|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.
|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...
|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:
|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)
|Alpha 1 antagonist (blocker) selective: ||Prazosin (Minipress)
|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
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?
|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.|