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Med-Surg II - wk 2

Problems of Oxygenation & Perfusion: Nrs Management of Dysrhythmias

QuestionAnswer
perfusion movement of oxygen - bringing O2 to the cells (delivering)
telemetry monitoring remote monitoring of a patient. 3 electrodes & a little box (usually kept in the pocket).
EKG tracing. road map of the heart. where does the message originate, which is it communicating with, where does it go to make the contraction happen.
dysrhythmias electrical message in the heart "goes a different way." there is some problem that makes the impulse take a different route.
properties of cardiac tissue automaticity; excitability; conductivity; contractility.
automaticity the ability to initiate an impulse. SA node (where the impulse starts)
excitability ability to be electrically stimulated.
conductivity ability to transmit an impulse along the system. SA node communicates to the AV node.
Contractility heart muscle responds to impulse and contracts
conduction system of the heart originates in SA node -> (intraatrial pathways to LA) internodal pathways to AV node -> bundle of His -> R&L bundle branch -> purkinje fibers --> ventricular contraction
heart block something is blocking the conduction pathway.
Autonomic NS responsible for normal, regular control (rate of impulse formation, speed of conduction, strength of contraction).
parasympathetic NS Vagus nerve is main nerve.
Vagal Nerve Stimulation dec HR, slowed conduction, decreased force of contraction,
causes of Vagal Nerve Stimulation valsalva maneuver (bearing down) -- this is a nursing action for high HR, panic attack
sympathetic NS opposite of parasympathetic. increased HR, increased force of contraction
P wave atrial depolarization
PR interval beginning of P wave to beginning of QRS complex. time it takes for the atria to depolarize and repolarize
QRS complex ventricular depolarization.
ST segment flat line in normal heart. interval from the end of ventricular depolarization to the beginning of ventricular repolarization.
T wave ventricular repolarization
QT interval total time for ventricular depolarization and repolarization
ECG - vertical axis electrical potential
ECG - horizontal axis time - how long it takes
ECG - 5mm square 0.2 seconds x 0.5 mV
ECG 1mm square 0.04 seconds x 0.1 mV
Normal Sinus Rhythm 60-100 bpm. follows normal conductive pathway. look for P wave - P wave present = NSR.
Sinus Bradycardia sinus fires < 60 bpm. normal rhythm in aerobically trained athletes. can be problem w vagal nerve stim. some drugs do this (parasymphathomimetics). hypothermia can cause.
Sinus Bradycardia: Sx and Clinical Manifestations hypotensive. hypoxia. weak. dizzy. nauseous (if due to vagal nerve stim). angina. confusion.
Parasymphathomimetic Drugs mimic the parasympathetic NS. side effect = slows HR. ex: Pilocarpine (for dry mouth).
Sinus Bradycardia: Treatment Atropine. Pacemaker
Atropine anticholinergic drug. increases HR. may be given to reverse effects of muscarinic drugs (parasympathomimetics).
Sinus Tachycardia discharge rate from the sinus node is increased as a result of vagal inhibition. > 100 bpm.
Sinus Tachycardia: Causes anxiety. exercise. pain. fever. hypovolemia.
Sinus Tachycardia: Clinical Manifestations hypotension. dizzy, lightheadedness, SOB, angina (not enough O2 to the heart)
Sinus Tachycardia: Treatment beta-blocker (not for BP, to control/decrease HR). antipyretic (if caused by fever). analgesia (if caused by pain). IV fluids, increase oral intake (if caused by hypovolemia)
Treatment of Sinus Rhythms treat the CAUSE to get the patient out of that rhythm
Normal Sinus Rhythms NRS, sinus bradycardia, sinus tachycardia.
Premature Atrial Contraction NOT NSR. irregular. ectopic beat occurs occasionally, originating not from SA node. no lethal.
Premature Atrial Contraction: causes emotional stress, too much caffeine, too much alcohol, too much tobacco, electrolyte imbalances (some), COPD.
Premature Atrial Contraction: significance with heart disease can be a warning. check labs (K & Na). have meds been taken?take apical pulse 1 min. inform provider.
Premature Atrial Contraction: Treatment depends on the symptoms. find and eliminate the source. drugs secondary. beta-blocker (to control the rate). decrease caffeine/nicotine intake, halter monitor.
Paroxysmal Supraventrical Tachycardia (PSVT) person is in NSR, run of tachy, then back to NSR. > 130 bpm in 6s strip (up to 200 bpm). sustained or non-sustained.
PSVT - sustained emergency. BP can bottom out.
PSVT: Cauess over exertion. stimulants. emotional stress. digitoxicity. known CAD.
Digitoxicity signs nausea. lack of appetite. "yellow halos" in vision. blurry vision.
PSVT: causes in known CAD could mean things are not going well. take vitals, symptoms, info from tele-clerk. Report to Dr.
PSVT: Clinical Manifestations c/o palpitations. Hypotensive. dyspnea. angina
PSVT: Treatment vagal maneuvers. if not effective, then drugs. Adenosine
Adenosine potent anti-arhythmic. interrupts pathway to the AV node, slows AV node conduction, which slows HR. rapid response team will push this (not you - unless told to). want monitor by bedside.
Atrial Flutter originates from a single ectopic focus w/in atria. very typical pattern (sawtooth mtns). tx depends on what pattern looks like.
Atrial Flutter - rapid ventricular response TX directed at controlling vent rate (~160 bpm).BP drops, dizzy lightheaded, decreased CO.
Atrial Flutter: associated with... CAD, HTN, valve disorders, lung disease
Atrial Flutter: risks risk for stroke. risk for clots (blood not ejected from As, stasis --> clots --> stroke).
Atrial Flutter: clinical significance has to do with how fast the ventricles are contracting.
Atrial Flutter: Treatment goal: slow HR. beta-blockers, Ca Channel Blockers, anti-dysrhythmic. elective cardioversion.
Amdiodarone anti-dysrhythmic. slows sinus rate, increases PR interval. many side effects. IV push under controlled circumstances. more potent than beta- or Ca- blockers.
elective cardioversion controlled shock to get the heart out of a bad rhythm.
Atrial Fibrillation irregular impulse coming from multiple ectopic focuses in atria. less organized than flutter, atria become very disorganized. most common dysrhythmia. prevalence increases w age.
Atrial Fibrillation: common with... CAD. HF (sometimes first sign of HF). alcohol intoxication. too much caffeine. electrolyte imbalances (K & Na). post-cardiac surgery.
Atrial Fibrillation: Clinical Manifestations exactly same as A flutter. decreased CO. some may have rapid ventricular response. high risk for embolus.
Atrial Fibrillation: Goals of Treatment rapid ventricular response: slow HR, prevent thrombus formation. drugs: beta-blockers, Ca channel blockers, amiodarone. elective cardioversion.
Atrial Fibrillation: Elective Cardioversion can only be done if we know when the AFib started. Don't want to cardiovert someone with thrombi. unknown: anticoagulant for 3-4 weeks.
Premature Ventricular Contractions (PVC): causes stimulants (caffeine, alcohol, epinephrine, recreational drugs). electrolyte imbalances (K, usually too low). Known CAD.
PVC: known CAD or lasix usage watch for these patients. lasix - pulls fluid off, K follows fluid, K imbalance.
PVC: Clinical Manifestations CO can fall. hypoxia. angina.
PVC: Treatment O2 (hypoxia, angina). electrolyte replacement (K and Na). drugs (beta-blockers, amiodarone, lidocaine).
Multifocal PVCs QRSs are not the same. tells us that an impulse is coming from different places (weaker/stronger). not much of Q at first glance (distorted and wide = ineffective CO). patterns (couplets or triplets = both are bad).
PVC: Ventricular Bigeminy one normal complex, then wide distorted one, repeate
Ventricular Tachycardia EMERGENCY. can move from pulse VTach to pulseless VTach. activate rapid response team.
V Tach: Treatment shock them. ACLS protocol.
Ventricular Fibrillation can see this when they have an MI and progress to VFib.
Created by: malysab14