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Cardiac Pharm Barry

Cardiac Pharmacology Barry

QuestionAnswer
Preload determines how well the pump is primed. Directly related to... Tension developed in the ventricle.
Filling pressure of the ventricles at the end of diastole. Preload.
Right ventricular end-diastolic volume is the product of... Systemic venous return.
Left ventricular end-diastolic volume is the product of... Pulmonary circulation entering the left side of the heart.
Frank Starling Principle: Increased myocardial fiber length (preload) improves contractility up to a point of ultimate decompensation.
Preload can be measured by... CVP (RVEDP) and LAP or indirect PCWP (LVEDP).
Impedence to left ventricular outflow. Afterload.
Afterload formula: MAP-RAP divided by CO X 80 (800-1200 dynes/sec/cm5)
Afterload can be altered with drugs that... Dilate or constrict vascular beds- mostly arterial vessels.
Arterial vasodilators decrease resistance to ventricular contraction but can decrease... Preload.
Clinical indicator for right ventricular afterload is... Pulmonary vascular resistance (37-200 dynes/sec/cm5)
Left ventricular afterload is measured as... SVR. (peripheral vascular resistance)
Force of ventricular contraction and is defined as the... Inotropic state of the heart.
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
What is cAMP? Cyclic adenosine monophosphate
CO is the volume of blood that the heart ejects each minute. What are normal values? Normal 4-8L/min
Formula for CI: CO divided by BSA (2.5-4.0 L/min).
3 primary factors that determine CO: -Preload -Afterload -Contractility
Myocardial oxygen supply is determined by: Oxygen content of arterial blood and coronary perfusion.
How is coronary perfusion influenced by heartrate? Slower heartrate increases diastolic time thus allowing for increased coronary perfusion.
Coronary perfusion pressure is determined by... Diastolic pressure.
Coronary blood flow is regulated by... Coronary vascular tone.
Myocardial O2 demand is influenced by... Preload, afterload, inotrophy and heartrate.
Myocardial O2 demand is increased by... Increase in preload (increase in ventricular diameter) and increase in inotrophy.
Myocardial O2 demand is decreased by... Decrease in afterload and HR.
The neurotransmitter responsible for most adrenergic activity of the sympathetic nervous system. Norepinephrine.
Norepinephrine is released by... Postgangionic sympathetic fibers at end organ tissues.
Action of Norepinephrine is terminated by... Reuptake into the postganglionic nerve ending.
Adrenergic receptors are divided into... Alpha and beta receptors.
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.
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
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.
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.
Alpha nonspecific agonist drugs: Epi and NE.
Specific alpha 1 agonist: Phenylephrine Methoxamine (Vasoxyl) 3-5mg IV push 1mg/min onset: 1 min duration 1 hr.
Alpha 2 agonist selective: Clonidine Dexmedetomidine (Precedex) Bolus 1ug/kg over 10 min. GTT 200ug/50ml @ 0.2-0.7 ug/kg/hr.
Alpha antagonist nonspecific: Phentolamine (Regitine) Phenoxybenzamine (Dibenzyline)
Alpha 1 antagonist (blocker) selective: Prazosin (Minipress) Cardura (Doxazosin) Hytrin (Terazosin)
Alpha 2 antagonist (blocker) selective: Yohimbine
What do catecholamines do? Stimulate adrenergic receptors.
Endogenous catecholamines are: Dopamine, norepinephrine, and epinephrine.
Non-endogenous catecholamines are: Isoproterenol and dobutamine.
Dopamine directly stimulates... Dopamine, beta and alpha receptors.
What makes dopamine unique? It stimulates dopamine (dopaminergic) receptors and increases renal blood flow and diuresis.
Effects of dopamine at different doses: - Beta + alpha effects occur at 10-20ug/kg/min - Predominate alpha effects at 20u/kg/min and higher.
Three things about dopamine: 1. High doses can inhibit insulin and cause hyperglycemia 2. Rapid metabolism 3. Extravasation can cause intense vasoconstriction- Phentolamine
Norepinephrine is an endogenous neurotransmitter for... Alpha and beta receptors.
NE causes vasoconstriction which Increases systemic vascular resistance.
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
Epinephrine stimulates Alpha 1, Beta 1 and Beta 2 receptors, and increases perfusion in... Heart and brain.
Epinephrine stimulation of alpha 1 receptors in the skin, mucosa, and hepatorenal vasculature causes... vasoconstriction and decreased flow.
How does Epinephrine cause vasoconstriction and decreased flow? Stimulation of alpha 1 receptors in skin, mucosa, and hepatorenal vasculature.
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
What is the principal pharmacologic treatment for anaphylaxis and ventricular fibrillation? Epinephrine.
What are some complications of Epinephrine? Include cerebral hemorrhage, coronary ischemia, and ventricular arrhythmias. Halothane and potentate the dysrhythmic effects of epi.
Isoproterenol is a synthetic catecholamine with what effects? Pure beta agonist with potent Beta 1 and Beta 2 effects.
Isoproterenol increases what? Heartrate, myocardial contractility, systolic blood pressure.
What alpha effects of Isoproterenol? No alpha effects.
Secondary to Isoproterenol, excessive tachycardia and decreased diastolic pressure may decrease... Coronary blood flow.
Isoproterenol has high incidence of what bad thing? Cardiac dysrhythmias.
Dobutamine is a synthetic catecholamine with structural charateristics of... Dopamine and Isoproterenol.
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)
How are symphatomimetics classified? Classified as direct-acting (mimic the effects of norepinephrine) or indirect-acting (evoke the release of endogenous norepinephrine)
Phenylephrine mimics the effects of NE and is a... Direct acting alpha 1 agonist.
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
What is Ephedrine's primary mode of action? Indirect acting sympathomimetic. Increases blood pressure by stimulating release of norepinephrine.
What is Ephedrine's secondary mode of action? Direct acting (Directly stimulates postsymaptic adrenergic receptors)
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.
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.
What is Clonidine (Catapress)? Alpha 2 agonist.
What does Clonidine do? - Decreases outflow of the sympathetic nervous system - Decreases CO, SVR and BP - Sedative and analgesic effects decrease anesthesia requirements
Where in the body does Clonidine act? Central acting- acts on alpha 2 receptors located in the dorsal horn of the spinal cord.
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
What is Phentolamine (Regitine)? Alpha antagonist.
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
What is Phenoxybenzamine? Non-selective alpha blocker.
Phenoxybenzamine blockage at alpha 1 vs alpha 2: Blockage at Alpha 1 is greater than Alpha 2.
Why do we use Phenoxybenzamine? Used mostly for chronic control of pts with pheochromacytoma or Raynaud’s. It overcomes vasoconstriction.
What is Yohimbine and what does it do? Selective Alpha 2 antagonist. Leads to enhanced release of NE from nerve ending.
What is Prazosin (Minipress)? Alpha 1 receptor antagonist.
What does Prazosin (Minipress) do? - Dilates both arterioles and veins - Decreases SVR and Preload - Virtually no tachycardia secondary to no alpha 2 antagonistic effects.
Sodium Nitroprusside relazes both arterial and venous vessels. How? Forms nitric oxide- A naturally occurring potent vasodilator released by endothelial cells.
When do we use inhaled Nitric Oxide? In pulmonary hypertension.
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.
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.
S/s of acute cyanide toxicity: - Acute resistance - Metabolic acidosis - Cardiac dysrhythmias - Increased mixed venous O2 (secondary to inability to metabolize O2)
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.
NTG relaxes smooth muscle similarly in mechanism to Nipride. Arteral vs venous? Venous dilatation predominates over arterial dilatation.
Four things NTG is used for? 1. Relieves myocardial ischemia and spasm 2. Hypertension 3. Ventricular failure 4. Decreases preload
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.
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
What is Trimethaphan/Arfonad? Ganglionic blocker (Blocks sympathetic and parasympathetic receptors).
What does Trimethaphan/Arfonad do? - Directly vasodilates perph vasculature - Causes arterial dilation and venodilation - Can trigger Histamine release (avoid in asthmatics)
What is Trimethaphan/Arfonad used for? Used to control autonomic hyperrflexia (syndrome with massive sympathetic discharge in patients with upper spinal cord injuries).
Possible metabolism of Trimethaphan/Arfonad? Possibly by plasma cholinesterase.
What do beta blockers do? Block the effects of catecholamines on heart and lungs.
Is Inderal/ Propranolol selective or nonselective? Nonselective.
Actions of Inderal/Propranolol? - Decreases HR, CO, greater Beta 1 effects - Decreases spontaneous SA node firing
Uses of Inderal/Propranolol? - Afib/Aflutter/SVT - Angina (decreases Myocardial O2 requirements by decreasing HR and CO)
Potential negative SE of Inderal/Propranolol? Bronchospasm.
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
What is Metoprolol/Lopressor? Selective beta 1 antagonist.
Action/uses of Metoprolol/Lopressor? - Action: Decreases HR and CO - Uses: Afib/ Aflutter, HTN, SVT
What is Esmolol? What does it do? Selective beta 1 antagonist. Decreases HR and CO.
Metabolism of Esmolol: Hydrolysis by RBC’s and plasma esterases to inactive metabolites. Half life 9 minutes.
What is Atenolol/Tenormin? Why do we use it? Beta 1 selective antagonist. Use: Mostly PO for HTN – long acting.
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.
Three examples of beta agonists: Terbutaline, Albuterol, Ritodrine.
What is Labetolol/Trandate? Mixed alpha and beta antagonist. Blocks alpha 1 and beta 1 and 2.
Labetolol/Trandate decreases BP with no reflex decrease in HR. Ratio of alpha to beta action? 1:7
How do calcium channel blockers work? Selectively interfere with inward Ca ion movement across cell membranes.
What do calcium channel blockers do? Decrease contractility, HR, conduction thru the AV node. Cause small muscle relaxation and vasodilation.
When do we use calcium channel blockers? HTN, SVT, Coronary artery spasm, angina and cerebral artery vasospasm.
Verapamil is a calcium channel blocker. What is it derived from? Papaverine.
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
Use Verapamil with caution in patients who are... Beta blocked.
For what cardiac condition is Verapamil contraindicated? Why? Do not use in WPW. Inhibits intrinsic conduction pathway.
Diltiazem is a calcium channel blocker. What does it do and why is it used? Selective coronary vasodilation. Uses: Angina, HTN, SVT, Afib, Aflutter.
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
Nicardipine(Cardine) is a calcium channel blocker. What does it do and how is it used? Vasodilator. Uses: HTN, myocardial ischemia.
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.
What do ACE inhibitors do? Blocks the conversion of angiotension I to angiotension II in the lungs. Prevents angiotension II mediated vasoconstriction.
What do we use ACE inhibitors for? What's a potential SE? Uses: HTN, CRI, Chronic heart failure. Allergic rxn: Chronic cough.
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.
Created by: Chelsea Leigh Jones Chelsea Leigh Jones on 2010-10-01



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