heart failure Flashcards

1
Q

Heart failure (HF) definition

A

= is a syndrome and not a single pathological process in which there is impairment of the heart as a pump supporting physiological circulation.

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2
Q

s/s

A

Patients with heart failure will have the following features:

  1. symptoms typical of heart failure e.g. - breathlessness and exhaustion at rest or with less than the normal degree of exertion, fatigue and
  2. signs of fluid retention e.g. - pleural effusion, increased JVP, peripheral oedema and
  3. objective evidence of an abnormality of the structure or function of the heart at rest e.g. - cardiac murmurs, third heart sound
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3
Q

ways HF is classified

A
  1. low/high output
  2. L/R ventricular failure
  3. systolic/diastolic failure
  4. acute vs chronic
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4
Q

pathophys of heart failure

A

1. decreased CO initially = compensation

  • starling effect dilates heart to improve contractility
  • remodelling = hypertrophy
  • release of ANP/BNP
  • sympathetic activation

2. progressive decrease in CO

  • progressive dilation => impaired contractility + functional valve regurg
  • hypertrophy = relative myocardial ischemia
  • RAS activation = na+ fluid retention
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5
Q

low output HF causes

ie. CO is low and fails to increase with exertion.
nb. systolic + diastolic features tend to coexist

A

1.pump failure

a) systolic failure [impaired cntraction of ventricles thus low CO, EF = <40%] due to:

  • ischemia/mi
  • dilated cardiomyopathy
  • htn
  • myocarditis

b) diastolic failure [inability of ventricles to relax and fill normally thus get increased filling pressure, EF = >50%

  • pericardial effusion/tamponade/constriction
  • cardiomyopathy- restrictive/hypertrophic

c)arrhythmias [low hr]

  • bradycardia
  • heart block
  • tachycardias
  • anti-arrhythmics

2. excessive pre-load [EDV]

  • AR
  • MR
  • fluid overload

3. excessive after-load–ventricular pressure @ end of systole [ESP]

  • AS
  • HTN
  • HOCM
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6
Q

high output HF causes

A.T.P!!

A

increased needs causes RVF initially, then LVF!

  1. anemia, AVM
  2. thyrotoxicosis, thiamine deficiency [beriberi]
  3. pregnancy, pagets
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7
Q

LVF causes

A
  1. ihd
  2. idiopathic dilated cardiomyopathy
  3. systemic htn
  4. mitral/aortic vale disease
  5. specific cardiomyopathies
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8
Q

LVF symptoms

A

symptoms:

  1. fatigue
  2. exertional dyspnoea
  3. orthopnoea + pnd
  4. nocturnal cough [and/or pink frothy sputum]
  5. wt loss + muscle wasting

signs:

  • cold peripheries
  • often in AF
  • cardiomegaly w/displaced heart
  • S3 + tachycardia = GALLOP RHYTHM
  • cardiac asthma [wheeze]
  • basal creps in both lung bases
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9
Q

RVF causes

A
  1. LVF
  2. cor pulmonale
  3. tricuspid/pulmonary valve disease eg. pulm stenosis
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10
Q

RVF s/s

A

symptoms:

  1. anorexia
  2. nausea

signs:

  1. raised JVP + jugular vein distention
  2. tender, smooth + pulsatile hepatomegaly
  3. pitting oedema up to thigs, sacrum, abdo wall
  4. ascites
  5. facial engorgement
    nb: RVF/LVF may occur independently or together as CCF
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11
Q

acute vs chronic onset HF

A

acute

  • new onset or decompensation of chronic
  • peripheral/pulm oedema
  • and/or evidence of hypoperfusion

chronic

  • develops/progresses v slowly
  • venous congestion = common
  • arterial pressure maintained till v late
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12
Q

general summary of HF s.s

A

common symptoms are:

  • breathlessness
    • exertional
    • at rest - can be orthopnoea and paroxysmal nocturnal dyspnoea (PND)
  • fatigue
  • exercise intolerance
  • fluid retention - ankle swelling
  • other non specific symptoms include:
    • nocturia
    • anorexia
    • abdominal bloating and discomfort
    • constipation,
    • cerebral symptoms - confusion, dizziness and memory impairment

signs such as:

  • tachycardia
  • displaced apex beat
  • third heart sound
  • gallop rhythm
  • reduced pulse volume
  • pulsus alternans
  • raised JVP –
    • in right heart failure
    • has a high predictive value in the diagnosis
    • but is often absent
  • oedema
  • rales, or basal crepitations
  • hepatomegaly
  • ascites
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13
Q

Heart failure: NYHA classification

A

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure:

NYHA Class I

  • no symptoms
  • no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

NYHA Class II

  • mild symptoms
  • slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

NYHA Class III

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

NYHA Class IV

  • severe symptoms
  • unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
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14
Q

HF ix

A
  • chest radiology

πŸ’ ALVEOLAR SHADOWING - or classic perihilar β€˜bat wings’ appearance

πŸ’ KERLY B LINES- thickened oedematous interlobular shadowing

πŸ’ CARDIOMEGALY- cardiothoracic ratio >50%

πŸ’ UPPER LOBE DIVERSION- upper lobe pulm vein dilation

πŸ’ EFFUSIONS-

πŸ’ FLUID IN THE FISSURES

  • the ECG - is recommended in every patient with suspected HF (1), may elucidate the cause of heart failure:
    • left ventricular hypertrophy which may be caused by chronic hypertension or aortic stenosis
    • evidence of ischaemic heart disease
    • p-mitrale of mitral stenosis
  • echocardiography identifies:
    • focal or diffuse myocardial dysfunction
    • valvular disease
    • pericardial disease
    • left ventricular systolic dysfunction
  • biochemistry, haematology and urinalysis:
    • defines electrolyte disturbances and assesses renal function
    • fbc excludes anaemia
    • tfts exclude thyrotoxicosis in patients with atrial fibrillation
    • lfts excludes causes of oedema such as liver disease, nephrotic syndrome and acute renal failure
    • natriuretic peptides - testing for Brain-type natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and N-terminal (NT)-ANP has been shown to increase the reliability of diagnosis of heart failure in primary care
      • these peptides are released from ventricular myocytes in response to volume overload (stretch), and their concentration has been shown to an extremely sensitive marker for heart failure
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15
Q

Heart failure: diagnosis

A

NICE issued updated guidelines on diagnosis and management in 2010. The choice of investigation is determined by whether the patient has previously had a myocardial infarction or not.

Previous myocardial infarction

  • arrange echocardiogram within 2 weeks

No previous myocardial infarction

  • measure serum natriuretic peptides (BNP)
  • if levels are β€˜high’ arrange echocardiogram within 2 weeks
  • if levels are β€˜raised’ arrange echocardiogram within 6 weeks
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16
Q

what is serum bnp

A

Serum natriuretic peptides

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.

Very high levels are associated with a poor prognosis.

17
Q

Factors which alter the BNP level:

A
18
Q

mx of adult with chronic HF

A

1. manage any depression

2. lifestyle advice: no smoking, exercise[group rehab programmes], healthy diet [decreased salt, optimise wt perhaps with help of dietician!]

3. pharm mx:

first-line treatment for all patients is both of these:

  • ACE-inhibitor eg. lisinopril [or candesartan as substitute].
  • beta-blocker eg. carvediol/bisoprolol/nebivolol. nb. start low go slow.
  • loop diuretic eg. furosemide/bumetanide for fluid overload

second-line treatment :

  • if intolerant of ACEi, can try these vasoldilators/additional rx in afrocaribbean pts: hydralazine in combination with a nitrate
  • in pts who still have symptoms: aldosterone antagonist eg. spironolactone. *specialist advice needed first. be careful of hyperkalemia in renal patients*

third line: if symptoms persist cardiac resynchronisation therapy or digoxin* should be considered.

  • An 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%

🍜 offer annual influenza vaccine

🍜 offer one-off** pneumococcal vaccine

Loop diuretics do not have prognostic benefit in heart failure and so would only give symptom relief. ACE-I/ARBs, B blockers and Aldosterone receptor antagonists improve mortality in heart failure

4. invasive therapies

  • cardiac resynchronisation and or ICD [implantable cardioverter defib] - detects life threatening rapid heart beat
  • intra aortic balloon counter pulsation- temporary mechnical ventilatory support
  • LVAD- l ventricular assist device- helps weakened heart pump blood
  • heart transplant- [70% 5 yrs]

*digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties. Digoxin is strongly indicated if there is coexistent atrial fibrillation

**adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years

19
Q

HF - exacerbating factors to avoid!

A
  • alcohol
  • cocaine
  • nsaids- fluid retention
  • verapamil- negatively inotropic
20
Q

complications

A

resp failure

cardiogenic shock

death