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Cardiology Flashcards

1
Q

Midline sternotomy +…

Metallic click

A

Mechanical valve replacement

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2
Q

Midline sternotomy +…

Murmur

A

Tissue valve

Valvotomy

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3
Q

Midline sternotomy +…

Vein harvest scars

A

CABG

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4
Q

Midline sternotomy +…

Old scar, young patient

A

Repair of congenital defect

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5
Q

Midline sternotomy +…

Immunosuppression

A

Heart transplant

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6
Q

Midline sternotomy +…

No other findings

A

Trauma: tamponade,

Internal mammary artery CABG

Tissue valve

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7
Q

Cardiac Causes of Clubbing

A

Infective endocarditis

Congenital cyanotic heart disease

  • Fallot’s tetralogy
    1. VSD
    2. Pulmonary stenosis
    3. Right ventricular hypertrophy
    4. Overriding aorta
  • Transposition of the Great Vessels

Atrial myxoma

Associated with Carney Complex LAMES syndrome

Lentigines: spotty skin pigmentation

Atrial Myxoma

Endocrine tumours: pituitary

Schwannomas

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8
Q

Causes of Collapsing Pulse

A

Caused by hyperdynamic circulation

ATAP

Aortic regurgitation

Thyrotoxicosis

Anaemia

Pregnancy

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9
Q

Causes of Absent Radial Pulse

A

Arrest

Trauma

Thrombosis/ embolism

Co-arctation of aorta

Takayasu’s arteritis

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10
Q

Impalpable Apex Beat

A

COPD

COPD

Obesity

Pericardial effusion

Dextrocardia

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11
Q

Features of Pulmonary Hypertension

A

Increased JVP

Left parasternal heave

Loud P2 + Pan-systolic murmur of Tricuspid regurgitation

Pulsatile hepatomegaly

Ascites and peripheral oedema

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12
Q

Heart sounds

A

S1 = mirtal valve closure

S2 = aortic valve closure

S3 = rapid venitrcular filling of dilated left ventricle

S4 = atrial contraction against stiff ventricle

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13
Q

Signs on Examination of Aortic Stenosis

A

Slow-rising pulse

Narrow pulse pressure <30mmHg

Precordium

Pacemaker

Aortic thrill

Apex: forecful, non-displaced

HS: Quiet A2, S4 (forceful atrial contaction against hypertrophied left ventricle)

Murmur

Early, ejection systolic murmur

Right 2nd ICS

Loudest sitting forward at end-expiration

Radiates to carotids

SEVERE AS
Quiet, absent A2

S4

Narrow pulse pressure

Decompensation: LVF

Significant negatives

Infective endocarditis

LVF

Indicators of severity

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14
Q

Clinical Signs of Severe Aortic Stenosis

A

Quiet A2

S4

Narrowed pulse pressure

LVF

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15
Q

Differential for Aortic Stenosis

A

Aortic sclerosis: no radiation to carotids, normal pulse character

Mitral regurgitation (also, systolic murmur)

HOCM: valsalva increases murmur, squatting decreases murmur

Pulmonary stenosis: right sided

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16
Q

Causes of Aortic Stenosis

A

Age-related senile calcification

Biscuspid aortic valve

Rheumatic heart disease

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17
Q

Clinical symptoms of Severe Aortic Stenosis

A

Angina: 50% dead in 5 years

Syncope: 50% dead in 3 years

Dyspnoea: 50% dead in 2 years

Clinical signs

Quiet A2

S4

LVF

Narrowed pulse pressure

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18
Q

Echo features of severe Aortic stenosis

A

Valve area <1cm2

Pressure gradient >40mmHg

Jet velocity >4m/s

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19
Q

Management of Aortic Stenosis

A

MDT: GP, Cardiologist, Cardiothoracic surgeons, dietician, specialist nurse

Conservative

  • Monitor, regular follow-ups with echo

Medical

  • Optimise CV risk factors: atorvastatin, Anti-HTN, DM, anti-platelets

Surgical

  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
  • balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
  • TAVI
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20
Q

Signs of Mitral Regurgitation on Examination

A

Peripheral inspection: warfarin bracelet

Pulse: Atrial fibrillation

Precordium

Left parasternal heave

Apex: THRUSTING displaced - volume oberload as ventricle has to pump forward systolic volume and regurgitant volume —> eccentric hypertrophy

HS: Soft S1, S2 not heard separately from the murmur (+/- loud P2 if pulmonary hypertension)

Murmur

Blowing: pansystolic murmur

Loudest at apex, left lateral position and on end-expiration

Radiates to axilla

Clinical signs of severe Mitral Regurgitation

Left ventricular failure

Atrial fibrillation

Significant negatives: Infective endocarditis, AF, LVF (indicators of severity)

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21
Q

Differential for Mitral Regurgitation

A

Aortic stenosis (systolic)

Ventricular septal defect

Tricuspid regurgitation: right-sided

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22
Q

Clinical Signs of Severe Mitral Regurgitation

A

LVF

AF

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23
Q

Causes of Mitral Regurgitation

A

Functional: Left ventricular dilatation secondary to hypertension or idiopathic

Annular calcification —> contraction

Rheumatic heart disease

Mitral valve prolapse

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24
Q

ECG changes in Mitral Regurgitation

A

P-mitrale (atrial hypertrophy)

Arrhythmias

  • Atrial premature beats
  • Paroxysmal supraventricular tachycardia
  • Ventricular premature beats
  • Complex ventricular ectopy

Left ventricular hypertrophy

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25
Q

Echo features of severe Mitral Regurgitation

A

Jet width of >0.6cm

Systolic pulmonary flow reversal

Regurgitant volume >60ml

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26
Q

Management of Mitral Regurgitation

A

MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse

Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM

Specific

AF: rate control and anti-coagulate

Reduce afterload: ACE-inhibitor or b-blocker (esp Carvedilol)

Surgical:

Valve replacement or repair

If unfit: ?Percutaneous mitral valve leaflet repair for mitral regurgitation

Aim to replace the valve before significant LV dilatation and dysfunction

Indications for surgery: symptomatic

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27
Q

Eponymous signs of Aortic Regurgitation

A

Quincke’s sign: capillary pulsation in nail beds

Corrigan’s: visible vigorous carotid pulsation

De Musset’s: head bopping

Traube’s: pistol-shot femorals (pistol-sound heard over femorals)

Durozieze’s: systolic murmur over femoral artery with proximal compression, diastolic murmur with distal compression

Mueller’s: systolic pulsations of uvula

Rosenbach’s: systolic pulsations of the liver

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28
Q

Causes of Aortic Regurgitation

A

Marfan’s

Tall, thin, long arms, high-arched palate

Ankylosing spondylitis: cervical kyphosis

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29
Q

Signs of Aortic Regurgitation on Examination

A

Pulse: Collapsing

Wide pulse pressure e.g. 180/45

Precordium

Aortic thrill

Apex: displaced (volume overload)

HS: soft S2, +/- S3

Murmur

High-pitched early diastolic murmur

Loudest on lower left sternal edge (parasternal 3rd IC), sitting forward in end-expiration

Additional murmurs:

Ejection systolic flow murmur

Austin-flint murmur = rumbling mid-diastolic murmur secondary to regurgitant jet fluttering the anterior of mitral valve

Clinical Signs of Severe Aortic Regurgitation

Collapsing pulse

Wide pulse pressure

Left ventricular failure

Significant negatives: infective endocarditis, indicators of severity (LVF, wide pulse pressure, collapsing pulse)

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30
Q

Clinical Signs of Severe Aortic Regurgitation

A

Collapsing Pulse

Wide pulse pressure

Left ventricular failure

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31
Q

Causes of Aortic Regurgitation

A

Chronic

Bicuspid aortic valve

Rheumatic heart disease

Autoimmune: ankylosing spondylitis

Connective tissue disease: Marfan’s, Ehlers-Danlos

Acute

Infective endocarditis

Type A aortic dissection

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32
Q

Differential for Aortic Regurgitation

A

Mitral stenosis

Pulmonary regurgitation, tricuspid stenosis: right-sided

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33
Q

Echo findings in Aortic Regurgitation

A

Severe

Jet width >65% of outflow tract

Regurgitant jet volume

Premature closure of mitral valve

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34
Q

Management of Aortic Regurgitation

A

MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse

Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM

Specific

Reduce afterload: ACE-inhibitor, or b-blockers (carvedilol) OR diuretics

Surgical: valve replacement (before LV dilatation)

Indications: NYHA >2, LV dysfunction

Pulse pressure >100mmHg

ECG changes: T invesion in lateral leads

LV enlargement on CXR or EF <50%

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35
Q

Signs of Mitral Stenosis on Examination

A

Peripheral inspection: middle-aged female, wafarin bracelet, malar flush

Pulse: Atrial fibrillation

Precordium

Left parasternal heave: Right ventricular hypertrophy secondary to pulmonary hypertension

Apex: Tapping (palpable S1), non-displaced

HS: Loud S1, +/- Loud S2 if Pulmonary hypertension

Murmur

Rumbling mid-diastolic murmur

Loudest at the apex, left lateral position, with the bell, radiating to axilla

+/- Graham Steell (early diastolic) murmur due to pulmonary regurgitation secondary to pulmonary hypertension

Clinical Signs of Severe Mitral Stenosis

Malar flush

Long murmur

LVF

Significant Negatives: infective endocarditis, indicators of seveirty, evidence of pulmonary hypertension (raised JVP with large v waves, left parasternal heave, loud P2)

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36
Q

Causes of Mitral Stenosis

A

Rheumatic heart disease

Other rarer causes: prosthetic valve, congenital

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37
Q

Echo features of Severe Mitral Stenosis

A

Valve orifice <1cm2

Pressure gradient >10mmHg

Pulmonary artery systolic pressure >50mmHg (pulmonary hypertension)

38
Q

Management of Mitral Stenosis

A

MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse

Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM

Specific

AF: Rate control with b-blockers, anti-coagulate

Diuretics for symptomatic relief

Surgical

Indicated in mod-severe mitral stenosis

Percutaneous balloon valvuloplasty

CI: atrial mural thrombus

Valve replacement

39
Q

Pathophysiology of Rheumatic Fever

A

Antibiody cross-reactivity following Strep pyogenes infection

Leading to a Type II hypersensitivity reaction (molecular mimicry)

Antibodies cross-react with myosin, muscle glycogen and smooth muscle cells

Histology: Aschoff bodies and Anitschkow myocytes

40
Q

Revised Jones Criteria

A

Evidence of Group A strep infection

AND

either

2 major criteria

OR

1 major + 2 minor criteria

41
Q 
Major Criteria (Jones) Rheumatic Fever
**PASES**
A

PASES

Pancarditis

Arthritis

Subcutaneous nodules

Erythema marginatum

Sydenham’s chorea

42
Q

Minor Criteria (Jones) Rheumatic Fever

A

FEPAP

Fever

ESR / CRP raised

Prolonged PR interval (not if carditis is major)

Arthralgia (not if arthritis is major)

Previous rheumatic fever

43
Q

Management of Rheumatic Fever

A

Bed rest for 2 weeks

Benpen for strep throat

Naproxen for arthritis

Diazepam if chorea not settling

44
Q

Causes of recurrence of rheumatic fever

A

Strep throat infection again

Pregnancy

OCP

45
Q

Valve disease in rheumatic heart disease

A

Mitral: 70%

Aortic: 40%

Tricuspid: 10%

Pulmonary: 2%

Regurgitation —> stenosis

46
Q

Rheumatic fever prognosis

A

resolves within ~3 months

60% of those with carditis will have rheumatic heart disease

47
Q

Secondary prophylaxis against rheumatic fever

A

Pen V 250mg / 12h

For at least five years or until age 21 years, whichever is longer.

This should be for ten years for RF with carditis but no valvular disease (or well into adulthood, whichever is longer).

However, with substantial valvular disease this should be continued longer. In severe valvular damage, or with valve surgery, prophylaxis should be continued for life

48
Q

Signs of Valve Replacement on Examination

A

General: audible click, bruising from anti-coagulation, warfarin bracelet, anaemia

Scars

  • Midline sternotomy: CABG, aortic valve replacement, mitral valve replacement
  • Left lateral inferior thoracotomy: mitral valve replacement, mitral valvotomy
  • Neck scars: central line insertion
  • Groin / femoral / wrist scars from angiography
  • Vein harvesting

Pulse:

AF suggestive of mitral replacement due to mitral stenosis

Time click with pulse, occurs in time = mitral valve (systole –> mitral closure)

Precordium

3 artifical sounds = Starr-Edwards

1 artifical sound = tilting disc or bileaflet

No sounds - biological valve

Aortic replacement: lub-click

+/- systolic flow murmur

Mitral replacement: click-dub

+/- diastolic flow murmur

Murmurs

well-seated valves –> flow murmurs

Aortic: systolic

Mitral: diastolic

Poorly seated valves –> regurgitation

Aortic: diastolic

Mitral: systolic

49
Q

Starr-Edwards Valve

A

3 artifical sounds

Quiter click as valve opens

Loud thud as valve closes

Rumbling sound as ball rolls in cage

50
Q

Tilting disc valve

Bileaflet valve

A

1 artificial sound

high-pitched click as valve closes

51
Q

Complications of valve replacement

A

Thromboembolism: 1-2% per annum despite warfarin

Anaemia: haemolysis

Bleeding

Infective endocarditis

Failure

Acute: breakage, thrombus, dehiscence

Chronic: stenosis or incompetence

52
Q

Risk Factors for Infective Endocarditis

A

IVDU

Skin wounds

Immunosuppression: Chronic Renal Failure, Diabetes Melitus

53
Q

Organisms causing Infectiv Endocarditis

A

Strep viridans (most common)

Staph aureus (IVDU)

S.epidermidis

S. bovis (needs colonoscopy for colonic neoplasm)

HACEK = culture negative IE

54
Q

Clinical Features of Infective Endocarditis

A

Hands

Clubbing

Splinter haemorrhages

Janeway lesions

Osler nodes

Cardiac

New/changing murmur

Mitral regurgitation: 85%

Aortic regurgitation: 55%

Other

Fever

Roth spots

Splenomegaly

Haematuria

55
Q

Duke Criteria for Infective Endocarditis

A

2 major

OR

1 major AND 3 minor

OR

All 5 minor

56
Q

Major Duke Criteria

A

1) Positive blood culture

Typical organism in 2 separate cultures OR persistently +ve cultures e.g. 3 >12 h apart

2) Endocardial involvement

+ve echo vegetation, abscess, dehiscence

OR

New valvular regurgitation

57
Q

Minor Duke Criteria (5)

A
  1. Predisposition: IVDU, cardiac lesion
  2. Fever >38
  3. Emboli: septic infarcts, splinters, janeway lesions
  4. Immunological phenomena: Glomerulonephritis, Osler nodes, Roth spots, RF
  5. +ve blood culture not meeting major criteria
58
Q

Treatment of Infective Endocarditis

A

Acute severe:

Flucloxacillin OR Vancomycin IV

+ Gentamicin IV

Subacute:

Benpen + Gentamicin IV

59
Q

Apex Beat Displacement

A

Thrusting displaced apex beat is caused by volume overload: an active large stroke volume ventricle eg aortic or mitral regurgitation or left to right shunts.

Sustained apex beat is caused by pressure overload eg aortic stenosis, gross hypertension.

Tapping apex beat - mitral stenosis.

Diffuse pulsation asynchronous with apex beat - left ventricular aneurysm.

Double or triple impulse may occur in hypertrophic obstructive myopathy.

Impalpable apex beat - obesity, overinflated chest, pericardial effusion. Also consider dextrocardia.

60
Q

Signs of Atrial Fibrillation on Exmaination

A

On inspection:

Hyperthyroidism: tremor, thin, palmar erythema, sweating, eye signs

Mitral stenosis: malar flush

Pneumonia: bronchial breath sounds + added sounds

Pulse: irregularly irregular

Precordium

Mitral stenosis: mid-diastolic murmur

Mitral regurgitation: pan-systolic murmur

Significant negatives: murmur, evidence of hyperthyroidism, LVF, bruising from warfarin

61
Q

Causes of Atrial Fibrillation

A

Common

IHD

Rheumatic herat disease

Thyrotoxicosis

HTN

Other

Pneumonia

PE

Post-op

Potassium: hypokalaemia

Poison: alcohol

Painful joints: rheumatoid arthritis

62
Q

Differential diagnosis of irregularly irregular pulse

A

AF

Remains when exercising the patient

Multiple ventricular ectopics

As patient exercises, pulse appears regular as there is reduced window for ectopics

63
Q

Pulse deficit

A

Difference ub HR at the wrist and at the apex

64
Q

CHA2DS2-VASc Score

A

Determine the necessity of anticoagulation in AF

Congestive heart failure/left ventricular dysfunction (heart failure with reduced ejection fraction, or people with recent decompensated heart failure requiring hospitalization, irrespective of ejection fraction) = 1

Hypertension (defined as a resting blood pressure greater than 140 mmHg systolic and/or greater than 90 mmHg diastolic on at least 2 occasions or current antihypertensive pharmacologic treatment) = 1

A2ge older than or equal to 75 years = 2

Diabetes mellitus (defined as fasting plasma glucose level of 7.0 mmol/L [126 mg/dL] or more or treatment with oral hypoglycaemic drugs and/or insulin) = 1

S2troke/TIA/thromboembolism = 2

Vascular disease (prior myocardial infarction, peripheral arterial disease, or aortic plaque) = 1

Age 65–74 years = 1

Sex category (female) = 1

Anticoagulation treatment = CHA2DS2VASc score of 2 or above,

Consider offering it to men with a CHA2DS2VASc score of 1

Weigh up with HASBLED

65
Q

HAS-BLED Score

A

Identify people at high risk of bleeding who could benefit from increased vigilance and a specific focus on correction of modifiable risk factors

  • Uncontrolled hypertension
  • Poor control of INR
  • Concurrent medication (for example concurrent use of aspirin or a nonsteroidal anti-inflammatory drug)
  • Harmful alcohol consumption

Hypertension (uncontrolled, greater than 160 mmHg systolic)

Abnormal liver function / Abnormal renal function

Stroke (previous history, particularly lacunar)

Bleeding (bleeding history or predisposition)

Labile international normalized ratios (INRs, therapeutic time in range less than 60%)

Elderly (aged over 65 years)

Drugs (antiplatelet agents or nonsteroidal anti-inflammatory drugs)

Harmful alcohol consumption

66
Q

Management of new-onset AF

A

Admit if they present with severe symptoms or a serious complication of AF.

  • Identify and manage any underlying causes or triggers of AF.
  • Treat the arrhythmia :
    • rate-control treatment (beta-blocker or a rate-limiting calcium-channel blocker) is recommended for most people with AF
  • Referral for rhythm-control treatment (cardioversion) may be appropriate for people:
    • With new-onset AF.
    • Whose AF has a reversible cause (for example a chest infection).
    • Who have heart failure thought to be primarily caused, or worsened, by AF.
    • With atrial flutter and is considered suitable for an ablation strategy to restore sinus rhythm.
  • Rate-control or rhythm-control treatment should be considered for people with AF presenting acutely with non-life threatening haemodynamic instability, depending on the time of onset of arrhythmia.
  • Assess stroke risk using the CHA2DS2VASc assessment tool.
  • Assess risks and benefits of anticoagulation , and start treatment if appropriate.
  • The HAS-BLED assessment tool should be used to assess the risk of a major bleed and to identify and manage modifiable risk factors for bleeding, such as uncontrolled hypertension, harmful alcohol consumption, and concurrent use of aspirin or a nonsteroidal anti-inflammatory drug.

Arrange follow up :

  • After starting rate-control treatments — to assess their effectiveness and tolerability.
  • After starting anticoagulation treatment — to assess compliance and adverse effects.

Provide advice and information on AF, its treatments, and where to find support groups.

67
Q

Management of AF

A

1st Line

  • Offer a rate-control treatment to most people with atrial fibrillation
  • Offer a beta-blocker (see Choice of beta-blocker) or a rate-limiting calcium-channel blocker (diltiazem [off-label use] or verapamil)
  • Consider digoxin monotherapy for people with non-paroxysmal AF only if they have a sedentary lifestyle (that is, they do little or no exercise)Follow up within 1 week of starting rate-control treatment to assess tolerance to treatment and to review symptom control, heart rate, and blood pressure.

Refer to a cardiologist for consideration of rhythm-control treatment (cardioversion), people:

  • With new-onset AF.
  • Whose AF has a reversible cause (for example a chest infection).
  • Who have heart failure thought to be primarily caused, or worsened, by AF.
  • With atrial flutter who are considered suitable for an ablation strategy to restore sinus rhythm.
  • For whom a rhythm-control strategy would be more suitable based on clinical judgement.

For people with AF presenting acutely with non-life threatening haemodynamic instability, rate-control or rhythm-control treatment should be considered, depending on the time of onset of arrhythmia.

  • If the onset of arrhythmia is within 48 hours, offer rate-control treatment or refer the person to an acute medical unit for consideration of immediate cardioversion (without the need for anticoagulation treatment).
  • If the onset of arrhythmia is more than 48 hours or uncertain, start rate-control treatment. If referral for consideration for rhythm-control treatment (cardioversion) is thought to be necessary using clinical judgement, cardioversion should be delayed until the person has been maintained on therapeutic anticoagulation for a minimum of 3 weeks.

Rhythm-control treatments used by specialists include:

  • Electrical cardioversion.
  • Pharmacological cardioversion with antiarrhythmic drugs (such as amiodarone or sotalol).
  • For people having cardioversion for atrial fibrillation (AF) that has persisted for longer than 48 hours, electrical (rather than pharmacological) cardioversion is used
68
Q

Contrainidcations to Warfarin

A

Coagulopathues

Compliance issues

Risk of falls

PUD

Pregnancy

Patient choice

69
Q

Signs of Pacemaker on Examination

A

Inspection: groin scars from insertion, Medic alert bracelet

Pulse: AF

Precordium

Left infraclavicular incisional scar

Palpable pacemaker: if large ? defibrillator

Murmur ?aortic stenosis

Significant negatives: AF, LVF, valvuar pathology, complications of pacemaker (infection or erosions)

70
Q

Signs of pacemaker on ECG

A

Pacing spikes

Physiological ECG trace does not include vertical signals

Evidence of ischaemia

71
Q

Permanent pacemaker indications

A

Complete AV block

Mobitz type II

Symptomatic bradycardia e.g. sick sinus syndrome

Drug-resistant tacharrhythmias

Biventricular pacing in chronic heart failure

72
Q

Letters of pacemaker

A

1st: chamber paced (A, V, or D)
2nd: chamber sensed (A, V, or D)
3rd: Response (Inhibited, Triggered, Dual)

73
Q

Number of Pacemaker Leads

A

Single lead: one lead senses and responds

e.g. VVI

Dual lead: sense and respond in either chamber

Biventricular: leads to both ventricles +/- right atrium

Used for cardiac resynchronisation therapy in HF

74
Q
A

Dual lead pacemaker

One lead in rigth atrium

One in right ventricle

75
Q
A

Single lead pacemaker

76
Q
A

Biventricular pacemaker

Right atrium and right venbtricle lead inserted intravenously

Left ventricle lead was placed epicardially via mini-sternotomy and tunneled up to the prepectoral pocket

77
Q

Implantable defibrillator

A

Can be incorporated into any pacemaker

78
Q

Complications of a Pacemaker

A

Insertion

Bleeding

Arrhythmia

Post-insertion

Erosion

Lead migration

Pocket infection

Malfunction

79
Q

Definition of Chronic Heart Failure

A

Cardiac output is inadequate for the body’s requirments despite adequate filling pressures

80
Q

Caues of Left-sided heart failure

A

Ischaemic heart disease

Idiopathic dilatated cardiomyopathy

Systemic hypertension

Mitral and aortic valve disease

81
Q

Signs and Symptoms of Left-Sided Heart Failure

A

Signs

Cold peipheries +/- cyanosis

AF

Cardiomegaly with displaced apex beat

S3 + tachycardia = gallop rhythm

Wheeze (cardiac asthma)

Bibasal crepitations

Symptoms

Fatigue

Exertional dyspnoea

Orthopnoea and paroxysmal nocturnal dyspnoea

Nocturnal cough (+forthy pink sputum)

Weight loss and muscle wasting

82
Q

Causes of Right-Sided Heart Failure

A

Left ventricular failure

Cor pulmonale

Tricuspid and pulmonary valve disease

83
Q

Signs and Symptoms of Right-Sided Heart Failure

A

Signs

Increased JVP + jugular venous distension

Tender smooth hepatomegaly (may be pulsatile)

Pitting oedema

Ascites

Symptoms

Anorexia

Nausea

84
Q

New York Classification of Heart Failure

A

I: nil shortness of breath

II:comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

III: marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

IV: Shortness of breath at rest

85
Q

NT-proBNP

A

Secreted from ventricles in response to stretch and increased HR

Increased levels are sensitive marker of HF

If low, revise diagnosis

86
Q

CXR changes in heart failure

A

Alveolar shadowing

Kerley B lines

Cardiomegaly

Upper lobe Diversion

Effusions

Fluid in the fissures

87
Q

ECG findings in chronic heart failure

A

Ischaemia

Hypertrophy

AF / arrhythmias

88
Q

Echo findinds in CHF

A

Focal / global hypokinesia

Hypertrophy

Valve lesions

Ejection fraction reduced (normally 60%)

Can be normal HF PEF

89
Q

Management of CHF

A

MDT: Gp, cardiologist, physio, dietician, specialist nurse

Optimise CVS risk factors: statins, Anti-HTN, DM, anti-platelet

Specific

1st-line treatment for all patients is both an ACE-inhibitor and a beta-blocker

2nd- line treatment is now either an aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate

3rd -line: If symptoms persist cardiac resynchronisation therapy or digoxin* should be considered. A

n alternative supported by NICE in 2012 is ivabradine. The criteria for ivabradine include that the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), has a heart rate > 75/min and a left ventricular fraction < 35%

Adjuncts

diuretics should be given for fluid overload

offer annual influenza vaccine

offer one-off** pneumococcal vaccine

90
Q

Trials for Heart Failure Drugs

A

ACE inhibitors (SAVE, SOLVD, CONSENSUS)

spironolactone (RALES)

beta-blockers (CIBIS)

hydralazine with nitrates (VHEFT-1)

91
Q
A

PACES (10 decks)

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