CRR

• Heart failure is an inability of the heart to deliver blood and, therefore, oxygen at a rate commensurate with the requirements of the metabolising tissues despite normal or increased cardiac filling pressures.
• The physiological definition of heart failure may be acute or chronic and it may arise as a consequence of myocardial, valvular, pericardial, endocardial, electrical problems or some combination of these.
• Risk factors and outcomes of heart failure include age, some viral infections, congenital heart defects, medical conditions such as valvular heart disease, coronary heart disease, MI, HTN, sleep apnoea, arrhythmias, obesity, smoking, alcohol, and heart failure is commonest in men over 75.
• The prevalence of heart failure is increasing as more survive myocardial infarct.
• An average GP (list size 2000) will see about 20 people with heart failure each year.
• The prognosis of heart failure is worse than for many cancers and it significantly impairs quality of life, leading to depression.
• Preload measures the pressure that drives the blood into the left ventricle, prior to contraction, and depends on the venous pressure and the rate of venous return.
• Preload is a measure of how much blood returns to the heart to pump.
• Excessive preload damages heart muscle.
• Monitor blood pressure, renal function, and potassium when using Sacubitril.
• Patients with signs of sodium and water retention, such as peripheral oedema, pulmonary oedema, or an elevated jugular venous pressure, should receive diuretic therapy.
• Hydralazine/Nitrate combination is used as an alternative first-line treatment or option for second-line treatment for LVSD in Afro-Caribbeans.
• Sacubitril is a pro-drug of LBQ657 which inhibits neprilysin (neutral endopeptidase; NEP), an enzyme that normally degrades peptides such as natriuretic peptides.
• Sacubitril is used for symptomatic chronic heart failure with reduced ejection fraction, NYHA class II to IV, left ventricular ejection fraction of 35% or less, and who are already taking a stable dose of ACE inhibitors or ARBs.
• Breathless patients without these signs probably also get a better symptomatic response to diuretics than any other treatment.
• Nitrates, such as Isosorbide dinitrate, are primarily venodilators with a dose-dependent increase in arterial dilatation.
• Hydralazine is an arteriolar dilator with an uncertain mechanism.
• Loop diuretics should be monitored for declines in renal function, Na, and K.
• Diuretic resistance can be due to poor absorption from the gastrointestinal tract or low glomerular filtration rate.
• Ivabradine blocks IF current in SA pacemaker cells, contributing to depolarisation prior to cardiac action potential, reducing heart rate and so cardiac work.
• Verapamil and diltiazem may be used as monotherapy, reducing heart rate, contractility and afterload.
• Nicorandil is a potassium channel opener and NO donor, dilating arteries and veins (NO), also dilating arterioles.
• Verapamil and Diltiazem may be used with nitrates, but not usually with b-blockers.
• Aortic pressure, obesity, Thyrotoxicosis, anxiety, sympathomimetics, (Preload) are factors that contribute to increased blood pressure.
• Cardioselective calcium entry blockers, like verapamil, reduce heart rate and contractility, with little or no demonstrable effect on veins (preload).
• Nicorandil has been shown to be effective as add on therapy in the IONA Study 2002.
• If a patient does not tolerate nitrates, they are unlikely to tolerate Nicorandil due to its mechanism of action.
• Calcium entry blockers, such as nifedipine and nicardipine, dilate peripheral arteries and arterioles, reducing afterload.
• Nifedipine and nicardipine are less useful as monotherapy because of reflex tachycardia, making them ideal candidates for combination with b-blockers.
• Diltiazem does not cause tachycardia because of its negative chronotropic actions.
• Nicorandil is not suitable if there is LV dysfunction or hypotension.
• Afterload measures the pressure that the heart must overcome to pump blood out into the circulation, ie to open the aortic and pulmonary artery valves, and is largely dependent on aortic pressure.
• The higher the afterload, the less blood the heart can pump.
• Cardiac function curve shows how well the heart can pump blood out through the body.
• Right atrial pressure measures blood returning to the heart (venous return).
• Cardiovascular reserve is the degree to which CVS can perform in the face of circulatory demand and/or afterload or contractility.
• Due to a decrease in the contractility of the left ventricular heart muscle, a failing heart is unable to pump enough blood to meet the body’s demands.
• Increasing Ca 2+ influx can be achieved through b-adrenergic activation or phosphodiesterase inhibition.
• Activation of b1 receptor, leads via Adenylate Cyclase, cAMP to activation of Protein Kinase A.
• Post synaptic beta1 receptors are predominant adrenergic receptors in heart.