Heart Failure Treatment 1 Flashcards
Define Heart Failure
Pathological state when the heart is unable to pump blood (reduce stroke volume & cardiac output) at a rate that meets the requirements of tissue
Normal conditions = dynamic relationship between
venous capacitance, ventricular preload, CO, afterload, peripheral resistance
Define Acute Hemodynamic Stress
Sharp decrease in blood volume –> decreased cardiac output –> activation of compensatory mechanisms to support the circulation
RAS –> BP and CO
Increased AngII which leads to peripheral resistance and increased sodium and water which allows recovery of BP and CO
SNS –> BP and CO
Increased myocardial contractility and increased heart rate via beta 1
Increased peripheral resistance via alpha 1 and 2
Therapy for HF involves:
Reduction of preload and/or afterload
Enhancement of inotropic state (contraction force)
Vasodilators
ACEi
Direct vasodilators
Positive inotropic drugs
Cardiac glycosides
Adrenergic/dopaminergic receptor agonists
Phosphodiesterase inhibitors
Diuretics in HF work on
Vasoconstriction and sodium/water retention
- Long term effects via: decrease peripheral resistance
Loop Diuretics are
Furosemide
Dumetanide
Torsemide
Loop Diuretics MOA
Inhibit NKCC symporter
Act in the thick ascending limb of loop of Henle
Loop Diuretics Main effects
Profound diuresis (25%) which increases urine flow Increased excretion of Na, Cl, K, Ca and Mg
Loop diuretics Main Adverse Effects
Ototoxicity
Hypokalemia
Hyperglycemia
Thiazide diuretics main representatives
HCTZ (microzide)
Chlorthalidone (Hygroton)
Indapamide (Lozol)
Metolazone (zaroxolyn)
Thiazide diuretics MOA
Act in the distal convoluted tubule (5% of Na reabsorption)
Inhibit Na Cl symporter
Thiazide diuretics effects on urine flow and ion excretion
Moderate increase in urine flow
Increased excretion of Na, Cl and increased excretion of K
Chronic use of thiazide diuretics
Decreased excretion of Ca and uric acid
Thiazide Main Adverse Effects
Hypokalemia
Increased risk of gout
Hyperuricemia
Aldosterone antagonists drugs
Spironolactone and eplerenone
Aldosterone antagonists MOA
Aldosterone (steroid hormone) binds to receptors then are translocated to the nucleus where it binds DNA and stimulates expression of aldosterone induced proteins
ACEi drugs
End in -pril
ACEi MOA
Reduction of Ang II which is involved in vasoconstriction, increased peripheral resistance, decreased sodium and water, slight decrease in aldosterone secretion and decreased sympathetic tone
Alternative MOA of ACEi
Increased bradykin which decreased peripheral resistance via vasodilation and Ang 1-7 which is an antagonists of Ang II and natriuresis
ACEi side effects
Dry cough, angioedema
Direct vasodilators
Nitroglycerin
Nitroprusside (Nipride)
Nesiritide (Natrecor)
Direct vasodilators MOA
Nitropresside and nitroglycerin either breakdown into NO or are NO and stimulate the process
Nitroglycerin
Prodrug metabolized into NO
Infused IV
Selective for venous capacitance vessels (reduction of left ventricular filling pressure)
Limitations of Nitroglycerin
Severe headache
Have to taper off
Development of resistance with chronic use
Long infusion + increased EtOH
Na nitroprusside
Metabolized into cyanide and NO
IV administered
Dilates both arteries and veins so it can reduce ventricular filling pressure and peripheral restance
Na nitroprusside Limitations
Hypotension
Cyanide toxicity
Can cause tissue hypoxia, decreased oxidative metabolism, and liver or renal toxicity
Cyanide toxicity causes
Altered mental status
CV instability
Anion gap metabolic acidosis
Nesiritide
Recombinant brain natiuretic peptide
Causes vasodilation of arteries and veins, nauresis and diuresis
IV administration
Nesiritide Limitations
Hypotension
Expensive
Debatable effectiveness
