Treatment of Heart Failure Flashcards
What are the different stages of heart failure treatment?
- treat risk factors -
- ACE- i and beta blockers- in selected patinets
- ACE-i, Beta blockers and diuretics
- palliative therapy, mechanical assistance device, heart transplant
Describe the terms wet/dry and cold/warm as it relates to heart failure
volume overload = wet/dry
Low output = cold/warm
how do ACE inhibitors work?
they decrease afterload by interfering with the renin-angiotensin-aldosterone system - resulting in peripheral vasodilation.
They also affect left ventriculer hypertrophy, remodeling and renal blood flow
specifically: ACE-inhibitors competitively block the converting enzyme that transforms angiotensin I into angiotensin II. The reduction in angiotensin II levels explains its arteriovenous vasodilatory actions, as angiotensin II is a potent vasoconstrictor that augments sympathetic tone in the arteriovenous system. Additionally, angiotensin causes vasopressin release and produces sodium and water retention, both through a direct renal effect and through the liberation of aldosterone. Since converting enzyme has a similar structure to kinase II that degrades bradykinin, ACE-inhibitors increase kinin levels that are potent vasodilators (E2 and F2) and increase release of fibrinolytic substances such as tPA.
What is the effect of heart failure on the RAAS axis?
aldosterone production by the adrenal glands is increased in heart failure to stimulate renal sodium retention and potassium excretion - promoting ventricular and vascular hypertrophy
aldosterone antagonists counteract the many effects of aldosterone. Diuretics decrease preload by stimulating natriuresis in the kidneys
How does Digoxin work?
it effects the Na+/K+ ATPase pump in the myocardial cell increasing contractility -
specifically:
Digoxin attaches to specific receptors which form a part of the enzyme,
Na+/K+-dependent ATP-ase(sodium pump), inhibiting it. This blockade produces a progressive increase in the intracellular concentration of Na, which in turn activates the exchange of Na+-Ca++and increases the influx of Ca++and its intracellular concentration, [Ca++]i. This increase in the [Ca++]iat the level of the contractile proteins explains the resultant increase in cardiac contractility.
How do Beta blockers work?
inhibit the sympathetic nervous system and adrenergic receptors - slowing the heart rate, decreasing blood pressure and have a direct benefit on the myocardium enhancing reverse remodeling.
How does Nesiritide (brain natriuretic peptide) work?
deccreases preload by stimulating diuresis and decreases afterload by vasodilation
What is the objective when treating heart failure?
- increase survival
- decrease morbidity
- increase exercise capacity
- increase quality of life
- decrease progression of disease and symptoms related
what are the 3D’s in the treatment of heart failure?
Diet
Drugs
Devices/surgery
what are some precipitants in the diet of heart failure?
- alcohol
- nicotine
- other drugs of abuse
- salt
- fluid intake
- stress
Why do diuretics make patients with heart failure feel so much better?
They control symptoms secondary to fluid retnetion
- paroxysmal nocturnal dyspnoea
- orthopnea
- ascites
- peripheral oedema
*they don’t make you live longer, but they inmprove quality of life*
How do thiazide diuretics work?
inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle
how do K-sparing diuretics work?
They inhibit reabsorption of Na in the distal convoluted and collecting tubules
How do Loop diuretics work?
inhibit exchange of Cl-Na-K in the thick ascending loop of henle
what are some adverse effects of loop diuretics?
could potentially decrease potassium to a level below that which is needed for normal cardiac function = sudden death
otherwise
- hyperuricemia
- hypotension
- Ototoxicity
In what ways do we see diuretic resistance?
- neurohormonal activation
- rebound Na+ uptake after volume loss
- hypertrophy of distal nephron
- reduced tubular secretion
- decreased renal perfusion
- altered absorption of diuretic
- noncompliance with drugs
what do ACE inhibitor drug names end with?
“pril”
ex) captopril, enalapril, lisinopril etc
Why are ACE inhibitors so important?
constitute the cornerstone of drug therapy for heart failure, in that administration over time leads to amelioration of symptoms, beneficial hemodynamic changes, increased functional capacity, regression of structural changes, and, unequivocally, prolongation of survival.
what are some contraindications of ACE inhibitors?
bilateral renal artery stenosis
pregnancy
renal insufficiency
hyperkalemia
severe hypotension
How do angiotensin 2 receptor blockers work?
There are two types of tissue receptors for angiotensin: AT1 and AT2. Stimulation of AT1 receptors has a proliferative and vasoconstrictor effect, while stimulation of
AT2 receptors has the opposite effects, that is, vasodilatory and antiproliferative. In the treatment of heart failure, specific blockade of the AT1 receptors is desirable. Drugs which create a selective and competitive block of the AT1 receptors include:losartan, valsartan, irbersartanand candersartan.
what do angiotensin 2 receptor blocker drug names end with?
They end with “sartan”
ex) Valsartan, irbersartan, and candersartan
Are beta blockers useful?
Yes, they reduce mortality by 30% across all classes of heart failure except the final stages
what do beta blocker drug names end with?
They end with “prolol”
ex) bisoprolol, metoprolol, etc
how do aldosterone inhibitors work?
Aldosterone acts directly on specific receptors. At the renal level it produces retention of sodium and water, resulting in an increase in preload and afterload, edema formation and the appearance of symptoms of pulmonary and systemic venous congestion. In addition, it increases the elimination of potassium and magnesium, creating an electrolyte imbalance which may be responsible in part for cardiac arrhythmias. At the tissue level, aldosterone stimulates the production of collagen, being in large part responsible for the fibrosis that is found in hypertrophied myocardium and in the arterial walls of patients with
heart failure. The beneficial effects of aldosterone inhibitors derive from the direct and competitive blockade of specific aldosterone receptors. Aldosterone inhibitors therefore have three types of effects:
- Diuretic effect, which is most noticeable when fluid retention and increased levels of aldosterone are present.
- Antiarrhythmic effect, mediated by the correction of hypokalemia and hypomagnesemia.
- Antifibrotic effect. This effect, demonstrated in animal models, can contribute to a decrease in the progression of structural changes in patients with heart failure.
What sort of surgery/devices can we give patients with heart failure
CABG or angioplasty in selected cases
valve surgery when that is the problem
left ventricular reconstruction (only in ischaemic cardiomyopathy)
cardiac transplantation
