Heart Failure Flashcards

1
Q

What is the prognosis for heart failure?

A

High mortality shortly after diagnosis – 30-40% die within a year

Mortality following is 10%

Admission required – 5yr mortality = 75%

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2
Q

What are community support programmes for chronic disease?

A

Expert patient programmes:
6 week course led by a ‘lay’ patient that has experience living with the specific chronic disease
Better lifestyle, communication, pain management, mental health, problem solving and planning

Specialised nurses:
1-2x/yr regular; more frequent if poorly controlled disease
Work closely with patients to improve care

DAFNE + DESMOND:
Diabetes specific courses

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3
Q

What are examples of levels of prevention of disease in heart failure?

A

Primary:
NHS health check
Education and doing re lifestyle factors

Secondary: 
Regular monitoring – BP, Echos etc 
Daily low dose aspirin 
BP meds 
Statin 
DM/renal management 
Diet/exercise programmes 

Tertiary:
Cardiac rehab
Community support

Population: 
Salt and sat fats guidance/labelling 
Physical activity encouragement – change4life, cycle lanes etc 
Sugar and alcohol taxes 
Collection of population health data
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4
Q

What is the definition of heart failure?

A

Inability of the heart to pump adequate amounts of blood to meet the body’s metabolic demands → the end stage of all heart disease

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5
Q

What are the different types of heart failure?

A

Systolic - inability of heart to contract efficiently to eject adequate volumes of blood to meet metabolic demands (most common)

Diastolic - reduction of heart compliance → reducing in ventricular filling and ejection

Left - leads to pulmonary oedema and usually results in right sided heart failure due to pulmonary hypertension (cor pulmonale)

Right - leads to peripheral oedema, hepatic congestion and tenderness

Congestive = L+R heart failure

Low-output - HF from low CO

High-output - due to metabolic demand-
supply mismatch i.e. reduced blood O2 carry-
ing capacity or increased body metabolism

Acute - usually the result of acute event - MI

Chronic - slow symptom progression due to
underlying disease

Acute-on-chronic - acute degeneration of a
chronic cause i.e. caused by infection

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6
Q

What is the pathophysiology of heart failure?

A

NEEDS BETTER CLARITY:

HR and contractility increase to maintain cardiac output - over time this causes hypertrophic changes to the cardiac tissue - with too much growth this tissue becomes under perfused, unable to deal with the increased demand and undergoes ischemic injury

Also stimulation of RAAS due to reduced renal perfusion:
Angiotensin II creation leads to vasoconstriction + aldosterone + ADH release - increase in Na and H2O retention, increasing stroke volume and total peripheral resistance, but also more fluid stretches the heart = reduced contractile ability + pulmonary and peripheral oedema

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7
Q

How does heart failure present?

A

The Framingham criteria:
SAW PANIC HEART ViNo

Major:
S3 heart sound present (‘gallop’ sound)
Acute pulmonary oedema (left side of heart is unable to clear fluid from lungs)
Weight loss of more than 4.5kg in 5 days when treated (patients lose their retained fluids)
Paroxysmal nocturnal dyspnoea
Abdominojugular reflux (JVP waveform rises when pressure applied over liver area)
Neck vein distended (i.e. JVP elevated at rest)
Increased cardiac shadow on X-ray (cardiomegaly = cardiothoracic ratio of >0.5; double density sign = enlarged L atrium)
Crackles heard in lungs

Minor:
Hepatomegaly
Effusion, pleural
Ankle oedema bilaterally
exeRtional dyspnoea
Tachycardia
Vital capacity decreased by a third of maximum value
Nocturnal cough
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8
Q

How do you investigate heart failure?

A

CXR:
- Cardiomegaly, pulmonary oedema

ECG:
- Can help confirm HF, define underlying cause - MI, BBB, arrhythmias

Echo:
- Look at ejection fraction, wall thickness, cardiac kinetics etc

Bloods:
- Causes and severity: anaemia, hypernatraemia, hypo/hyperkalaemia

Brain natriuretic peptide (BNPs):

  • Peptides that cause natriuresis, diuresis and vasodilation (body’s “natural defence” against hypervolaemia)
  • Levels correlated with cardiac filling pressures
  • Recommended in all patients with suspected HF

Renal function/U+E:
- Cardio-renal axis dysfunction will often occur with long term CCF patients due to the relationship between the two axes and the effects/side effects of medications (e.g. ACEis, diuretics etc)

Liver function/LFTs:

  • Can become deranged in biventricular failure due to systemic hypervolaemia and increased back pressures in liver
  • Should settle with cardiac management and diuresis

Angiography

Thyroid function - rule out thyrotoxicosis
PFTs - to discount lung disease

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9
Q

What non-pharmacological management options are there for heart failure?

A
Exercise
Diet control - plant based whole-food diet, reduce salt intake
Monitor weight, lose weight if obese 
Fluid restriction 
Reduce alcohol intake
Quit smoking
Flu vaccination
Watch for depression and act accordingly
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10
Q

What is the pharmacological management of heart failure?

A

ABCD = ACE-I, B-blocker, Ca blocker + nitrates, Diuretics + Digoxin

Stepwise approach:
ACE inhibitors or ARB
ADD diuretic
ADD beta-blocker
ADD aldosterone antagonist
ADD digoxin
Consider another vasodilator, e.g. isosorbide dinitrate or hydralazine
Drugs to avoid
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11
Q

What ACE-Is are used in HF?

A

Enalapril, lisinopril etc

Reduce afterload and fluid retention → slows LV disease progression
Strong vasodilators

SE: dry cough - if intolerable = angiotensin II inhibitors (candesartan)

Caution: concomitant use with spironolactone (can cause hyperkalaemia)

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12
Q

What Diuretics are used in HF?

A

Promote renal Na excretion and thus water excretion; decrease ventricular filling pressures, decreasing pulmonary and systemic congestion - if congestion controlled, can cease diuretics and maintain strict fluid/salt balance with diet

Furosemide (loop, moderate/severe HF) (1st line)
SE: gout, electrolyte imbalance, postural drop (elderly)

Bendroflumethiazide (thiazide, first line in mild HF)
SE: gout, electrolyte imbalance, postural drop (elderly)

Spironolactone (potassium sparing)
SE: gynaecomastia

DONT use as monotherapy, always with ACE-I

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13
Q

What B-blockers are used in HF?

A

Beta blockers:
Bisoprolol, cavedilol etc (cardioselective options)

Reduce afterload and HR to prevent arrhythmias

SE: dizziness, nausea, headache, change in sex drive/performance

Contraindications: asthma, heart block, bradycardia

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14
Q

What Ca-blockers and vasodilators are used in HF? What should be avoided?

A

CaB:
Amlodipine

Hydralazine + nitrates
-ve chrono/inotrophic

Used if intolerant to ACE-I/ARB

AVOID:
Diltiazem, Verapamil

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15
Q

When is Digoxin indicated in HF?

A

Sinus rhythm patients that remain symptomatic even after other pharmacological interventions (third line after ACE-i and diuretics)

Patients with severely impaired left ventricular function

Recurrent hospital admissions

Treating AF in CHF

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16
Q

When is amiodarone indicated in HF?

A

In arrhythmic patients

17
Q

What drugs should be avoided in heart failure?

A

Felcanide
Verapamil, diltiazem and other calcium channel blockers (other than amlodipine)
Tricyclic antidepressants
Lithium
NSAIDs
Corticosteroids
Drugs known to prolong QT interval (e.g. erythromycin)

18
Q

What other treatment options are there for HF?

A

Implantable devices:
Pacemaker
Biventricular pacemakers are useful in patients with heart failure and bundle branch block
ICD – implantable cardiac defibrillator
Left ventricular assist device (e.g. VentrAssist)

Surgery:
Revascularization in IHD [CABG or Angioplasty (PTA)]
Valvular replacement
Cardiac transplant

19
Q

How do you manage acute heart failure?

A

Monitor sats + titrate oxygen appropriately - may need high flow or NIV (or Invasive ventilation if unresponsive/deteriorating)

Do an ECG, FBC, U/E, Cardiac enzymes, BNP (-ve = less than 100ng/L), ABG, CXR, transthoracac Doppler 2D echo to look for cardiac abnormalities

Mainstay of treatment:
Furosemide IVI, slow infusion starting at 50mg - increased in steps of 20mg every 2 hours if required; maximum 1.5 g per day
If already taking diuretic - start on higher dose

Monitor, daily:

  • Weight - aim for 0.5-1kg weight loss/day
  • Urine output/fluid balance - ?catheterise
  • Renal function - as diuretics can upset

Do NOT routinely offer:
Opiates
Nitrates (unless people also have myocardial ischemia, severe HTN or valve disease)
Sodium nitroprusside
Inotropes/vasopressors (unless cardiac shock)

After stabilised e.g. IV diuretics stopped:
Start/restart B-blocker
Offer ACE-i/ARB/aldosterone antagonist