs/symptoms?

A
  • lower limb trauma or surgery or immobilisation in a plaster cast (+1)
  • bedridden for more than 3 days or surgery within the last 4 weeks (+1)
  • malignancy (including treatment up to 6 months previously) (+1)
  • tenderness along deep venous system (+1)
325
Q

what is the Wells score for clinical probability of a DVT for clinical findings?

A
  • entire limb swollen (+1)
  • calf swelling more than 3cm compared to asymptomatic side, measured at 10cm below tibial tuberosity (+1)
  • pitting oedema (greater in symptomatic leg) (+1)
  • dilated collateral superficial veins (non-varicose) (+1)
326
Q

what is the Well’s score for clinical probability of a DVT for possible alternative diagnosis?

A

alternative diagnosis (e.g. musculoskeletal injury, haematoma, chronic oedema, cellulitis of the leg, arthritis of the leg, Baker’s cyst) as likely or greater than that of DVT (-2)

327
Q

what are differential diagnoses of DVT?

A
  • MSK injury
  • haematoma
  • chronic oedema
  • cellulitis of the leg
  • arthritis of the leg
  • Baker’s cyst
328
Q

what are the different scores for Wells score for clinical probability of a DVT?

A
<0 = 3% (low)
1-2 = 17% (moderate)
>3 = 75% (high)
329
Q

what is the mechanism of adenosine?

A
  • adenosine is a purine nucleotide.
  • it acts on adenosine receptors and enhances the flow of potassium out of myocardial cells; it produces hyperpolarization of the cell membrane and stabilizes the cell membrane.
  • it has potent effects on the sinus (SA) node, causing complete heart block for a fraction of a second after i.v. administration and producing sinus bradycardia.
330
Q

what are the indications for adenosine?

A

the main indication is reversion to sinus rhythm of atrioventricular junctional tachycardia.

331
Q

what are the preparations and doses of adenosine?

A
  • 3mg/mL
  • by rapid i.v. injection into a central or large peripheral vein, 6 mg over 2 seconds with cardiac monitoring and resuscitation equipment available; if necessary, followed by 12 mg after 1–2 minutes, and then 12 mg after a further 1–2 minutes; increments should not be given if high-level AV block develops at any dose.
332
Q

what are side effects of adenosine?

A

unwanted effects are common; however, they are usually transient. patients should be warned before drug administration of side effects usually lasting less than 1 minute:

  • bradycardia and AV block
  • facial flushing, headache, chest pain or tightness
  • bronchospasm, sense of impending doom
333
Q

what are cautions/contraindications of adenosine?

A

contraindicated in asthma, second- or third-degree AV block and sick sinus syndrome (unless pacemaker fitted).

334
Q

what is the mechanism of action of amiodarone hydrochloride?

A

class III (Vaughan Williams’ classification) drug action, which prolongs the duration of the action potential, thus increasing the absolute refractory period. inhibits the potassium channels involved in repolarization.

335
Q

what are indications for amiodarone hydrochloride?

A
  • intravenous injection of amiodarone is used in cardiopulmonary resuscitation for ventricular fibrillation or pulseless tachycardia unresponsive to other interventions.
  • oral and i.v. amiodarone is used in the treatment of arrhythmias
  • in the non-emergency setting it should only be initiated under specialist supervision.
  • amiodarone causes little or no myocardial depression.
336
Q

what are the preparations and doses of amiodarone hydrochloride?

A

tablets: 100 mg, 200 mg. Injection: 30 mg/mL or concentrate 50 mg/mL.
- oral administration is 200 mg three times daily for 1 week reduced to 200 mg twice daily for a further week
- IV administration is via central line catheter, initially 5 mg/kg in 250 mL glucose 5% over 20–120 minutes with ECG monitoring. This may be repeated if necessary to a maximum of 1.2 g in 24 hours in 500 mL. as soon as an adequate response has been obtained, oral therapy should be initiated and the i.v. therapy phased out.

337
Q

what are side effects of amiodarone hydrochloride?

A
  • amiodarone therapy can be proarrhythmogenic in patients with significant structural heart disease.
  • amiodarone contains iodine and can cause both hypothyroidism and hyperthyroidism.
  • liver toxicity can also occur
  • other side effects are reversible corneal microdeposits, phototoxic skin reactions, slate-grey skin pigmentation, pneumonitis and peripheral neuropathy.
338
Q

what are contraindications to amiodarone hydrochloride?

A
  • it is contraindicated in sinus bradycardia or sinoatrial heart block, unless pacemaker fitted, iodine sensitivity and thyroid dysfunction.
  • many drugs interact with amiodarone, including warfarin and digoxin. it has a very long half-life (extending to several weeks) and months may be required to achieve steady-state concentrations
339
Q

what is the mechanism of action of flecainide?

A
  • class Ic (Vaughan Williams’ classification) antiarrhythmic drug. it is a membrane-depressant drug that reduces the rate of entry of sodium into the cell (sodium channel blocker).
  • this may slow conduction, delay recovery or reduce the spontaneous discharge rate of myocardial cells.
340
Q

what are indications for flecainide?

A
  • AV nodal reciprocating tachycardia, arrhythmias associated with accessory conducting pathways, paroxysmal atrial fibrillation.
  • occasionally it is used in ventricular tachyarrhythmias resistant to other treatments.
341
Q

what are preparations and doses of flecainide?

A
  • SVT – 50 mg twice daily, increased to maximum 300 mg daily.
  • ‘on demand’ treatment for AF – 200 mg or 300 mg if weight greater than 70 kg, at the onset of paroxysm.
342
Q

what are side effects of flecainide?

A
  • include dizziness, visual disturbances, dyspnoea, palpitations, proarrhythmic effects, headache, fatigue and nausea
  • rarely, bronchospasm, heart block, bone marrow suppression and increased ventricular rate in AF/flutter are seen.
343
Q

what are cautions/contraindications of flecainide?

A
  • class Ic agents increase mortality in post-MI patients with ventricular ectopy and should be reserved for patients who do not have significant coronary artery disease, left ventricular dysfunction, or other forms of significant structural heart disease.
  • interactions with other drugs, including β-blockers and calcium-channel blockers, can occur
344
Q

what is the mechanism of action of digoxin?

A
  • this drug blocks AV conduction and reduces heart rate by enhancing vagal nerve activity and inhibiting sympathetic activity.
  • it is positively inotropic (enhancing strength of cardiac contraction) by inhibition of Na+/K+-ATPase and secondary activation of the Na+/Ca2 + membrane exchange pump, thereby increasing intracellular calcium levels.
345
Q

what are indications for digoxin?

A
  • digoxin is used in heart failure with atrial fibrillation or patients in sinus rhythm who remain symptomatic despite ACEI, β-blocker and diuretic uses.
  • it is also used for rate control in sedentary patients with atrial fibrillation/flutter.
346
Q

what are preparations and doses of digoxin?

A

tablets: 62.5, 125 and 250 μg. Injection: 250 μg/mL.
- check renal function and electrolytes before starting therapy; reduce dose in the elderly and in renal impairment.
- oral: rapid digitalization for atrial fibrillation/flutter 0.75–1.5 mg in divided doses over 24 hours and then maintenance of 125–250 μg once daily according to heart rate and renal function
- IV infusion: intravenous infusion for emergency loading dose for atrial fibrillation or flutter 0.75–1 mg over at least 2 hours and then maintenance dose the next day by mouth.

347
Q

what are the side effects of digoxin?

A
  • side effects include nausea, vomiting, diarrhoea, conduction disturbances, blurred or yellow vision and ventricular arrhythmias.
  • hypokalaemia and renal impairment (reduce dose) increase the risk of toxicity.
  • plasma digoxin concentrations should be measured if toxicity is suspected; concentrations of > 2 mmol/L usually suggest toxicity. In severe toxicity, give anti-digoxin antibodies.
348
Q

what are contraindications to digoxin?

A
  • contraindicated in arrhythmias associated with accessory conduction pathways because the accessory pathway is not affected.
  • blocking the normal pathway can increase the speed of conduction in the abnormal pathway and lead to ventricular arrhythmias.
  • caution should be demonstrated in left ventricular outflow tract obstruction.
  • diltiazem, verapamil, spironolactone and amiodarone inhibit renal excretion of digoxin; avoid with amiodarone and measure plasma levels with other drugs
  • tetracycline, erythromycin and possibly other macrolides enhance the effect of digoxin. Rifampicin reduces serum concentrations.
349
Q

what are indications for beta blockers?

A
  • angina
  • MI
  • arrhythmias
  • stable heart failure
  • hypertension
  • alleviation of symptoms of anxiety
  • prophylaxis of migraine
  • prevention of variceal bleeding
  • symptomatic treatment of hyperthyroidism
350
Q

where are different beta blockers used?

A
  • atenolol and metoprolol are used in angina
  • stoalol in management of supraventricular and ventricular arrhythmias
  • propanolol in treatment of hyperthyroidism, prevention of variceal bleeding and prophylaxis of migraine (usually)
  • bisoprolol and carvedilol in the management of heart failure (usually specialist initiated)
  • nebivolol in the treatment of stable mild–moderate heart failure in patients over 70 years old.
351
Q

what are the preparations of propanolol?

A
  • portal hypertension: initially 40 mg twice daily, increased according to heart rate; maximum 160 mg twice daily
  • angina: initially 40 mg two to three times daily; maintenance dose 120–240 mg daily
  • arrhythmias: anxiety, hyperthyroidism, migraine prophylaxis, essential tremor, 10–40 mg three times daily
  • hypertension: initially 80 mg twice daily, increased at weekly intervals as required; maintenance 160–320 mg daily.
  • intravenous: arrhythmias and thyrotoxic crisis: 1 mg over 1 minute; if necessary, repeat at 2-minute intervals; maximum 10 mg.
352
Q

what are the preparations of atenolol?

A
  • angina: 25–100 mg daily in one or two doses
  • after MI: 25–100 mg daily
  • hypertension: 25–50 mg daily.

intravenous
- for arrhythmias: 2.5 mg at a rate of 1 mg/min, repeated at 5-minute intervals to a maximum of 10 mg, or by infusion 150 μg/kg over 20 minutes, repeated every 12 hours if required.

353
Q

what are the doses and preparations of bisoprolol?

A

Tablets: 1.25 mg, 2.5 mg, 3.75 mg, 5 mg, 7.5 mg, 10 mg.

  • hypertension and angina, usually 5–10 mg once daily; maximum 20 mg daily
  • heart failure, initially 1.25 mg daily titrated up at weekly intervals over 8–10 weeks to maximum 10 mg daily.
354
Q

what are the doses and preparations of metoprolol?

A

Tablets: 50 mg, 100 mg. Injection: 1 mg/mL.

  • after MI: 100 mg twice daily
  • angina, arrhythmias, anxiety, thyrotoxicosis, migraine prophylaxis, essential tremor: 50–100 mg two to three times daily
  • hypertension: 50–100 mg twice daily.

intravenous
- for arrhythmias: up to 5 mg at a rate of 1–2 mg/min, repeated after 5 minutes to a maximum of 10–15 mg.

355
Q

what are the doses and preparations of sotalol?

A

Tablets: 40 mg, 80 mg, 160 mg, Injection: 10 mg/mL.

  • sotalol use is limited to the treatment of ventricular arrhythmias or the prevention of supraventricular arrhythmias.
  • oral: 80 mg daily in one to two divided doses, increased gradually at intervals of 2–3 days to usual dose of 160–320 mg daily.
  • IV: over 10 minutes: 20–120 mg with ECG monitoring repeated at 6-hourly intervals if necessary.
356
Q

what are the side effects of beta blockers?

A
  • bradycardia
  • exacerbation of intermittent claudication
  • lethargy
  • nightmares
  • hallucinations
  • deterioration of glucose tolerance and interference with metabolic and autonomic responses to hypoglycaemia in diabetics.
357
Q

what are contraindications to beta blockers?

A
  • asthma
  • severe peripheral arterial disease
  • second- or third-degree heart block
  • marked bradycardia
  • hypotension
  • phaeochromocytoma (apart from specific use with α-blockers).
358
Q

what are the mechanisms of action of ACE inhibitors?

A

these drugs inhibit the conversion of angiotensin I to angiotensin II and reduce angiotensin II-mediated vasoconstriction.

359
Q

what are the indications for ACE inhibitors?

A
  • ACEIs improve symptoms and significantly improve survival in all grades of heart failure.
  • recommended in patients at risk of developing heart failure (e.g. ischaemic heart disease).
  • other indications are hypertension and diabetic nephropathy.
360
Q

what are the preparations and doses for perindopril?

A

Tablets: 2 mg, 4 mg, 8 mg.

  • hypertension, initially 4 mg once daily, subsequently adjusted according to response to maximum 8 mg daily
  • heart failure: initially 2 mg once daily, increased after at least 2 weeks to maintenance usually 4 mg daily
  • ischaemic heart disease, diabetic nephropathy: 4 mg daily increased after 2 weeks to 8 mg daily.
361
Q

what are the preparations and doses for lisinopril?

A

Tablets: 2.5 mg, 5 mg, 10 mg, 20 mg.

  • hypertension: initially 10 mg once daily, usual maintenance 20 mg daily, maximum 80 mg daily
  • heart failure: initially 2.5 mg once daily, increased by 10 mg every 2 weeks if tolerated to maintenance 35 mg daily
  • ischaemic heart disease, diabetic nephropathy: 5–10 mg daily. Immediately post-STEMI start at 2.5 mg if systolic BP 100–120 mmHg and gradually increase to maintenance dose of 5–10 mg. Do not give if systolic BP < 100 mmHg.
362
Q

what are preparations and doses of ramipril?

A

Tablets: 1.25 mg, 2.5 mg, 5 mg, 10 mg.

  • hypertension: initially 1.25 mg daily, increased weekly to maintenance 2.5–5 mg daily, maximum 10 mg once daily
  • heart failure: initially 1.25 mg daily, increased if necessary to maximum 10 mg daily
  • ischaemic heart disease, diabetic nephropathy: 2.5 mg twice daily, maintenance 2.5–5 mg daily.
363
Q

what are side effects of ACE inhibitors?

A

after the first dose, side effects can include hypotension in heart failure and patients taking diuretics, dry cough, hyperkalaemia, sudden deterioration in renal function in patients with renal artery stenosis and in patients taking NSAIDs, loss of taste, rashes and hypersensitivity reactions.

364
Q

what are cautions/contraindications for ACE inhibitors?

A
  • bilateral renal artery stenosis
  • pregnancy
  • angio-oedema
  • severe renal failure
  • severe or symptomatic mitral or aortic stenosis
  • hypertrophic obstructive cardiomyopathy (risk of hypotension)
365
Q

what are indications for angiotensin II receptor antagonists?

A
  • hypertension
  • heart failure
  • diabetic nephropathy in patients intolerant to ACE inhibitors due to cough
366
Q

what are preparations and doses of candesartan?

A

Tablets: 2 mg, 4 mg, 8 mg, 16 mg, 32 mg.

  • hypertension: initially 8 mg daily, increased as necessary to 32 mg daily
  • heart failure: initially 4 mg once daily increased at intervals of at least 2 weeks to target dose of 32 mg.
367
Q

what are preparations and doses of valsartan?

A

Capsules: 40 mg, 80 mg, 160 mg.

  • hypertension: 80 mg once daily and increased if necessary after 4 weeks to 160 mg daily
  • ischaemic heart disease: 20 mg twice daily increased gradually to 160 mg twice daily.
368
Q

what are side effects of angiotensin II receptor antagonists?

A
  • postural hypotension
  • rash
  • abnormalities in liver biochemistry
  • hyperkalaemia
369
Q

what are cautions/contraindications of angiotensin II receptor antagonists?

A
  • lower doses should be given in liver and renal impairment, patients taking high-dose diuretics and the elderly (over 75 years).
  • caution should be applied in renal artery stenosis, aortic or mitral valve stenosis and in obstructive hypertrophic cardiomyopathy.
370
Q

what are the overall effects of nitrates, calcium-channel blockers and potessium-channel activators?

A

have a vasodilating effect, leading to a reduction in venous return, which reduces left ventricular work and dilatation of the coronary circulation

371
Q

what is the mechanism of action of nitrates?

A
  • an increase in cyclic guanosine monophosphate (cGMP) in vascular smooth muscle cells causes a decrease in intracellular calcium levels and smooth muscle relaxation with dilatation of veins and arteries, including the coronary circulation.
  • nitrates reduce venous return, which reduces left ventricular work.
372
Q

what are the indications for nitrates?

A

prophylaxis for and in the treatment of angina, as an adjunct in congestive heart failure and intravenously in the treatment of acute heart failure and acute coronary syndrome

373
Q

what are the preparations and doses of short acting glyceryl trinitrate?

A

sublingual tablets: 300 μg, 500 μg, 600 μg. spray: 400 μg/dose.

  • angina: one or two tablets or sprays under the tongue repeated as required. more effective if taken before exertion known to precipitate angina.
374
Q

what are the preparations and doses of isosorbide mononitrate?

A

Tablets: 10 mg, 20 mg, 40 mg.

  • 10–40 mg twice daily, 8 hours apart rather than 12 to prevent nitrate tolerance.
375
Q

what are side effects of nitrates?

A
  • mainly due to vasodilating properties and are minimised by initiating therapy with a low dose
  • flushing
  • headache
  • postural hypotension
  • methaemoglobulinaemia
376
Q

what are cautions/contraindications of nitrates?

A
  • hypotension and hypovolaemia, hypertrophic obstructive cardiomyopathy, aortic stenosis, mitral stenosis, cardiac tamponade and constrictive pericarditis.
  • nitrates potentiate the effect of other vasodilators and hypotensive drugs.
  • sildenafil is contraindicated in patients taking nitrates.
377
Q

what is the mechanism of action of calcium channel blockers?

A
  • block calcium channels and modify calcium uptake into myocardium and vascular smooth muscle cells.
  • dihydropyridine calcium-channel blockers (e.g. amlodipine, nifedipine, nimodipine) are potent vasodilators with little effect on cardiac contractility or conduction.
  • verapamil, and to a lesser extent diltiazem, are weak vasodilators but depress cardiac conduction and contractility.
378
Q

what are indications for calcium channel blockers?

A
  • hypertension and prophylaxis for angina
  • verapamil used in treatment of some arrhythmias
  • nimodipine for prevention of ischaemic neurological deficits following aneurysmal subarachnoid haemorrhage
379
Q

what are the preparations and doses of amlodipine?

A

Tablets: 5 mg, 10 mg.

  • 5–10 mg once daily.
380
Q

what are the preparations and doses of verapamil?

A

Tablets: 40 mg, 80 mg, 120 mg, 160 mg. Oral solution: 40 mg/5 mL.

  • angina: 80–120 mg three times daily.
  • hypertension: 240–480 mg daily in two to three divided doses.
  • supraventricular arrhythmias: oral 40–120 mg three times daily
381
Q

what are preparations and doses of nifedipine modified release?

A

Adalat LA tablets: 20 mg, 30 mg, 60 mg.

  • angina: initially 30 mg once daily, increased if necessary to 90 mg once daily
  • hypertension: initially 20 mg once daily, increased if necessary.
382
Q

what are preparations and doses of diltiazem?

A

Tablets: 60 mg.

  • angina: 60 mg three times daily.
383
Q

what are preparations and doses of diltiazem slow release?

A

Capsules for twice daily use: 90 mg, 120 mg, 180 mg. Capsules for once daily use: 120 mg, 180 mg, 240 mg, 300 mg.

  • hypertension: 120 mg twice daily
  • angina: 90 mg twice daily
  • angina and hypertension: 240 mg once daily,
384
Q

what are side effects of calcium channel blockers?

A
  • these are mainly due to vasodilator properties: flushing, dizziness, tachycardia, hypotension, ankle swelling and headache. - side effects are minimized by starting with a low dose and increasing slowly.
  • constipation occurs with verapamil.
  • worsening heart failure can be seen with verapamil and diltiazem.
385
Q

what are cautions/contraindications of calcium channel blockers?

A
  • the major contraindication is aortic stenosis.
  • verapamil and diltiazem diminish cardiac contractility and slow cardiac conduction; thus they are relatively contraindicated in patients taking β-blockers, left ventricular failure, sick sinus syndrome and heart failure.
  • verapamil is contraindicated for treatment of arrhythmias complicating Wolff–Parkinson–White syndrome.
  • short-acting calcium antagonists increase mortality and are contraindicated immediately after MI.
386
Q

what is the mechanism of action of potassium-channel activators?

A
  • the mechanism of action here is a hybrid of nitrates and calcium-channel blockers.
  • potassium-channel activators cause an increase in potassium flow into the cell, which indirectly leads to calcium-channel blockade and arterial dilatation.
387
Q

what are indications for potassium-channel activators?

A

use is indicated in cases of refractory angina in patients who are uncontrolled on standard regimens of aspirin, beta-blockers, nitrates, calcium antagonists and statins

388
Q

what is an example of a potassium-channel activator? what is its preparation and dose?

A
  • nicorandil
  • tablets: 10mg, 20mg
  • 5-30mg twice daily
389
Q

what are side effects of potassium channel activators?

A
  • headache
  • flushing
  • nausea
  • vomiting
  • dizziness
  • hypotension
  • tachycardia
390
Q

what are cautions/contraindications of potassium channel activators?

A
  • contraindicated in left ventricular failure and cardiogenic shock
  • sildenafil is contraindicated in patients taking nicorandil