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Medicine block (Y3) > Week 4: Cardiology (3)(pathology con) > Flashcards

Week 4: Cardiology (3)(pathology con) Flashcards

1
Q

heart failure

A

Inability of the heart to meet the demands of the body.

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2
Q

causes of HF

A
  1. Ischaemic heart Disease (most common)
  2. Hypertension
  3. Valvular heart disease (Rheumatic fever in elderly)
  4. Atrial fibrillation
  5. Chronic lung disease (right sided- cor pulmonale)
  6. Cardiomyopathy (Hypertrophic, dilated and right ventricular, post viral, post-partum)
  7. Previous cancer chemo drugs
  8. HIV
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3
Q

Signs and symptoms of HF

A
  • a persistent cough, which may be worse at night.
  • wheezing.
  • a bloated tummy/ ankles
  • loss of appetite.
  • weight gain or weight loss.
  • confusion.
  • dizziness and fainting.
  • a fast heart rate.
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4
Q

HF patients with bad prognosis

A
  • severe fluid overload
  • very high NT-proBNP
  • severe renal impairment
  • advanced age
  • mulit-morbdiity
  • frequent admissions
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5
Q

investigations for HF

A

Investigations

  • bloods
    • renal function
    • FBC, LFTs, TFTs
    • Ferritin and transferrin (haemochromatosis)
    • BNP
  • CXR
  • Echocardiography. cardiac MRI – assessment of LV function
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6
Q

What makes sure the heart pumps effectively?

A
  • One way valve ensuring blood flows in one direction
  • Chamber size if too small reduced preload (stretch of ventricles)
  • Functioning muscle  MI will damage heart
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7
Q

preload

A

stretch of ventricles before contraction

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8
Q

After load-

A

what the heart has to pump against i.e. bp

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9
Q

ejection fraction

A
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10
Q

HF can be classified either via

A

EJ or ventricle involvement

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11
Q

ejection fraction classification of HF

HFrEF

A
  • Reduce EF <40%
  • Contractility problem
  • most common
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12
Q

ejection fraction classification of HF: HFpEF

A
  • Preserved ejection fraction
  • Filling problem
    • Stiff/smaller ventricles
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13
Q

causes and presentation of left sided HF

A
  • Causes: IHD, MI, HTN, valvular
  • Presentation: pulmonary oedema, fatigue, tiredness, SoB
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14
Q

causes and presentation of left sided HF

A
  • Causes: IHD, MI, HTN, valvular
  • Presentation: pulmonary odema, fatigue, tiredness, SoB, PND
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15
Q

causes and presentation of right sided HF

A
  • Causes: chronic hypoxia
  • Presentation: peripheral oedema, fatigue, tiredness, jugular vein distention
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16
Q

HFNEF (heart failure normal ejection fraction)

A
  • Clinical features of heart failure however have echocardiograms that suggest just mild impairment or even normal systolic function.
  • Similar clinical course and outcome as patients with LV systolic dysfunction.
  • Patients with HFNEF are often more elderly, overweight and have hypertension and atrial fibrillation.
  • It is hypothesised that the physiology behind HFNEF relates to impaired filling or diastolic dysfunction
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17
Q

lifestyle management of HF

A
  • Smoking cessation
  • Reduce alcohol consumption
  • Salt restriction
  • Fluid restriction may be indicated in presence of hyponatraemia
    • Daily weight monitoring can help identity fluid accumulation earlier
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18
Q

medical management of HF

A

Medication: think BAD

  • Diuretics
    • Loop diuretics most effective (
      • Furosemide
        • IV (if very fluid overloaded)
      • Bumetanide
        • Better absorbed orally
    • If hypokalaemia starts- spironolactone
  • ACEi
  • ARBs e.g. valsartan and candesartan
  • ARNI (angiotensin receptor – neprilysin inhibitor)
  • Beta blockers (low and go slow)
    • Carvedilol
    • Bisoprolol
  • Vasodilators: hydralazine and isosorbide mononitrate
  • Ivabradine
  • Complex device therapy
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19
Q

CXR in heart failure

A
  1. Cardiomegaly
  2. Could be pleural effusions
  3. Perihilar shadowing/consolidations
  4. Alveolar oedema
  5. Air bronchograms phenomenon of air-filled bronchi (dark) being made visible by the opacification of surrounding alveoli
  6. Increased width of vascular pedicle
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20
Q

Patients being diuresised

A
  • Fluid balance (- 1000)
  • Clinical condition
  • Daily
  • Blood test for dehydration

Diuretics will not cause low sodium.

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21
Q

Nitrates and HF

A
  • Nitrates reduce preload; reduce pulmonary oedema and reduce ventricular size.
  • There is a beneficial effect of using IV nitrates in acute heart failure if there is underlying ischaemia, hypertension or regurgitant aortic and mitral valve disease.
  • In chronic heart failure they can be especially useful for relief of orthopnoea and exertional dyspnoea.
  • Caution should be applied with aortic and mitral stenosis, HOCM and pericardial constriction.
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22
Q

Cardiac resynchronisation pacemaker (CRP)

A
  • When? Evidence of left bundle branch block
    • This means the QRS duration is broad and essentially depolarisation of electricity is delayed from the septum to lateral wall resulting in mechanical reduction.
  • If we pace at these two points then we can alter the QRS duration to becoming narrow again then the heart muscle can pump normally.
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23
Q

Implantable cardiac defibrillators

A
  • Do not improve symptoms
  • Only purpose is to prevent sudden cardiac death associated with heart failure by detecting and cardioverting VT/VF
  • Delivers and electric shock
  • Used for secondary prevention in survivors of sudden cardiac arrest or for primary prevention
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24
Q

Valvular heart disease

A

aortic stenosis and regurg, mitral stenosis and regurg

  • Left uncorrected valvular heart disease can often lead to irreversible ventricular dysfunction or pulmonary hypertension
  • Best to correct early
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25
Q

aortic stenosis causes

A
  • Age related
  • Congenital bicuspid valve
  • Chronic kidney disease
  • Previous rheumatic fever
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26
Q

Symptoms of aortic stenosis

A
  • Angina
  • Heart failure
  • Syncope
  • Decreased exercise tolerance
  • Dyspnoea on exertion
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27
Q

aortic stenosis :Murmur

A
  • Best heard: aortic area (2nd intercostal space right side)
  • Ejection systolic radiating to the carotid/neck
28
Q

assessment for aortic stenosis

A
  • Echocardiogram – quantification of severity and assess the rest of the heart
29
Q

intervention for aortic stenosis

A
  • Symptoms caused by AS (regardless of severity).
  • Asymptomatic severe AS with left ventricular systolic dysfunction.
  • Asymptomatic severe AS with abnormal exercise test (symptoms, drop in BP ST changes).
  • Asymptomatic severe AS at the time of other cardiac surgery (e.g. CABG).

In older patients with significant co-morbidities transcatheter aortic valve implantation (TAVI)- via the femoral artery

30
Q

Aortic regurgitation

A

Increased volume load on the left ventricle leads to progressive LV dilation and heart failure

31
Q

causes of aortic regurg

A

Causes

  • Idiopathic dilation of the aorta (pulling valve leaflets apart)
  • Congenital abnoramility of aortic valve (bicsid valve)
  • Calcific degeneration
  • Rheumatic disease
  • Infective endocarditis
  • Marfans syndrome
32
Q

symptoms of aortic regurg

A

Causes

  • Idiopathic dilation of the aorta (pulling valve leaflets apart)
  • Congenital abnoramility of aortic valve (bicsid valve)
  • Calcific degeneration
  • Rheumatic disease
  • Infective endocarditis
  • Marfans syndrome
33
Q

aortic regurg: murmur

A
  • Best heard at the left sternal edge
  • Early diastolic blowing murmur
  • Associated with a collapsing pulse
  • on end expiration, with the patient sitting up and leaning forward.
34
Q

aortic regurg assessment

A

Assessment

  • Echocardiogram
  • Quantification of severity of the regurg and assessment of the rest of the heart
35
Q

aortic regur intervetion

A

Intervention

  • Afterload reduction i.e. reducing BP ( with ACEi) can slow rate of left ventricular dilatation and is now standard therapy in patients with severe AR and LV dilation
36
Q

aortic regurg: indication for surgery

*

A
  • Symptomatic severe AR
  • Asymptomatic severe AR with evidence of early LV systolic dysfunction (EF < 50% or LV end-systolic diameter > 5 cm or LV end-diastolic diameter > 7·0 cm)
  • Asymptomatic AR of any severity with aortic root dilatation > 5·5 cm (or > 4·5 cm in Marfan syndrome or bicuspid aortic valve).
37
Q

mitral regurg pathophysiology

A
  • Mitral valve prolapse is one aetiology more common in patients with Marfans syndrome and those with pectus excavatum
    • 1-2% of population and may be familial
  • Prognosis worse when there is moderate ot severe MR and when the EF is <50%
  • Usually worsens over time
38
Q

causes of mitral regurg

A
  • Marfans
  • Rheumatic heart disease
  • IHD
  • Infective endocarditis
  • Certain drugs
  • Collagen vascular disease
  • Secondary to a dilated annulus from LV dilation
  • Severe MR
    • Ruptured chordae
    • Ruptured papillary muscle
    • Infective endocarditis
39
Q

symptoms of mitral regurg

A
  • May remain asymptomatic for many years
  • Average interval from diagnosis to onset of symptoms is 16 years
40
Q

mitral regurg: murmur

A
  • Pan-systolic blowing murmur
  • Best heard over mitral area (5th ICS mid clavicular line) and radiates to axialla
  • accentuation maneouver: Roll the patient onto their left side and listen over the mitral area with the diaphragm of the stethoscope during expiration to listen for a pansystolic murmur caused by mitral regurgitation.
41
Q

mitral regurg

A
  • Echocardiography- assess LV function and size together with the severity of the jet of blood coming through the valve
42
Q

Indication for surgery: mitral regurg

A
  • Mitral valve replacement or mitral valve repair (performed if anatomy of valve is suitable- better operative mortality)

Surgical intervention is generally indicated in severe MR for:

  • Symptomatic patients (with symptoms due to the MR).
  • Asymptomatic patients with mild-moderate LV dysfunction (EF 30 - 60% and LVESD 4·5 - 5·5 cm).
43
Q

medical therpay for mitral regurg

A
  • Diuretic
  • If ischaemic MR- ACEi
  • LV systolic dysfunction- ACEi and B-blockers and CRT
44
Q

infective endocarditis RF

A

Risk factors

  • Mitral valve prolapse
  • Prosthetic material (valve and aptches, but not coronary stents
  • Rheumatic heart disease
  • Degenerative and bicuspid aortic valve disease
  • Congenital heart disease
  • Normal heart valve
  • Infection due to intravascular device
  • Intravenous drug use
45
Q

pathophysiology of IE

A

Pathophysiology

  • Native-valve IE- viridans group of streptococci (50% episodes) and staphylococcus aureus (20%)
  • IVDU – S. aureus is commonest (50-60% of episodes)
  • Early IE occurring up to a year after implantation of prosthetic heart valve is though to be due to perioperative contamination – staphylococci (coagulase negative)
  • Late IE commonly due to viridans streptococci’s, S. aureus and coagulase negative staphylococci
  • Enterococcal endocarditis represents about 10% of all cases disease of GU or lower GI tract
  • 10% of cases are caused by fungi (candida and aspergillus spp) particularly in patients with immunosuppression, IV drug use, cardiac surgery, prolonged exposure of Abx drugs and IV feeding
  • 5% of patients with proven IE the conventional blood cultures are negative
    • May be due to recent Abx or infection with slow growing or fastidious organisms
46
Q

IE should be suspected in patients with

A

unexplained fever, bacteraemia or systemic illness and/or with apparently new murmur. Patients should be admitted if suspects.

47
Q

Investigations for IE

A

Should be suspected in patients with unexplained fever, bacteraemia or systemic illness and/or with apparently new murmur. Patients should be admitted if suspects.

Routine initial investigations should include:

  • Full blood count
  • ESR and CRP
  • U&Es
  • Liver function tests
  • Urine dipstick analysis and MSU for microscopy/culture
  • Chest X-ray
  • ECG
  • However, the key diagnostic investigations are: BLOOD CULTURES & Transosopheageal ECHOCARDIOGRAM
48
Q

Blood cultures and IE

A
  • At least 3 (preferably 6) should be taken from diff sites over several hours
  • If pt stable reasonable to delay abx to allow comprehensive sampling- once abx been given much harder to identify causative organism
  • If cultures are negative despite high suspicion, samples can be taken in special media that allows growth of fastidious organisms
49
Q

Echocardiogram and IE

A
  • Transthoracic echocardiography will detect 65% of vegetations.
  • Transoesophageal echocardiography (TOE) will detect 95% of vegetations.
    • TOE is particularly useful for the detection of mitral valve and prosthetic valve vegetation
    • More sensitive at detecting aortic root and septal abscesses and leaflet perforations
50
Q

the key diagnostic investigations for IE are

A

BLOOD CULTURES & ECHOCARDIOGRAM

51
Q

extra heart sound heard when: aortic stenosis

A

systolic

52
Q

extra heart sound heard when: aortic regurg

A

diastolic

53
Q

extra heart sound heard when: pulonary stenosis

A

systolic

54
Q

extra heart sound heard when: pulmonary regurg

A

diastolic

55
Q

extra heart sound heard when: mitral stenosis

A

diastolic

56
Q

extra heart sound heard when: mitral regurg

A

systolic

57
Q

extra heart sound heard when: tricuspid stenosis

A

diastolic

58
Q

extra heart sound heard when: tricuspid regurg

A

systolic

59
Q

major criteria for IE

A
  • Positive blood cultures
    • typical organism from 2 blood cultures
    • persistent positive blood cultures taken > 12 hours apart
    • > 3 positive blood cultures taken over more than 1 hour
  • Endocardial involvement
  • Positive echo findings (vegetation, abscess)
  • New valvular regurgitation
  • Dehiscence of prosthesis
60
Q

minor criteria for IE

A
  • Predisposing valvular or cardiac abnormality
  • IV drug abuser
  • Pyrexia > 38°C
  • Embolic phenomenon
  • Vasculitic phenomenon
  • Blood cultures suggestive (organism grown but not achieving major criteria)
  • Suggestive echo findings (but not meeting major criteria)
61
Q

Management of IE involves

A

Antibiotic therapy and sometimes surgery

62
Q

antibiotics for endocarditis caused by viridans streptococci (think endocarditis)

A

benzylpenicillin IV (or vancomycin if penicillin-allergic) plus low- dose gentamicin (e.g. 80 mg BD)

63
Q

antibiotics for endocarditis caused by enterococcus faecalis

A

antibiotics for endocarditis caused by virdians streptococci

64
Q

antibiotics for endocarditis caused by staphyloccus

A
  • eg. Staph. aureus, Staph. Epidermidis: flucloxacillin (or benzylpenicillin if penicillin-sensitive, or vancomycin if penicillin allergic or MRSA) plus gentamicin (or fusidic acid).
65
Q

how is reponse to therapy in IE measured

A

It is important to monitor response to therapy closely. As well as regular bedside reviews of clinical status, you should also check:

  • Echocardiogram (once weekly) - to assess vegetation size and look for complications (e.g. valve destruction, intracardiac abscesses)
  • ECG (at least twice weekly) - to detect conduction disturbances, which may indicate development of an aortic root abscess in aortic valve infection
  • Blood tests (twice weekly) - ESR, CRP, full blood count and U&Es
  • Duration of antibiotics will depend on clinical response as well as local microbiology guidance: patients may need 6 weeks or more of treatment
66
Q

IE and surgery

A

Referral for consideration of surgery is indicated in patients with:

  • Moderate to severe cardiac failure due to valve compromise
  • Valve dehiscence (detachment)
  • Uncontrolled infection despite appropriate antimicrobial therapy
  • Relapse after optimal medical therapy
  • Threatened or actual systemic embolism
  • Coxiella burnetii and fungal infections
  • Paravalvar infection (e.g. aortic root abscess)
  • Sinus of Valsalva aneurysm
  • Valve obstruction

Medicine block (Y3) (38 decks)

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