Flashcards in Heart Failure Deck (40)
Factors affecting SV
contractility, filling pressure (preload) and peripheral resistance (afterload)
Definition of heart failure
inability of the heart to pump sufficient blood to meet the metabolic demands of the body. Decreased mechanical efficiency (decreased contractility)
A decrease in stroke volume will have what effect on the heart?
Leads to dilation (increased vent V) and hypertrophy (increased ventricular mass). Helps increases stroke volume
What is the flow of heart failure? Heart failure leds to a decreased CO which leads to....
an increase in sympathetic NS which leads to an increase in HR, preload, afterload and Ang II. The last three lead to an increase in blood V.
What is maladaptive remodeling?
alteration in dimension/shape in response to hemodynamic stress/injury in association with neurohormonal activation. (myocyte hypertrophy and apoptosis, fibroblast proliferation and oxidative stress)
What factors lead to maladaptive remodeling? (specifically)
Ang II, catecholamines, aldosterone, cytokines, ect.
What part of the heart failure flow does inotropi agents effect?
What inotropic agent do we need to know?
Digoxin (a cardiac glycoside), Dobutamine, Milrinone
What effect does Digoxin have on the heart?
increased contractility which leads to an increased stroke V. Decreases HR by an increase in vagal tone and slowing of AV conduction
What is the mechanism of Digoxin?
inhibits the Na-K-ATPase, increases intracellular Ca
What is the negative side to Digoxin?
A long half life (36 hours) and a low therapeutic index
What are the toxicities of cardiac glycosides?
N&V, diarrhea, visual changes.
arrhythmias (bradycardia, AV block, ventricular premature beats/tachycardia)
What kind of drug is dobutamine?
A dopamine derivative inotropic agent
What is dobutamine's mechanism?
beta (low dose) and alpha (high dose) agonist
What is dobutamine's mechanism?
Increases contractility which increases CO.
Causes tachycardia, but less so then isopropterenol.
When would you use docutamine? What is its effect on martaility of HF?
As a short term cardiac supper (IV only), pts will develop a tolerance to it.
It is proarrhythmic.
Only txs the side effects, doesn't effect mortaility of HF.
What is the mechanism of Milrinone?
It is a phosphodiesterase inhibitor. PDE inactivates cAMP so by inhibiting PDE it increases cAMP.
What effect does Milrinone have?
It increases contractility, SV and decreases afterload (vasodilation)
What are the limitations of Milrinone?
hypotesion, proarrhythmia, doesn't effect mortality of HF
What are the classes of neurohormonal modulators that we need to know?
Ang II modifiers, beta blockers, aldosterone antagonists and vasodilators.
What are the three Ang II modifiers and what class of drug do they belong?
Captopril and Enalapril (ACE inhibitors) and Losartan (ANG II receptor blockers).
What are the mechanisms for Ang II modifiers?
1. decrease afterload (vasodilation) increases SV
2. venodilation leads to a decreased preload which leads to a in congestion
3. a decrease in aldosterone leads to a decrease in blood volume
4. slows progression of hypertrophy/remodeling
What effect does ANG II modifiers have on the mortality of HF?
they decrease it because they slow the progression of hypertrophy and remodeling.
What are the adverse effects of Ang II modifiers (2 for the group, 2 for ACE inhibitors specifically)
Hypotension (1st dose, salt depleted), fetopathic potential (renal toxicity).
ACE inhibitor: cough and angioedema
What beta blockers do we need to know for HF?
metoprolol (beta 1 selective)
Carvedilol (beta-nonselective, alpha-1-antigonist)
How do beta blockers need to be dosed in acute situations?
Need to be given in low doses because they will lower HR and ejection fraction.
What is the chronic effect of beta blockers?
Gradual increase in the dose will eventually lead to an increased EF.
What is the antiarrhythmic effect of beta blockers?
blockade of toxic catecholamine effects
What effect does beta blockers have on the mortality of HF?
Slows the progression of vent hypertrophy/remodeling. Decreases mortality.
What are the limitations and adverse effects of betablockers?
asthma (nonselective blockers/bronchospasm) and diabetes (prolongation of hypoglycemia).
Bradycardia (SA and AV nodal) and insomnia/nightmares.
What aldosterone antagonist do we need to know?
What is the mechanism of spironolactone?
blocks minneralcorticoid receptor, deceases Na and water reabsorption, decrease K excretion, reduces sympathetic tone, decrease LV remodeling, increases EF, decreases apoptosis and fibrosis. Maybe reduces mortality.
What are the limitations of spironolactone?
hyperkalemia and male impotence.
What vasodilators do we need to know for HF?
nitroglycerin and hydralazine
What is the mechanism of nitro?
it dilates veins > arterioles (NO).
What effect does nitro have?
decreases preload and thus decreases filling pressure and congestion.
What is the limitation of vasodilators?
What is the mechanism of Hydralazine?
dilator of arterioles > veins (NO)
What effect does hydralazine have?
decreases TPR = decrease in afterload = increase in SV