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Medicine 2 - 05 Heart Failure > 7 Cardiac Failure - Clinical Management > Flashcards

7 Cardiac Failure - Clinical Management Flashcards

1
Q

Define Chronic heart failure

and give its prevalence

A

‘Abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate commensurate with requirements of the metabolising tissue’

Seen in 1-2% of the adult population, rising to >10% in over 70s

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2
Q

Describe some signs and symptoms of heart failure, as a clinical ‘syndrome’

A

Typical symptoms:

  • Breathlessness
  • Fatigue
  • Peripheral Oedema

Signs:

  • Raised JVP
  • Pulmonary crepitations
  • Peripheral oedema

Chronic heart failure is a structural/functional cardiac abnormality causing a reduction in cardiac output +/- raised intracardiac pressure at rest or during stress

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3
Q

Define and describe Ejection Fraction,

and describe how it can be used to determine heart failure

A

Ejection fraction - measurement of the quantification of Left Ventricular Systolic function

The most common way of measuring this is using an echocardiogram

Normal EF > 50%
Reduced EF < 40%
Severely impaired EF <35%

heart failure can be thought of as:
- HF with reduced EF (HFrEF)

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4
Q

List some causes of Heart failure

A

Mainly:

  • Ischaemic Heart Disease
  • Toxic damage (drug abuse, heavy metals, radiation)
  • Immune-mediated + inflammatory damage (infection, auto-immune diseases)
  • Infiltration (related to malignancy etc.)
  • Metabolic derangements (disease to hormone producers, deficiencies)
  • Genetic abnormalities
  • Hypertension
  • Valve + myocardium structural defects (acquired or congenital - VSD or ASD)
  • Pericardial + endomyocardial pathologies (peri/endo myocardial - pericarditis, effusion)
  • High output states (severe anaemia, sepsis, pregnancy)
  • Volume overload (renal failure, iatrogenic fluid overload)
  • Arrhythmias (tachycardia, bradycardia - atrial, ventricular, SAN dysfunction, conduction)
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5
Q

Describe the goals of treatment for chronic heart failure

A
  • Identify/treat any cause (valvular disease, IHG - PCI or CABG)
  • Reduce cardiac workload
  • Increase cardiac output
  • Counteract maladaptation
  • Relieve symptoms
  • Prolong quality life - reduce hospitalisations
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6
Q

Briefly describe the pharmacological management available for Chronic Heart Disease

A

it is stage-dependent

ALL patients with LVSD should commence on:
- an ACE inhibitor AND a beta-blocker

ALL patients with pulmonary or peripheral oedema should receive a Diuretic

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7
Q

Describe Angiotensin-converting enzyme inhibitors (ACE inhibitors)

and give their Mechanism of Action

A

Now recognised as 1st line of treatment
e.g. Ramipril, Enalapril, Lisinopril

ACE inhibitors:

  • they reduce arterial and venous vasoconstriction (hence reducing after and preload)
  • they reduce salt/water retention (hence, they reduce the circulating volume)

MOA:
- ACE inhibitors inhibit the RAAS
- by blocking the conversion of Angiotensin I to Angiotensin II
> (which is responsible for activating vasoconstriction and aldosterone production - promotes salt/water retention)
> it may prevent cardiac remodelling

(also given for hypertension)

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8
Q

Describe the use of ACE inhibitors in the treatment of Chronic heart disease

ALSO, give any side effects + contraindications

A

When giving ACEi’s

  • start a low dose, then titrate up
  • MONITOR urea/creatin and K+ levels before and during treatment

SIDE EFFECTS + contraindications
- May cause severe hypotension, so consider giving at night (or withdraw diuretic therapy for a few days before, if BP is low)
- May cause deterioration of renal function in pre-existing renal disease
- May cause dry, irritating cough (10%) - due to elevated pulmonary bradykinin
> ACE is involved in the breakdown of Bradykinin (which causes the contraction of smooth muscle + dilation of blood vessels)
- RARELY, they cause angio-oedema

AVOID IN known renovascular disease
(e.g. Bilateral renal artery stenosis)

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9
Q

Describe AT1 receptor antagonists (or Angiotensin Receptor Blockers - ARBs)

and give their MOA

and give some Side effects

A

Example of ARBs:
- Losartan, Valsartan, Candesartan

MOA:

  • Angiotensin II acts at AT I receptors
  • AT1 receptor antagonists block the action of Ang II

Side Effects:
- Far less likely to give a cough (than ACEi)

ARB’s are given as a 2nd line alternative to ACE inhibitors (if not tolerated)

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10
Q

Describe the use of B-blockers

and give their MOA

A

B Blockers

  • used to be contraindicated
  • but are now 1st line WITH ACEi’s

Beta 1 selective
e.g. Bisoprolol, metoprolol, carvedilol

B blockers:
- Of use in stable chronic heart failure (take care with px who have COPD)
- They reduce sympathetic stimulation
> Heart Rate
> O2 consumption
- They are antiarrhythmic: will control rate in atrial fibrillation
- They oppose the neurohormonal activation (which leads to myocyte dysfunction)

It is especially useful in Heart failure associated with ischaemia

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11
Q

Describe the SE of B-blockers, and any contraindications

A

When giving B-blockers,
- start with a low dose
‘start low go slow’
- symptoms may initially deteriorate

AVOID IN:
- COPD
- decompensated heart failure
- or in presence of pulmonary oedema 
(and asthmatics, or bradycardia)
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12
Q

Describe the use of Diuretics in the treatment of Cardiac failure

MOA

Side effects

A

Loop diuretics like Furosemide (and. thiazides)

  • they reduce the circulating volume
  • Reduces preload on the heart
  • Relive pulmonary and peripheral oedema

Side effects:
- Thiazides (especially)/loop diuretics may cause Hypokalaemia

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13
Q

Describe the use of Mineralocorticoid Receptor Antagonist (MRA) in the treatment of Cardiac failure

MOA

Side effects

A

MRA

  • e.g. Spironolactone - aldosterone receptor antagonist
  • e.g. Eplerenon - similar to spironolactone, but has less anti-androgenous Side effects (anti-testosterone)

MOA:

  • Causes a reduction in salt and water retention
  • Reduction in left ventricular retention

Caution:
- May cause severe Hyperkalaemia
(ESPECIALLY in combination with ACEi’s)

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14
Q

Describe the MOA of Digoxin

and uses

A

Digoxin

  • is a cardiac glycoside
  • used to be a mainstay, but out in and out of fashion

MOA:
- Digoxin is a +ve inotrope (increases the strength of contraction)
> by inhibiting Na+/K+ ATPase
> and so Na+ accumulates in myocytes, and exchanged with Ca2+
> leading to increased contractility
(if there is more Ca2+ in cells, there is more myocyte contraction, giving a longer Action Potential -ve chronotrope)

  • Digoxin is also a -ve Chronotrope (decreases heart rate)
    > due to longer action potential)
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15
Q

Describe the use of Digoxin

it’s role in Chronic heart failure treatment (with other drugs)

and AF

A

Digoxin
- Impairs AV conduction + increases vagal activity (via CNS)
- The resulting bradycardia is beneficial in heart failure with AF
> as slowing the heart rate improves cardiac filling

BUT, digoxin is largely replaced by B blockers in clinical practice

Digoxin is reserved for refractory chronic heart failure
- when ACEi/ARB/B-blockers fail/not tolerated

Digoxin can be useful to control ventricular response to AF in acute heart failure with pulmonary oedema

When giving:
- titrate dose to ventricular rate aiming for <100beats/min

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16
Q

Describe digoxin toxicity

A

This is a major problem with digoxin,
- as it has a narrow therapeutic window

SE:

  • Anorexia
  • Nausea (suggests dose is too high)
  • Visual disturbances
  • Diarrhoea

If digoxin is used in AF, the pulse should be monitored

17
Q

List some specialist treatment options available for chronic heart failure

A
  • Ivabradine

- Entresto (sacubitril + valsartan)

18
Q

Describe the use of Ivabradine in chronic heart failure treatment

give its MOA

SE and contraindications

A

Ivabradine works by inhibiting if current
- Pacemaker Na/K currents in the SA node

It reduces the heart rate

  • BUT not the force of contraction (heart failure use)
  • Those with symptomatic angina had increased SV death

STOP ivabradine treatment if:

  • the resting heart rate remains below 50bpm
  • or symptoms of bradycardia persist

Can be given in addition to ACEi, ARB, and MRA
- CAUTION when adding to a B-blocker

19
Q

Describe the use of Entresto (sacubitril + valsartan) in the treatment of chronic heart failure

MOA

SE

A

It is an ARTI (angiotensin receptor neprilysin inhibitor.
Made of two drugs:
- Angiotensin receptor (Valsartan)
- Sacubitril (neprilysin inhibitor)
> inhibits neprilysin inhibitor
> prevents the breakdown of neuro-endopeptidase e.g. natriuretic peptides and bradykinin

Patients should initially be stable on ACEi or ARB

SHOULD NOT BE CO-PRESCRIBED with ACEi or ARB

Entresto is used for symptomatic HFrEF
- with EF < 35%

20
Q

Describe some add-on treatment available to give when there is ACEi/ARB intolerance/resistance

A

Nitrates

  • Isosorbidfe dinitrate
  • Veno-dilation to reduce preload
  • Beneficial in IHD

Alpha-blocker
- Hydralazine

21
Q

List some medications that can be given to a patient who has heart failure AND type 2 diabetes

A
  • SGLT2 inhibitors (Dapagliflozin)

- GLP1 inhibitors (liraglutide)

22
Q

Describe the use of SGLT2 inhibitors, as a treatment for heart failure (with Diabetes type 2)

A

SGLT2 inhibitors

  • Sodium-glucose co-transporter inhibitors
  • Reduction in CV death and hospitalisation for heart failure in patients with Type 2 diabetes

e. g. Dapagliflozin/Empagliflzin
- benefit in patients WITHOUT diabetes (and is now given to other px w/o DM)

23
Q

Describe the use of GLP1 inhibitors, as a treatment for heart failure (with Diabetes type 2)

A

GLP1 inhibitors

  • Glucagon-like peptide 1 inhibitors
  • Reduction in all causes and CV mortality in patients with MI and CVA
  • Some reduction in Heart Failure hospitalisations

e.g. Liraglutide

24
Q

Describe the importance of monitoring, when giving treatment for Heart Failure

A

Monitor HR, BP, and renal function after initiation of new agent or up-titration:

Renal function

  • patients often elderly, GFR may be impaired
  • Important for drug handling - e.g. dose of digoxin

Use of ACEi
- caution in Renovascular disease

25
Q

Describe the importance of careful monitoring of Potassium (K+) levels, in the treatment of heart failure

A

Hypokalaemia
- side effect of digoxin

Hyperkalaemia
- Serious possibility of hyperkalemia with ACEi/ARB if used with an MRA/K+ sparing diuretic

Medicine 2 - 05 Heart Failure (8 decks)

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