This is when the heart is unable to pump blood in sufficient amounts from the ventricles to meet the body's metabolic needs.
Heart failure may be caused by a defect outside of heart such as:
Heart failure can be caused by supraventricular dysrhythmias such as:
These drugs prevent sodium and water resorption by inhibiting aldosterone secretion resulting in diuresis which decreases preload and work of the heart.
These drugs are potent vasodilators. They decrease systemic vaxular resistance (afterload).
This beta blocker can be used for heart failure and has a negative inotropic, chronotropic, dromotropic effect and is used mainly as a vasodilator which causes a decrease in the afterload and blood pressure
This aldosterone antagonist drug used to treat heart failure is potassium-sparing.
This aldosterone antagonist used to treat heart failure is a selective aldosterone blocker.
this heart failure drug was the first drug approved for a specific ethnic group, namely African Americans.
This B-type natiuretic peptide is used in severe, life-threatening heart failure.
This B-type natiuretic peptide works like a human hormone released by ventricles in response to fluid and pressure overload. It reduces preload, after-load, and indirectly increases cardiac output. It helps to excrete Na and water, should only be given IV and hypotension is the most common side effect.
These heart failure drugs work by inhibiting the enzyme phosphodiesterase and results in positive inotropic response and vasodilation.
These drugs are phosphodiesterase inhibitors and are describes as inodilators.
The indication for this type of drug is for short-term management of heart failure. It is given when a patient does not respond to treatment with digoxin, diuretics, and/or vasodilators. AHA and ACC advise against long term infusions.
These drugs are no longer used as a first-line treatment for heart failure. They were originally obtained from the Digitalis plant foxglove and is used to control ventricular response to atrial fibrillation or flutter.
The mechanism of action for these drugs is increased myocardial contractility, change in the electrical conduction properties of the heart by decreasing rate of electrical conduction and prolonging the refractory period between the SA and AV node resulting in reduced heart rate and improved cardiac efficiency.
The effects of these type of drugs have a positive inotropic effect (increased force and velocity of myocardial contraction), negative chronotopic effect (reduced heart rate), and negavie dromotropic effect (decreased automaticity at the SA node, decreased AV node conduction, and other effects.
The effects of these drugs increase stroke volume, reduce heart size during diastole, and decreases in venous BP and vein engorgement. They increase coronary circulation and promote diuresis due to improved blood circulation and helps with nighttime paroxysmal dyspnea, cough, and cyanosis.
This cardiac glycoside has a long half-life and therapeutic concentration may not be achieved for a week or longer. Drug levels must be monitored and it has a very narrow therapeutic window. It is frequently administered by giving a loading dose and then decreasing to a maintenance dose. It is giving PO or IV. Giving IM can be irritating.
Side effects of this drug include bradycardia or tachcardia with toxicity, anorexia, N/V, diarrhea, abdominal cramps, and fatigue. Other effects are headache, lethargy, confusion, changes in vision (yellow-blue or yellow-green halo vision).
Patients with hypokalemia, hepatic dysfunction, hypercalcemia, dysrhythmias, hypothyroid, respiratory or renal disease, use of a pacemaker or advanced age are all predisposed to this cardiac glycoside toxicity.
A patient is on digoxin and has an apical pulse of 59 what should be done?
Treatment for this include holding the drug and calling the physician, checking lab lytes and levels of the drug, possibly giving potassium, treating any GI symptoms and ECG monitoring.
What are some drug interactions of positive intotropic drugs such as digoxin?
When should the physician be called when taking an apical pulse on a patient taking digoxin?
A patient taking digoxin should report a weight gain of how much?
This drug given IV should not be mixed with dextrose and the solution color is true yellow.
This drug also known as an Ino Dilator is used for short term management of CHF.
Thrombocytopenia, dysrhythmia, nausea, hypotension, and elevated liver enzymes with long-term use.
Dysrhythmia (mainly mentricular), hypotension, angina, hypokalemia, tremor, and thrombocytopenia
What plant gives us the oldest and most effective group of drugs for some patients to treat heart failure?
Inside a resting cardiac cell there is what kind of charge that is relative to the outside of the cell.
This energy-requiring pump is needed to maintain the uneven distribution of ions during RMP.
What is used to classify antidysrhythmic drugs that is based on the electrophysiologic effect of particular drugs on the action potential.
These Class I drugs are membrane stabilizers, exert their effect on Na fast channels, slow the rate of conduction and has a negative dromotropic effect.
Class 1A drugs block sodium channels causing a delayed _________ and increase the ________ __________ duration.
This Class 1A drug has a direct action on the electrical activity and an indirect (anticholinergic) effect. This increases the rate of impulse formation and conduction, a significant adverse effect of asystole and PVCs.
Mild overdose of this Class 1A drug can cause tinnitus, hearing loss, blurred vision and GI upset.
This Class 1A drug's anticholinergic effects are weaker and used for atrial fib and VT. Significant adverse effects include lupus-like symptoms.
This Class 1 drug's side effects include anti-cholinergic, i.e. ataxia, dry mouth, tachy, urinary retention. Also dysrhythmia & cardiovascular depression. One should not use with poor LV function,
Class 1B sodium channel blockers act specifically on what? ischemic myocardial issue.
This Class 1B drug is indicated for ventricular dysrythmias only and is the drug of choice for accute dysrythmias associated with an IM.
This Class 1B drug can cause significant CNS toxicity with symptoms presenting as twitching, confusion, seizures, respiratory depression, hypotension, bradycardia, and dyshythmias.
Class 1C drugs block sodium channels but have little or no effect on what?
This drug is used for sustained ventricular tachycardia and has been used for atrial fibrillation at low doses. Its most common side effect is hypotension.
This Class 1C drug is used for life threatening ventricular dysryhthmias and significantly slows conduction in the heart.
This Class II heart drug is ultra short acting and indicated for supraventricular dysrhythmias, is cardioselective, and should only be given IV
This Class III potassium channel blocker is indicated for life threatening ventricular dysrhythmias, has been used for resistant atrial dysrhythmias, has a long half life but may see side effects for months. Its most serious side effect is pulmonary toxicity.
This Class III potassium channel blocker is indicated for atrial fib and flutter.
The action of this class is slow conduction, prolonged refractory period, prolonged repolarizaiton, and inhibition of slow channel pathways.
Verapamil (Calan) and diltiazem (Cardizem) are what class of heart drug?
This is a different kind of antidysrhythmic drug that slows conduction through the AV node and is used to convert supraventricular tachy to normal sinus rhythm. It has an extremely short half life (<10 secs) and is only administered fast IV push. It causes asystole for a few seconds but has minimal adverse effects.
Positive response to antidysrhythmic therapy includes what?
This type of HTN is also known as idiopathic HTN. It describes 90% of all cases of HTN and there is no known cause and is know as the "silent killer".
This type of HTN is caused by some other disease, such as pheochromocyoma, pre-eclampsia, or renal artery disease.
What is the cardiac output from the left ventricle measured against the force the left ventricle has to overcome to eject blood?
What do sympathetic stimulation, atherosclerosis, CHF, and kidney function all have in common?
What is it called when there is an increase in heart rate from the stimulation of beta 1 receptors or an increase in peripheral vascular resistance secondary to alpha 1 receptors?
What creates smaller internal vessel lumen and increases systemic vascular resitance?
According to what entity an increased DBP is no longer considered more dangerous than an increased SBP?
Studies show that an increased SBP is associated with what?
For patients 50 and older increased SBP is greater risk for this than increased DBP?
What type of HTN drug is more effective in African American patients?
What type of drug is used in conjunction with cardiac glycosides and diuretics for treatment of CHF?
When using the beta-blockers nadolol (Corgard) or propranolol (Indural) you should check if the patient has what disease before administering?
Atenolol (Tenormin), metoprolol (Lopressor), bisoprolol (Zebeta), and nebirolol (Bystolic) are beta-blockers that are also what?
What dual action alpha-1 and beta receptor blocker is indicated for reflex tachycardia/bradycardia occurrence, has a 1st pass effect.
What dual action alpha-1/beta receptor blocker should never be used in a patient that has asthma or COPD?
What type of drug has side effects of URI, insomnia, diarrhea, dyspnea, heartburn, nasal congestion, back pain, and hyperkalemia?
What HTN drug is a treatment for angina, migraine, dysrhythmia, and Reynaud's disease?
What are two calcium channel blockers slowly decrease heart rate?
Adverse reactions of this type of HTN drug may include rash, flushing, peripheral edema, and dermatitis.
What type of HTN drug decreases plasma and extracellular fluid volumes resulting in decreased preload, cardiac output and total peripheral resistance?
What type of HTN drug directly relaxes arteriole and/or venous smooth muscle resulting in decreased systemic vascular response, decreased afterload, and peripheral vasodilation?
What two vasodilators are used for acute HTN emergency?
What vasodilator should shows rapid results in about 2 minures, has a short half life should only be given in a bag covered IV due to light sensitivity?
What should levels should be monitored when giving a patient sodium nitroprusside for an extended period of time?
This happens when the supply of O2 and nutrients in the blood is insufficient to meet the demands place upon it.
What causes arteries to calcify causing increased O2 demand secondary to the arteries lack of dilation?
Tissue becomes ischemic due to lack of O2 secondary to CAD. This can build up in the tissues due to metabolism being converted to anaerobic.
When heart has poor blood supply due to atherosclerosis, CAD or myocardial infarction it becomes what and can cause necrosis or death to tissue becoming fatal.
This type of angina is known as "classic" or "effert" angina. It can be predictable as it is sometimes brought on by things such as caffeine or exercise.
This type of angina is known as "preinfarction" or "crescendo" angina and is less predictable than chronic stable angina and may be a warning of an impending heart attack.
This type of angina is also known as "Prinzmetal" or "variant" angina and is due to spasms of the coronary artery.
What drugs work by increasing O2 supply to the myocardium and decrease O2 demand overall?
What antiangina drugs relax smooth muscle of blood vessels, dilate peripheral arteries and veins, decrease preload and O2 demand, and alleviate coronary artery spasms?
This is the prototypical nitrate, has a large 1st pass effect with oral forms, is used for symptomatic treatment of ischemic heart conditions and is used sublingual for acute attacks.
These meds are used for the acute relief of angina and as a prophylaxis in situations that may produce angina.
This antianginal nitrate when used IV should never be mixed with other drugs, should be given IV push from a glass bottle (due to its absorption into plastic bottles) and with a paper bag to cover the bottle due to its photosensitivity.
This antianginal nitrate when used IV should not be used with a filter and should be administered with non-pcp tubing due to its absorption of plastics.
What should a nurse advise a patient to do at the first sign of anginal pain?
A patient has had an anginal attack and has taken a sublingual dose of nitroglycerin. What is the next thing they should do?
If there is no relief with one dose of nitroglycerin when should a nurse direct a patient to take a second dose?
Why should a nurse advise a male patient to keep their nitroglycerin in their shirt pocket and not their pants?
What should a nurse advise a patient in when staring a nitroglycerin patch?
To decrease tolerance to nitroglycerin patches a nurse should instruct her patient to do what?
When administering a nitroglycerin patch to a patient what should a nurse always do?
Beta-blocking drugs such as atenolol (Tenormin), metoprolol (Lopressor), and nadalol (Corgard)that are used for angina are more reliable and consistent in this type of patient?
Anticholinergics, antihypertensives and phenothiazines should not be used with this type of antianginal medication?
Calcium channel blockers are indicated for angina because of this behavior?
Calcium channel blockers are 1st line drug for treatment of angina, HTN, and what?
Calcium channel blockers are used for short-term management of what?
What calcium channel blocker is used for angina, vasospastic and chronic stable angina, HTN, and atrial dysrhythmias/
What calcium channel blocker was once administered by the unapproved method of "squeezing under the tongue"?
This calcium channel blocker is used to treat angina, HTN, and PSVT (paroxsysmal supraventricular tachycardia).
A nurse should advise a patient taking amlodipine ((Norvasc) to avoid drinking this citrus beverage due to its ability to decrease the metabolism of the drug?