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Cardiac Pharm Barry
Cardiac Pharmacology Barry
Question | Answer |
---|---|
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. |