heart failure Flashcards
long term activation of RAAS
- Long term activation of RAAS: makes the heart work harder and harder results in increase in preload/afterload
- Long term activation of SNS: myocardial stress, increased O2 use, cardiac hypertrophy, fibrosis, cardiac muscle cell necrosis and death, increased potential for dysrhythmias
what is preload
venous return (as the blood comes back to the heart = the load that the heart has to pump)
what is afterload
the pressure/resistance under which the heart has to pump
treatment of HF
– ACE inhibitors – Angiotensin II receptor antagonists – Neprilysin inhibitors – Diuretics – Beta adrenoceptor antagonists (beta blockers) – Spironolactone – Ivabradine – Digoxin (particularly if atrial fibrillation)
what is HF
Heart failure • Inability of the heart to pump sufficient blood to meet the metabolic needs of the tissues in the presence of an adequate filling pressure • Caused by o Ischemic heart disease o Hypertension o MI o Heart valve disease o Infections
ACE inhibitors
- Reduce mortality/morbidity
- Slow progression of HF
- Reduces preload and afterload – makes it easier for heart to do its job
- Decrease Angiotensin II levels
- Increase bradykinin levels
- Produce vasodilation
- Increase excretion of sodium and water
- Start with low dose, increase gradually
- Monitor renal function + potassium levels (expect decreased RF, increased K+) – can lead to hyperkalaemia
- Add diuretic if symptoms not adequately controlled
- Can cause cough
Angiotensin II receptor antagonists
- Can be used instead of ACE inhibitors i.e. if ACE not tolerated (cough)
- Monitor renal function + potassium – decrease RF, increase K+
- Reduce mortality/morbidity in patients with SHF
Neprilysin inhibitors
- Sacubitril inhibits the enzyme neprilysin
- Sacubitril inhibits the breakdown of natriuretic peptides and prolongs their actions = beneficial in treatment of systolic HF
Good actions of natriuretic peptides:
- Vasodilation
- Diuresis, natriuresis
- Inhibition of renin and aldosterone release
- Reduction in sympathetic activity
- Reduced preload and afterload
- Anti-hypertrophic and anti-fibrotic effects which reduce CV remodelling
- Sacubitril is combined with valsartan (Entresto)
- Never administer with an ACE inhibitor – risk of angioedema – 36hr washout period
Diuretics (loop and thiazide diuretics)
- Shouldn’t be used as mono therapy in the treatment of SHF – they don’t improve prognosis/mortality – they are add-ons to get rid of fluid
- Can be added to other therapy e.g. ACE inhibitors to control signs/symptoms of pulmonary and systemic congestion
- Increase sodium, water, potassium excretion – monitor electrolytes
Beta adrenoceptor antagonists (beta blockers)
- Reduce sympathetic activity on heart
- Reduce cardiac ischaemia + arrhythmias
- Reduce renin release (block of beta 1 receptors on the juxtaglomerular cells of the kidney)
- Apart from beta blockade, some also produce vasodilation – carvedilol, nebivolol
- Start with low dose, increase slowly. Symptoms may worsen to begin with before seeing an improvement
Spironolactone
- Potassium sparing diuretic
- Competitive antagonist of aldosterone
- Increases sodium + water excretion
- Decreases potassium excretion (hyperkalaemia)
- Anti-androgenic activity – can produce gynaecomastia
- Low doses (25mg daily) = beneficial in severe SHF – improves survival
- Not to be used on their own, but as an add on as the HF gets worse
- Combination with ACE inhibitor / A2RA requires extreme caution/monitoring – risk of hyperkalaemia, death
Ivabradine
Ivabradine is a heart-rate-lowering agent that acts by selectively and specifically inhibiting the cardiac pacemaker current (If), a mixed sodium-potassium inward current that controls the spontaneous diastolic depolarization in the sinoatrial (SA) node and hence regulates the heart rate.
Digoxin (particularly if atrial fibrillation)
- MOA: Inhibits the Na+/K+ in the heart (Cardiac cells). Increase of Na+ in the cardiac cells (intracellular Na+) reduces the amount of calcium pumped out of the cell = increases the force of contraction of the heart
- Increases parasympathetic tone on the heart (hence why it causes bradycardia)
- Reduces hospitalisations for pts with heart failure, but doesn’t improve mortality rate. Limited role in heart failure
- May be useful for pts with HF and AF (slows conduction through the AV node and increases the refractory period of the AV node)
- Low therapeutic index – toxicity, death
- Has a long half life
diogixin side effects type a adr
nausea, vomiting, diarrhoea, green/yellow vision, bradycardia, ectopic beats, arrhythmias
- Always check pts HR prior to administration – never give if HR <60 (causes bradycardia)
diogixin side effects type a adr
nausea, vomiting, diarrhoea, green/yellow vision, bradycardia, ectopic beats, arrhythmias
- Always check pts HR prior to administration – never give if HR <60 (causes bradycardia)
