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atrial fibrillation adverse consequences - \1. decreased cardiac output due to loss of atrial kick, rapid ventricular rate, irregular ventricular rhythm
- tachycardia induced cardiomyopathy - in rapid afib for prolonged period of time
- thromboembolism right bundle branch - -right side of the interventricular septum and right ventricle -impulse travels slower as the right ventricle is smaller/thinner left bundle branch - \two main divisions: anterior fascicle and posterior fascicle carrying impulses to the left ventricle PR interval - \delay of AV node to allow filling of ventricles QRS complex - \ventricular depolarization shape depends on the lead that is being monitored and the ventricular activation device T wave - \ventricular repolarization normally in the same direction as the QRS upright, flat, inverted pathologies of T wave -
\MI, E/L levels, drug effect, myocardial disease, and lead being recorded u wave - \repolarization of the purkinje fibres SHOULD BE POSITIVE especially when T wave is positive large u waves can be seen when repolarization is abnormally prolonged - E/L imbalances like hypokalemia, hypocalcemia, hypomagnesemia, IICP, LVH, certain medications ST segment - \early ventricular repolarization should be at isoelectric line J point - \where QRS complex ends and ST segment begins QT interval - \ventricular depolarization and repolarization varies with age, gender, and heart rate beginning of the QRS to the end of the T wave QT must be corrected to a HR of 60 bpm QTc - \corrected QT interval = QT/(square root of R-R interval) normalises for HR long QTc --> torsades, ventricular arrhythmia, Vfib vertical axis - \each small box is 1mm or 0.1 mV each large box is 5mm or 0.5 mV most common complication of ischemic heart disease and MI - \dysrhythmias best leads for differentiating wide QRS rhythms - \v1 and v
MOA: selective inhibition of funny sodium channels, prolonging slow depolarization phase (phase 4); decreases SA node firing; negative chronotropic effect without inotropy; reduces cardiac O2 requirements Use: chronic stable angina in patients who cannot take beta blockers; chronic HF with reduced ejection fraction Tox: luminous phenomena/visual brightness, hypertension, bradycardia medications that cause ST - \atropine, isoproterenol, epinephrine, dopamine, dobutamine, levo, nitroprusside persistent tachycardia - \decreased stroke volume, decreased cardiac output, and decreased coronary artery perfusion secondary to decreased diastolic time that occurs with rapid heart beats sinus dysrhythmia - \sinus node discharges irregularly and commonly associated with phases of respiration during inspiration, it fires faster, during expiration it slows down dig tox sinus arrest - \occurs when the sinus node firing is depressed and impulses are not formed when expected, absent P waves at expected time - QRS will also be missing unless there is a junctional or ventricular impulse when more than one impulse in a row fails to form sinus pause - \when only one sinus impulse fails to form causes of sinus arrest - \vagal stimulation, carotid sinus sensitivity, MI interrupting blood supply to sinus node medications like dig, BB, and CCB treatment for sinus pause and sinus arrest - \0.5 of atropine and a pacemaker PAC causes - \caffeine, alcohol, nicotine, heart failure, pulmonary disease, interruptions in arterial blood supply by myocardial ischemia or infarction, anxiety, hypermetabolic states
PR interval and QRS with PAC - \PR interval - normal or long depending on the prematurity of the beat - early PAC may find AV junction still partially refractory causing a prolonged PR QRS - may be normal, aberrant (wide) or absent depending on prematurity of the beat completely repolarized - normal QRS, relative refractory period of AV node, bundle branches or ventricles - QRS will be aberrant or wide, very early - absent QRS Wandering Atrial Pacemaker (WAP) - \site of impulse shifts from SA node to other ectopic areas in atria or in the AV junction when two supraventricular pacemakers compete for control of the heart varying p wave morphology occurs from atrial fusion resulting in variable P waves due to increased vagal tone or enhanced automaticity in atrial or junctional pacemakers competing with sinus node for control Multifocal Atrial Tachycardia (MAT) - \Same characteristics as WAP, Rhythm: IR, Rate: 101-150, Pw: changes in appearance w/ at least 3 variations in one lead, PR: V, QRS: N. Frequently mistaken for A-fib, often seen with emphysema, Congestive heart failure or acute mitral regurgitation, pneumonia, PE , HF, coronary valvular or hypertensive heart disease medication effective in suppressing atrial foci - \verapamil recurrent MAT medications - \beta blockers, verapamil, diltiazem MAINTAIN NORMAL MAG AND K Atrial Tachycardia - \Rate: 150-250 beats per minute due to abnormal automaticity or reentry into the atrium DIFFER IN SHAPE FROM SINUS P WAVE BECAUSE THEY ARE ECTOPIC
treatment of atrial flutter - \ventricular rate is priority control if cardiac output is decreased verapamil or cardizem, beta blockers conversion through medication (dofetilide or ibutilide) electrical cardioversion or overdrive atrial pacing Dofetilide - \Class III antiarrhythmic Ibutilide - \Class III antiarrhythmic flecainide and propafenone control what rate? and why do you have to ensure that AV nodal blocking agents are given in combination? - - control atrial rate
- atrial rate may decrease from 300 to a slower rate making it possible for AV node to conduct each impulse thereby increasing ventricular rates atrial fibrillation - \atherosclerosis, rheumatic heart disease, thyroid disease, HF, cardiomyopathy, valve disease, pulmonary disease, MI, congenital heart disease, cardiac surgery aberrant intraventricular conduction can occur if the atrial impulses reach the bundle branches during refractory period nonvalvular heart failure - \occurs in patients without mitral valve disease, prosthetic valves, history of valve surgery treatment of afib directed towards - \1. eliminating the cause
- controlling ventricular rate
- restoring and maintaining sinus rhythm
- preventing thromboembolism Wolf-Parkinson-White Syndrome - \∙An accessory conduction pathway from atria to ventricles through the bundle of Kent, causing premature ventricular excitation because it lacks the delay seen in the AV node. ∙Treatment is radiofrequency ablation.
∙Want to avoid AV nodal blocking agents. ∙Look for delta waves. medications for afib - \rate control - CCB (dilt, verapamil) and beta blockers - should be used in caution with HF or hypotension and are contraindicated with WPW antiarrhythmic recommendations - flecainide, dofetilide, propafenone, ibutilide (class I) and amiodarone (class II) AV nodal ablation - \destroys AV node ability to conduct impulses to ventricles results in complete AV block and requires a ventricular pacemaker, does not stop Afib so patients need to be adequately anticoagulated radiofrequency ablation - \triggers sites in pulmonary veins or atria - most common site is 2-4 cm in the pulmonary veins leading to left atrium segmental ostial pulmonary vein isolation (PVI) and circumferential PVI segmental ostial PVI - \specific sites of electrical conduction in the ostia of the pulmonary veins are ablated circumferential PVI - \continuous ablation lesions encircle the ostia of ALL FOUR pulmonary veins - completely isolate pulmonary veins from atrial myocardium MAZE procedure - \surgical procedure to treat atrial fibrillation in which a new conduction pathway is created that eliminates the rapid firing of ectopic pacemaker sites in the atria left atrial appendage - \cox maze procedure inserted into right femoral with a trans septal approach, seals the appendage from the rest of the body SVT - \any rhythm faster than 100 beats a minute which originates above the ventricles or utilises the atria, AV junction as part of the circuit that maintains tachycardia regular narrow complex QRS tachycardia in which the exact mechanism cannot be determined from the surface EKG
\irritable focus in the AV junction CAD or MI disrupting blood to the junction QRS complex can be normal or aberrant if the PJC conducts into the ventricles during the refractory period of the bundle Catecholamines - \hormones secreted by the adrenal medulla that affect the sympathetic nervous system in stress response Effect on adrenergic receptors Epi, levo, dopa Beta 1 and 2 How do inotropes work? - \They increase cardiac contractility and cardiac output Sympathetic stimulation or phosphodiesterase inhibitor Epi (inotropes) - \Of all the vasopressors this has the strongest effect on contractility Non-selective adrenergic agonist Low - beta 1 High - beta 2 1-10 mcg/min (1mg/250ml) Catecholamine SE: tachyarrhythmias, myocardial/mesenteric/renal/extremity ischemia and hyperglycemia Dopamine - \Beta 1 effects increase in HR and contractility 5-10 mcg/kg/min - affinity for beta 1 increase in cardiac output through HR and increased contractility 10 + affinity for alpha 1
400 mg/250 ml (2-20 mcg/kg/min) action within 5 minutes Catecholamine Dobutamine - \Primary effect on beta 1 and also beta 2 (watch for hypotension) 500 mg/250 ml (2.5-20 mcg/kg/min) titrate every 5 to 10 minutes Catecholamine management of elevated filling pressures and low cardiac output states like decompensated heart failure or cardiogenic shock, ongoing signs of hypoperfusion can be used with levo and maintained separately to maintain both blood pressure and cardiac output tachydysrhythmias, hypotension, ischemia Isoproterenol - \Primary beta 1 and beta 2 receptors *greater impact on heart rate than dobutamine - pure potent beta receptor agonist Used in bradycardia, strong inotropic, chronotropic and vasodilatory effect Can cause vasodilation - hypotension 1-4 mg/250 ml (2-20 mcg/min) Q 3-5 min Catecholamine SE: myocardial ischemia, tachyarrhythmias phosphodiesterase inhibitors - \inhibits enzyme type 3 PDE at low doses, non selective at high doses causes positive inotropic and vasodilation Cyclic adenosine monophosphate (CAMP) - more cAMP available to cells, more calcium is available to the cells stimulating contraction Prevent metabolism of cGMP leading to greater vasodilation (more so than beta 2) Milrinone - \PDE
4 mg/250 ml 16 mg/250 ml onset of 1 minute, every 3-5 minutes to titrate 1-12 mcg/kg/min - our policy is 0.02-.3 mcg/kg/min Phenylephrine (Neo-Synephrine) - \pure alpha agonist - baroreceptor mediated reflex bradycardia - can lead to mixed effect on cardiac output
- adjunct in salvage therapy or in light of dysrhythmias caused by levo -vino and arterial constriction 40 mg/250 dose is 50-200 mcg/min onset is 1 min, titrate every 3- vasopressin - -second line treatment with patients that are not responding to catecholamine medication -impacts arginine vasopressin system to increase blood pressure - direct systemic vasoconstrictor V1 receptor site agonist, causes water reabsorption in distal tubules and collecting ducts - also increases BP 20 units/100 ml 0.01-0.04 units/min onset is 5-15 minutes - no titration epinephrine - \last ditch in treatment of shock nonselective agonist in all adrenergic receptors higher doses have an affinity for alpha receptors 1mg/250ml 1-10 mcg/min onset is 1-2 minutes titrate every 5 dopamine - \indirect and direct acting agent - works indirectly by causing release of norepi from nerve terminal storage vesicles as well as directly by stimulating alpha and beta
400 mg/250 ml 2-20 mcg/kg/min WEIGHT BASED rate 1-3 renal dose 5-10 beta agonist 10-20 adrenergic alpha agonist onset is 5 min, titrate Q 15 Giapreza - \angiotensin II in IV form - just approved activates RAAS and AT2 receptors - causes vasoconstriction primary an action on arterial system 2.5 mg/250 ml or 2.5mg/500 ml .02-.08 mcg/kg/min titrate Q Why are manifolds/stopcocks important? - \if everything is y-sited together and you have to make a change to the vasopressor at the top, it will have to run through all of those additional lines before you see the change. manifolds allow you to see more immediate onsets when you are titrating medications. TKO flush line - \carries the medication in an manifold quicker therefore seeing medication effects quicker DO NOT use the infusion line on the swan, the line is far too long. use a line that is closer to the placement never FLUSH with pressors best practice for infusing pressors - \use a CVC - must verify prior to use - XRAY look a transducer waveforms if unsure if it is CVP or arterial waveforms the practice of trendelenburg position - \do not use. old practice. falsely elevating the pressure at the site of baroreceptors prevents the body from release it's own catecholamines - detrimental
benzapine derivative with selective dopamine 1 receptor agonist properties - dopaminergic stimulation continuous infusion: 0.1-1.6 mcg/kg/min sodium nitroprusside - \vasodilator affecting arterial and venous system, onset almost immediate, duration of action is 10 minutes if used for longer than 48 hours - risk of thiocyanate toxicity - serum concentration must remain below 10 mg/dL 0.5-10 mcg/kg/min SE: methemoglobinemia, cyanide toxicity use in caution with increased ICP, head trauma - increased cerebral pressure Nipride Indication - \hypertensive encephalopathy, infarction, SAH, malignant hypertension, aortic dissection, after general surgical procedures, major vascular problems, renal transplantation monitoring parameters for nipride - \blood pressure, renal function, thiocyanate concentration, acid-base status and hemodynamic parameters nitroglycerin - \preferential venous dilator at lower doses but relaxes arterial smooth muscle at higher doses - will see effects in 1-3 minutes duration of action less than 10 minutes tachyphylaxis can be seen with IV infusion, similar to use of topical nitro products HYPERTENSION WITH MYOCARDIAL ISCHEMIA OR INFARCTION - NET EFFECT IS REDUCING MYOCARDIAL OXYGEN CONSUMPTION 10-300 MCG/MIN Unfractionated Heparin and nitroglycerin drip - \increased doses may be needed to maintain therapeutic PTT - causes resistance hydralazine - \directly acts on peripheral vascular resistance by relaxing arterial vasculature
BP occurs within 5-20 min after and lasts for approximately 2-6 hours SE: HA, nausea, vomiting, palpitations, tachycardia - reflex tachycardia can precipitate anginal attacks co-administration of a beta blocker can decrease incidence of tachycardia 10-25 mg IV q 2-4 hours diazoxide - \hypertensive crisis to reduce PVR by directly relaxing arterial smooth muscle hypotension, nausea, vomiting, dizziness, weakness, hyperglycemia, reflex tachycardia have been associated with doses higher than 300 mg may cause excessive hypotension when used with other medications within 1-2 minutes, 3-12 hours 50-150 mg Q 5 min infusion 7.5 to 30 mg/min labetalol - \alpha and beta blocker beta to alpha is 7: onset is 5 minutes, duration is 2-12 hours CONSIDER PRIOR: for patients with asthma or reactive airway diseases, those with conduction disturbances, and negative inotropic effects which may worsen HF labetalol vs nipride - \labetalol used in setting of hypertension associated with head trauma/post craniotomy, spinal cord syndromes, autonomic dysreflexia, HTN associated with sympathomimetics (cocaine, meth, diet pills) OR withdraw from centrally acting antihypertensive agents (beta blockers, clonidine, methyldopa) alternative to phentolamine in setting of pheochromocytoma IV bolus: 10-20 mg over 2 min then 40-80 mg IV q 10 minutes to a total of 300 mg Continuous infusion: 1-4 mg/min and titrate to effect BP, HR, EKG, s/s of HF or bronchospasm Phentolamine -
ACE inhibitors - \blocks conversion from angiotensin 1 to angiotensin 2 - increase availability of bradykinin and other vasodilatory prostaglandins, also reduces plasma aldosterone concentrations
- net effect is a reduction in blood pressure in hypertensive patients and reduction in afterload in patients with HF adverse effects associated with ace inhibitors - \rash, change in taste, cough, angioedema, rarely - abdominal pain with diarrhoea initial hypotension will occur with patients that are hypovolemic, hyponatremic, or have been aggressively diuresed - can be minimised by holding diuretics for 24- hours can cause worsening renal function in patients with bilateral renal artery stenosis HYPERKALEMIA enalapril - \prodrug that is converted in the liver to enalaprilat which is a long acting ACE inhibitor Angiotensin Receptor Blockers - \prevent angiotensin II from reaching its receptors and the adrenal gland, causing vasodilation and decreased secretion of aldosterone - leads to increased sodium excretion and potassium sparing effects monitor E/L there is not a parenteral formulation making ARB not an adequate candidate for acute decrease in BP calcium channel blockers - \Negative Ino, Chrono, Dromo - not used in heart failure patients because of this inhibit the entry of calcium ions into heart muscle cells, causing a slowing of the heart rate, a lessening of the demand for oxygen and nutrients, and a relaxing of the smooth muscle cells of the blood vessels to cause dilation; used to prevent or treat angina pectoris, some arrhythmias, and hypertension CCB indications -
\hypertension, hypertensive encephalopathy, myocardial ischemia, malignant hypertension, eclampsia, renal tx nicardipine - \available in an oral and IV form, IV onset is 5 minutes with duration for 30 minutes continuous: 5 mg/h increase every 15 min to a max of 15 mg/hour oral: 20-40 mg q8h clevidipine - \onset faster than nicardipine, shorter duration injectable liquid emulsion (20% fat) - must be changed every 12 hours clonidine - \alpha 2 agonist - centrally sympatholytic agent stimulates receptors in medulla oblongata causing inhibition of sympathetic vasomotor centres can be used as maintenance therapy or in setting of hypertensive crisis - seen within 30 minutes, last between 8-12 hours can cause rebound hypertension - rarely used as first line in antihypertensive therapy Class I antiarrhythmics - \IA: Disopyramide, Quinidine, Procainamide "Double Quarter Pounder" IB: Lidocaine, Tocainide, Phenytoin, Mexiletine "Lettuce Tomato Pickles Mustard" IC: Moricizine, Fecainide, Propafenone "More Fries Please" NA channel blockers - inhibit potassium sparing depolarizing currents to prolong repolarization class Ia - - inhibit the fast sodium channel (phase 0 of action potential) -slows conduction -prolongs action potential duration and repolarization (prolongs QT) ADVERSE: can cause proarrhythmic effects by prolonging QT interval or depressing conduction and promoting reentry
