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

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

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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
aortic stenosis causes
* Age related * Congenital bicuspid valve * Chronic kidney disease * Previous rheumatic fever
26
**Symptoms of aortic stenosis**
* Angina * Heart failure * Syncope * Decreased exercise tolerance * Dyspnoea on exertion
27
**aortic stenosis :Murmur**
* Best heard: aortic area (2nd intercostal space right side) * Ejection systolic radiating to the carotid/neck
28
assessment for aortic stenosis
* Echocardiogram – quantification of severity and assess the rest of the heart
29
intervention for aortic stenosis
* **S**ymptoms 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
**Aortic regurgitation**
Increased volume load on the left ventricle leads to progressive LV dilation and heart failure
31
causes of aortic regurg
**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
symptoms of aortic regurg
**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
aortic regurg: murmur
* 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
aortic regurg assessment
**Assessment** * Echocardiogram * Quantification of severity of the regurg and assessment of the rest of the heart
35
aortic regur intervetion
**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
**aortic regurg: indication for surgery** *
* 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
mitral regurg pathophysiology
* 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
causes of mitral regurg
* 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
symptoms of mitral regurg
* May remain asymptomatic for many years * Average interval from diagnosis to onset of symptoms is 16 years
40
mitral regurg: murmur
* 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
mitral regurg
* **Echocardiography-** assess LV function and size together with the severity of the jet of blood coming through the valve
42
**Indication for surgery: mitral regurg**
* 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
medical therpay for mitral regurg
* Diuretic * If ischaemic MR- ACEi * LV systolic dysfunction- ACEi and B-blockers and CRT
44
infective endocarditis RF
**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
pathophysiology of IE
**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
IE should be suspected in patients with
unexplained fever, bacteraemia or systemic illness and/or with apparently new murmur. Patients should be admitted if suspects.
47
**Investigations for IE**
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
**Blood cultures and IE**
* 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
**Echocardiogram and IE**
* 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
the key diagnostic investigations for IE are
BLOOD CULTURES & ECHOCARDIOGRAM
51
extra heart sound heard when: aortic stenosis
systolic
52
extra heart sound heard when: aortic regurg
diastolic
53
extra heart sound heard when: pulonary stenosis
systolic
54
extra heart sound heard when: pulmonary regurg
diastolic
55
extra heart sound heard when: mitral stenosis
diastolic
56
extra heart sound heard when: mitral regurg
systolic
57
extra heart sound heard when: tricuspid stenosis
diastolic
58
extra heart sound heard when: tricuspid regurg
systolic
59
major criteria for IE
* 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
minor criteria for IE
* 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
**Management of IE involves**
**Antibiotic therapy and sometimes surgery**
62
antibiotics for endocarditis caused by viridans streptococci (think endocarditis)
benzylpenicillin IV (or vancomycin if penicillin-allergic) plus low- dose gentamicin (e.g. 80 mg BD)
63
antibiotics for endocarditis caused by enterococcus faecalis
antibiotics for endocarditis caused by virdians streptococci
64
antibiotics for endocarditis caused by staphyloccus
* eg. Staph. aureus, Staph. Epidermidis: flucloxacillin (or benzylpenicillin if penicillin-sensitive, or vancomycin if penicillin allergic or MRSA) plus gentamicin (or fusidic acid).
65
how is reponse to therapy in IE measured
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
IE and surgery
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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