Cardiac Pharmacology Barry
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| Preload determines how well the pump is primed. Directly related to... | Tension developed in the ventricle.
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| Filling pressure of the ventricles at the end of diastole. | Preload.
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| Right ventricular end-diastolic volume is the product of... | Systemic venous return.
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| Left ventricular end-diastolic volume is the product of... | Pulmonary circulation entering the left side of the heart.
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| Frank Starling Principle: | Increased myocardial fiber length (preload) improves contractility up to a point of ultimate decompensation.
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| Preload can be measured by... | CVP (RVEDP) and LAP or indirect PCWP (LVEDP).
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| Impedence to left ventricular outflow. | Afterload.
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| Afterload formula: | MAP-RAP divided by CO X 80 (800-1200 dynes/sec/cm5)
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| Afterload can be altered with drugs that... | Dilate or constrict vascular beds- mostly arterial vessels.
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| Arterial vasodilators decrease resistance to ventricular contraction but can decrease... | Preload.
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| Clinical indicator for right ventricular afterload is... | Pulmonary vascular resistance (37-200 dynes/sec/cm5)
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| Left ventricular afterload is measured as... | SVR. (peripheral vascular resistance)
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| Force of ventricular contraction and is defined as the... | Inotropic state of the heart.
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| Factors that influence contractility: | -Appropriate amts of K+, Na+, and Ca++
-SNS via beta 1 receptors stimulation (increased contractility, HR, ventricular automaticity, and myocardial O2 consumption
-Increased levels of cAMP
-Preload and afterload
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| What is cAMP? | Cyclic adenosine monophosphate
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| CO is the volume of blood that the heart ejects each minute. What are normal values? | Normal 4-8L/min
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| Formula for CI: | CO divided by BSA (2.5-4.0 L/min).
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| 3 primary factors that determine CO: | -Preload
-Afterload
-Contractility
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| Myocardial oxygen supply is determined by: | Oxygen content of arterial blood and coronary perfusion.
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| How is coronary perfusion influenced by heartrate? | Slower heartrate increases diastolic time thus allowing for increased coronary perfusion.
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| Coronary perfusion pressure is determined by... | Diastolic pressure.
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| Coronary blood flow is regulated by... | Coronary vascular tone.
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| Myocardial O2 demand is influenced by... | Preload, afterload, inotrophy and heartrate.
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| Myocardial O2 demand is increased by... | Increase in preload (increase in ventricular diameter) and increase in inotrophy.
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| Myocardial O2 demand is decreased by... | Decrease in afterload and HR.
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| The neurotransmitter responsible for most adrenergic activity of the sympathetic nervous system. | Norepinephrine.
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| Norepinephrine is released by... | Postgangionic sympathetic fibers at end organ tissues.
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| Action of Norepinephrine is terminated by... | Reuptake into the postganglionic nerve ending.
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| Adrenergic receptors are divided into... | Alpha and beta receptors.
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| Four things about alpha 1 receptors: | 1. Located in smooth muscle throughout the body.
2. Most important cardiovascular effect of alpha 1 stimulation is vasoconstriction.
3. Increased peripherial vascular resistance.
4. Increase in arterial blood pressure.
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| Three things about alpha 2 receptors: | 1. Located chiefly on the presynaptic nerve terminals.
2. Stimulation creates a neg. feedback loop that inhibits further norepi release. Decreases vasoconstriction
3. Blockage of Alpha 2 receptors causes a enhanced release of NE from nerve endings
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| Three things about beta 1 receptors: | 1. Most important Beta 1 receptors on post synaptic membranes in the heart.
2. Stimulation activates adenylyl cyclase, which converts ATP to cAMP(cyclic adenosine monophosphate)
3. Increases HR, conduction and contractililty.
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| Two things about beta 2 receptors: | 1. Located on post synaptic receptors in smooth muscle and gland cells.
2. Stimulation relaxes smooth muscle, resulting in bronchodilation, vasodilatation, and relaxation of uterus, bladder and gut.
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| Alpha nonspecific agonist drugs: | Epi and NE.
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| Specific alpha 1 agonist: | Phenylephrine
Methoxamine (Vasoxyl) 3-5mg IV push 1mg/min onset: 1 min duration 1 hr.
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| Alpha 2 agonist selective: | Clonidine
Dexmedetomidine (Precedex) Bolus 1ug/kg over 10 min. GTT 200ug/50ml @ 0.2-0.7 ug/kg/hr.
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| Alpha antagonist nonspecific: | Phentolamine (Regitine)
Phenoxybenzamine (Dibenzyline)
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| Alpha 1 antagonist (blocker) selective: | Prazosin (Minipress)
Cardura (Doxazosin)
Hytrin (Terazosin)
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| Alpha 2 antagonist (blocker) selective: | Yohimbine
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| What do catecholamines do? | Stimulate adrenergic receptors.
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| Endogenous catecholamines are: | Dopamine, norepinephrine, and epinephrine.
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| Non-endogenous catecholamines are: | Isoproterenol and dobutamine.
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| Dopamine directly stimulates... | Dopamine, beta and alpha receptors.
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| What makes dopamine unique? | It stimulates dopamine (dopaminergic) receptors and increases renal blood flow and diuresis.
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| Effects of dopamine at different doses: | - Beta + alpha effects occur at 10-20ug/kg/min
- Predominate alpha effects at 20u/kg/min and higher.
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| Three things about dopamine: | 1. High doses can inhibit insulin and cause hyperglycemia
2. Rapid metabolism
3. Extravasation can cause intense vasoconstriction- Phentolamine
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| Norepinephrine is an endogenous neurotransmitter for... | Alpha and beta receptors.
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| NE causes vasoconstriction which | Increases systemic vascular resistance.
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| NE receptor action: | - Beta 1 agonist effects are overshadowed by the alpha 1 effects
- Reflex bradycardia high doses
- Decreased renal blood flow
- Beta 2 effects are minimal
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| Epinephrine stimulates Alpha 1, Beta 1 and Beta 2 receptors, and increases perfusion in... | Heart and brain.
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| Epinephrine stimulation of alpha 1 receptors in the skin, mucosa, and hepatorenal vasculature causes... | vasoconstriction and decreased flow.
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| How does Epinephrine cause vasoconstriction and decreased flow? | Stimulation of alpha 1 receptors in skin, mucosa, and hepatorenal vasculature.
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| Beta 1 and beta 2 effects of epinephrine: | - Beta 1 stimulation causes increase in heartrate
- Beta 2 stimulation causes vasodilation in skeletal muscles and bronchial smooth muscle
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| What is the principal pharmacologic treatment for anaphylaxis and ventricular fibrillation? | Epinephrine.
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| What are some complications of Epinephrine? | Include cerebral hemorrhage, coronary ischemia, and ventricular arrhythmias. Halothane and potentate the dysrhythmic effects of epi.
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| Isoproterenol is a synthetic catecholamine with what effects? | Pure beta agonist with potent Beta 1 and Beta 2 effects.
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| Isoproterenol increases what? | Heartrate, myocardial contractility, systolic blood pressure.
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| What alpha effects of Isoproterenol? | No alpha effects.
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| Secondary to Isoproterenol, excessive tachycardia and decreased diastolic pressure may decrease... | Coronary blood flow.
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| Isoproterenol has high incidence of what bad thing? | Cardiac dysrhythmias.
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| Dobutamine is a synthetic catecholamine with structural charateristics of... | Dopamine and Isoproterenol.
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| Four things about Dobutamine: | 1. Acts on beta 1 receptors (selective beta 1 agonist)
2. Increases cardiac contractility (inotrophic effects)
3. Does not cause indirect release of norepinepherine
4. Decreases SVR (beta 2 agonist)
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| How are symphatomimetics classified? | Classified as direct-acting (mimic the effects of norepinephrine) or indirect-acting (evoke the release of endogenous norepinephrine)
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| Phenylephrine mimics the effects of NE and is a... | Direct acting alpha 1 agonist.
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| Five things about Phenylephrine: | 1. Primary effect is perph vasoconstriction
2. Increases systemic vascular resistance
3. No beta effects
4. Reflex bradycardia
5. Decreases renal blood flow
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| What is Ephedrine's primary mode of action? | Indirect acting sympathomimetic. Increases blood pressure by stimulating release of norepinephrine.
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| What is Ephedrine's secondary mode of action? | Direct acting (Directly stimulates postsymaptic adrenergic receptors)
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| Ephedrine's cardiovascular effects are similar to those of epinephrine: | Increases systolic and diastolic blood pressure, heartrate, and cardiac output.
Increased cardiac contractility and heartrate secondary to beta 1 receptor stimulation.
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| Three things about Ephedrine: | 1. Bronchodilator
2. Does not decrease uterine blood flow like direct acting alpha1 agonists
3. Subsequent doses are increased secondary to depletion of norepinephrine.
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| What is Clonidine (Catapress)? | Alpha 2 agonist.
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| What does Clonidine do? | - Decreases outflow of the sympathetic nervous system
- Decreases CO, SVR and BP
- Sedative and analgesic effects decrease anesthesia requirements
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| Where in the body does Clonidine act? | Central acting- acts on alpha 2 receptors located in the dorsal horn of the spinal cord.
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| Three things about Clonidine: | 1.Effective in suppressing the signs and symptoms of withdrawal from opioids
2. Lowers plasma catecholamine levels
3. Adverse effect is rebound hypertension when abruptly discontinued
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| What is Phentolamine (Regitine)? | Alpha antagonist.
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| What is Phentolamine (Regitine) used for? | - Smooth muscle relaxation
- Decrease BP (alpha 1) with reflex tachycardia (alpha 2)
- Extravasation of a alpha agonist 5-10mg locally infiltrated
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| What is Phenoxybenzamine? | Non-selective alpha blocker.
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| Phenoxybenzamine blockage at alpha 1 vs alpha 2: | Blockage at Alpha 1 is greater than Alpha 2.
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| Why do we use Phenoxybenzamine? | Used mostly for chronic control of pts with pheochromacytoma or Raynaud’s. It overcomes vasoconstriction.
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| What is Yohimbine and what does it do? | Selective Alpha 2 antagonist.
Leads to enhanced release of NE from nerve ending.
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| What is Prazosin (Minipress)? | Alpha 1 receptor antagonist.
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| What does Prazosin (Minipress) do? | - Dilates both arterioles and veins
- Decreases SVR and Preload
- Virtually no tachycardia secondary to no alpha 2 antagonistic effects.
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| Sodium Nitroprusside relazes both arterial and venous vessels. How? | Forms nitric oxide- A naturally occurring potent vasodilator released by endothelial cells.
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| When do we use inhaled Nitric Oxide? | In pulmonary hypertension.
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| Describe the process of metabolism from Sodium Nitroprusside to Cyanide: | Nipride enters red blood cells and receives an electron from the iron of oxyhemoglobin (Fe 2+). This electron transfer results in an unstable nitroprusside radical and methemoglobin (Fe 3+). Nitroprusside radicals decompose into cyanide ions.
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| Cyanide ions can be involved in one of three possible reactions. Most important: | Cyanide ions bind to tissue cytochrome oxidase which interferes with normal oxygen utilization.
Prevents O2 from being released from tissues.
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| S/s of acute cyanide toxicity: | - Acute resistance
- Metabolic acidosis
- Cardiac dysrhythmias
- Increased mixed venous O2 (secondary to inability to metabolize O2)
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| Treatment for acute cyanide toxicity: | - Mechanically ventilate with 100% O2
- Sodium Thiosulfate 150mg/kg over 15 min
- Thiosulfate converts cyanide to thiocyanate
- Thiocyanate is cleared via the kidneys.
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| NTG relaxes smooth muscle similarly in mechanism to Nipride. Arteral vs venous? | Venous dilatation predominates over arterial dilatation.
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| Four things NTG is used for? | 1. Relieves myocardial ischemia and spasm
2. Hypertension
3. Ventricular failure
4. Decreases preload
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| Nitroglycerine undergoes rapid reduction hydrolysis in the liver and blood. Dangerous potential metabolite/treatment? | - One metabolic product is nitrate, which can convert hemoglobin (Fe2+) to methemoglobin (Fe 3+)
- Methemoglobinemia is rare
- Methylene blue 1-2mg/kg over 5 minutes.
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| Hydralazine interferes with calcium utilization and is used for intraop hypertension. What does it do? | - Relaxes arteriolar smooth muscle
- Decreases systemic vascular resistance
- Decreases BP
- Increases HR and CO
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| What is Trimethaphan/Arfonad? | Ganglionic blocker (Blocks sympathetic and parasympathetic receptors).
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| What does Trimethaphan/Arfonad do? | - Directly vasodilates perph vasculature
- Causes arterial dilation and venodilation
- Can trigger Histamine release (avoid in asthmatics)
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| What is Trimethaphan/Arfonad used for? | Used to control autonomic hyperrflexia (syndrome with massive sympathetic discharge in patients with upper spinal cord injuries).
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| Possible metabolism of Trimethaphan/Arfonad? | Possibly by plasma cholinesterase.
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| What do beta blockers do? | Block the effects of catecholamines on heart and lungs.
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| Is Inderal/ Propranolol selective or nonselective? | Nonselective.
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| Actions of Inderal/Propranolol? | - Decreases HR, CO, greater Beta 1 effects
- Decreases spontaneous SA node firing
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| Uses of Inderal/Propranolol? | - Afib/Aflutter/SVT
- Angina (decreases Myocardial O2 requirements by decreasing HR and CO)
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| Potential negative SE of Inderal/Propranolol? | Bronchospasm.
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| Three things about Timolol/Blocadren: | - Mostly used to decrease IOP by decreasing formation of aqueous humor
- Non-selective beta blocker
- Used in the treatment of glaucoma
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| What is Metoprolol/Lopressor? | Selective beta 1 antagonist.
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| Action/uses of Metoprolol/Lopressor? | - Action: Decreases HR and CO
- Uses: Afib/ Aflutter, HTN, SVT
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| What is Esmolol? What does it do? | Selective beta 1 antagonist. Decreases HR and CO.
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| Metabolism of Esmolol: | Hydrolysis by RBC’s and plasma esterases to inactive metabolites. Half life 9 minutes.
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| What is Atenolol/Tenormin? Why do we use it? | Beta 1 selective antagonist. Use: Mostly PO for HTN – long acting.
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| What do beta agonists do? Why do we use them? | Relax bronchiole and uterine smooth muscles. Used to treat bronchospasm and to stop uterine contraction.
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| Three examples of beta agonists: | Terbutaline, Albuterol, Ritodrine.
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| What is Labetolol/Trandate? | Mixed alpha and beta antagonist. Blocks alpha 1 and beta 1 and 2.
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| Labetolol/Trandate decreases BP with no reflex decrease in HR. Ratio of alpha to beta action? | 1:7
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| How do calcium channel blockers work? | Selectively interfere with inward Ca ion movement across cell membranes.
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| What do calcium channel blockers do? | Decrease contractility, HR, conduction thru the AV node. Cause small muscle relaxation and vasodilation.
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| When do we use calcium channel blockers? | HTN, SVT, Coronary artery spasm, angina and cerebral artery vasospasm.
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| Verapamil is a calcium channel blocker. What is it derived from? | Papaverine.
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| What is Verapamil used for? What does it do? | Depresses transmission of impulses via SA node and AV node
Uses: SVT, Afib, Aflutter, chronic HTN
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| Use Verapamil with caution in patients who are... | Beta blocked.
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| For what cardiac condition is Verapamil contraindicated? Why? | Do not use in WPW. Inhibits intrinsic conduction pathway.
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| Diltiazem is a calcium channel blocker. What does it do and why is it used? | Selective coronary vasodilation.
Uses: Angina, HTN, SVT, Afib, Aflutter.
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| Nifedipine(Procardia) is a calcium channel blocker. What does it do and how is it used? | Coronary and peripherial arterial vasodilation.
Uses: HTN, angina, coronary vasospasm
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| Nicardipine(Cardine) is a calcium channel blocker. What does it do and how is it used? | Vasodilator. Uses: HTN, myocardial ischemia.
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| Nimodipine is a calcium channel blocker. What does it do and how is it used? | Enters CNS and may block influx of CA. Decreases cerebral artery vasospasm. Cerebral vasospasm can occur 4-14 days after a subarachnoid hemorrhage.
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| What do ACE inhibitors do? | Blocks the conversion of angiotension I to angiotension II in the lungs. Prevents angiotension II mediated vasoconstriction.
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| What do we use ACE inhibitors for? What's a potential SE? | Uses: HTN, CRI, Chronic heart failure.
Allergic rxn: Chronic cough.
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| What are ARB agents? What are they used for? | Prevents angiotension II from binding to receptor sites.
Used in pts with CHF, HTN, Diabetic neuropathy, CHF, pts who are intolerant of ACE inhibitors.
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