7 Cardiac Failure - Clinical Management Flashcards
Define Chronic heart failure
and give its prevalence
‘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
Describe some signs and symptoms of heart failure, as a clinical ‘syndrome’
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
Define and describe Ejection Fraction,
and describe how it can be used to determine heart failure
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)
List some causes of Heart failure
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)
Describe the goals of treatment for chronic heart failure
- 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
Briefly describe the pharmacological management available for Chronic Heart Disease
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
Describe Angiotensin-converting enzyme inhibitors (ACE inhibitors)
and give their Mechanism of Action
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)
Describe the use of ACE inhibitors in the treatment of Chronic heart disease
ALSO, give any side effects + contraindications
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)
Describe AT1 receptor antagonists (or Angiotensin Receptor Blockers - ARBs)
and give their MOA
and give some Side effects
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)
Describe the use of B-blockers
and give their MOA
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
Describe the SE of B-blockers, and any contraindications
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)
Describe the use of Diuretics in the treatment of Cardiac failure
MOA
Side effects
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
Describe the use of Mineralocorticoid Receptor Antagonist (MRA) in the treatment of Cardiac failure
MOA
Side effects
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)
Describe the MOA of Digoxin
and uses
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)
Describe the use of Digoxin
it’s role in Chronic heart failure treatment (with other drugs)
and AF
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
Describe digoxin toxicity
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
List some specialist treatment options available for chronic heart failure
- Ivabradine
- Entresto (sacubitril + valsartan)
Describe the use of Ivabradine in chronic heart failure treatment
give its MOA
SE and contraindications
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
Describe the use of Entresto (sacubitril + valsartan) in the treatment of chronic heart failure
MOA
SE
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%
Describe some add-on treatment available to give when there is ACEi/ARB intolerance/resistance
Nitrates
- Isosorbidfe dinitrate
- Veno-dilation to reduce preload
- Beneficial in IHD
Alpha-blocker
- Hydralazine
List some medications that can be given to a patient who has heart failure AND type 2 diabetes
- SGLT2 inhibitors (Dapagliflozin)
- GLP1 inhibitors (liraglutide)
Describe the use of SGLT2 inhibitors, as a treatment for heart failure (with Diabetes type 2)
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)
Describe the use of GLP1 inhibitors, as a treatment for heart failure (with Diabetes type 2)
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
Describe the importance of monitoring, when giving treatment for Heart Failure
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
Describe the importance of careful monitoring of Potassium (K+) levels, in the treatment of heart failure
Hypokalaemia
- side effect of digoxin
Hyperkalaemia
- Serious possibility of hyperkalemia with ACEi/ARB if used with an MRA/K+ sparing diuretic
