CARDIAC - RHYTHM STRIPS TEST WITH 100% CORRECT ANSWERS

Normal Sinus Rhythm Rate 60-100 BPM •Predisposing Factors: -NORMAL -Regular impulses at a normal rate. •ECG Appearance: -P wave, QRS wave, T wave -60-100 bpm -Equal distances bwt each beat -PRI: 0.12-0.20 sec. -QRS: < 0.12 sec •Hemodynamic Effects & Nursing Implications: -Normal •Treatment: -Normal Hemodynamic Effects & Nursing Implications: -Normal •Treatment: -Normal Sinus Arrhythmia •Predisposing Factors: -Normal -Varies with breathing •ECG Appearance: -NSR but irregular •Hemodynamic Effects & Nursing Implications: -Normal •Treatment: -Normal Brainpower Read More Previous Play Next Rewind 10 seconds Move forward 10 seconds Unmute 0:00 / 0:00 Full screen Sinus Bradycardia (slow low not enough CO to sustain) •**Sinus= arrhythmia originates in SA (sinus) node** •Predisposing Factors: -Meds: Beta blocker, Digoxin, Narcotics, CCB -Athletes that have low base HR -Sleep -Valsava Maneuver-straining with BM -Carotid Massage -Hypothyroid -Hypothermia -ICP -mi'S •ECG Appearance: -Same as NSR except <60 BPM •Hemodynamic Effects & Nursing Implications: -Sinus Brady is ok it pt. is asymptomatic •Symptomatic Sinus Brady can cause: -Hypotension -Diaphoresis -Chest Pain -SOB -Change in mental status _PALE COOL SKIN -weak -diz/syncope •Treatment: 1. Why brady? May be normal for pt. If not, assess pt. treat underlying cause first. - Ex. If cold=warm pt., constipated=stool softener, decr. thyroid=synthroid.(if RX stop offending RX or lower dose) 2. O2 3.Atropine- help inc. HR IV 4. trans pacing 4. Epi or dopamine gtts 5. Pacer perm Sinus Tachycardia ( everything normal but rt which is occurring Quickly. organs aren't getting perfused not refilling properly) > 100 BPM (if HR 100 -200 watch for (dysrhythmia if it continues) PRIMARY =WATCH AIRWAY •**Sinus= arrhythmia originates in SA (sinus) node** •Predisposing Factors: -Running, exercise, hypovolemia (dehydration), pain, anxiety, fever, infection, hypotension, anemia, hypoglycemia, hyperthyroid, Mi, fear, caff -emotional distress -CAD (heart thinks its not getting enough O2 out, ↑ HR), hyperthyroid -caused by vagal inhibition=vagal nerve slows down when stimulated - not getting stimulated OTC RX:cold meds, epinephrine, Sudafed Manifestations: -diz -dyspnea -hypotension -angina in pt with CHF •ECG Appearance: -Same as NSR except >100 bpm •Hemodynamic Effects & Nursing Implications: -Depends on pts. tolerance of Inc. HR. RX: can ^ RATE -epi -nor epi-levophed -atropine -Sudafed - cold meds -Theothyline -hydralazine •Treatment: 1. Why Tachy? If normal for pt. then no treatment. What is the underlying cause- assess and treat. -Ex. Limit Stimulants, Give O2, HF-Give Lasix, If r/t fever-treat fever, Dr. can do carotid massage. Vagal, manuevers., anxiety, stress 2. Meds to Dec. HR: CCB, beta block, antidysrhythmics Adenosine(adendocard) $$ clin unstab pt.=synchronized cardioversion Atrial Fibrillation -Paroxysmal starts and stops suddenly ( multiple ectopic folci) MOST COMM dysrth MORBIDITY and MORTALITY rates- prev incr with age 350-600 BPM (FIB QUIV) can be paroxysmal nor persistent lasting more than 7 days •**Disorganized uncoordinating twitching of atrial muscle** •Predisposing Factors: usually occ in pt with underlying heart disease -CAD, valvular heart disease, cardiomyopathy, HTN, HF, pericarditis -Possible Post-CABG OFTEN ACUTELY" $ thyrotoxicosis an alcohol intoxication $ caffeine $ electrolyte disturbances ( potassium) $stress $ heart surgery - •ECG Appearance: -No distinct 1 P wave; instead many fibrillatory waves. -Only QRS and T waves present. -QRS to QRS is irregular -Baseline present but wiggly INCR risk stroke, very very very little contraction, ★the embolized clot can develop and pass thru the brain and cause stroke a fib accounts for as many as 17% of all strokes The goal and treatment for Atrial fib is decreasing cardiac output because of ineffective atrial contractions (loss of atrial kick )and or rapid ventricular response. include a decrease in ventricular response so less than (100 BPM) prevention of stroke and conversion to sinus rhythm when possible. Ventricular rate is controlled is a priority for patients with atrial fibrillation •Goals: 1. HR control; 60-100 2. Convert to sinus rhythm and maintain 3. Prevent Clots •Treatment: Drugs to control ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most common) RX : rate control CCB, beta blockers, dronedarone, digoxin (Lanoxin)=rhythm control for some patient’s drug or Electro cardioversion of atrial fib to normal sinus rhythm may be considered especially if they're not tolerating very well if they are continuing to have shortness of breath, we would do electrical cardioversion ○electric cardioversion can be used to convert a-fib (SYNCH IT) If the patient is in a -fib for longer than 48 hours anticoagulation therapy with warfarin is needed for 3 to 4 weeks before the cardioversion and for several weeks after successful cardioversion anticoag therapy is necessary because the procedure can cause the clots to dislodge placing the patient at risk for stroke (even if we synch them) WE COULD CAUSE a stroke bc we can dislodge the clot TEE BEFORE they shock them may be performed to rule out clots in the Atria in the Atria if no clots are present anticoagulation therapy may not be needed before the cardioversion If drugs and cardioversion does not convert the atrial fibrillation to normal sinus rhythm long term anticoagulation therapy is needed Alternatives to warfarin are available for anticoagulant therapy in patients with nonvalvular atrial fibrillation. (dabigatran (Pradaxa) apixaban (Eliquis) Rivaroxaban (Xarelto)DO NOT REQ RTN LABS Pt refract – drugs don’t work cardioversion don’t work they don’t want anticoag for the rest of their life they can do ablation. But make sure they are on anticoag therapy before the surgery RISK could stimulate when they go up with the wire that could send you into a deathly rhythm (cath lab ACLS certified.) Atrial Flutter (single ectopic focus) ATR = 200-350/ Vent 150 BPM ( risk thrombus )-warfarin -coumadin $ REPRESENT ATRIAL FLUTTER WAVES REPRESENT ATRIAL DEPOLORIAZATION FOLLOWED BY REPLORIZATION ($$ IE: diff between flutter/ fib - fluter ONE ectopic focus _ONE shark tooth bite)-sawtooth •**Single irritable focus area in heart that has rapid repetitive impulses.** •Predisposing Factors: -CAD, Mitral valve dis, HTN, HF, hyperthyroid -Possible Post-CABG -Hyperthyroid -Heart Diseases -PE -chronic lung disorder -cor pulmonale -cardiomyopathy -CAN casue HF esp with underlying heart disease $$$RX that can cause it digoxin, quinidine, epinephrine •ECG Appearance: -QRS is normal -P waves have a sawtooth pattern -Usually regular rhythm •Hemodynamic Effects & Nursing Implications: -No atrial kick. -Ineffective atrial depolarization -Blood becomes stasis in heart -Risk of clots: PE, heart attack or stroke bc blood is stagnant -↓ CO -Irregularly irregular pulse -Palpitations, SOB, CP, fatigue, syncope, HF, change in mental status •Goals: 1. HR control; 60-100 2. Convert to sinus rhythm and maintain 3. Prevent Clots •Treatment:** (TX of choice is Radipofrqeuncy catheter down the rt atrium with the use of a low voltage high freq form of electrical energy catheter ablation done in EPS lab) Primary TX: 1. slow the Vent resp by decr the AV block --RX CCB, Breta blcr 2. Covert to NSR (meds): -antidysrhythmic RX: --convert atrial flutter to norm sinus $ibutilide (covert) $$$ maint sinus rhythm- amiodarone, flecainide, dronedarone(multaq) Only if clinically not stable 3. EC- to conver flutter into Sinus rhythm in emergency cardioversion: mild sedation, monitor rhythm, low joules. Do TEE first to check for clots (so you don't send the clots around the body when you shock!) 4.. Ablation:TX OF CHOICE for atrial flutter per PP slide 35 1st do the EC then ablation Junctional Dysrhythmias (start in the AV node to bundle of HIS AKA AV junct.) JUN. ESC. RHY. 40-60 BPM ACCELER. JUNCT. 61-100 BPM JUNCT.TACHY. 101-180 (No P wave, or may see it inverted Might see P wave Inverted because it's going in retrograde fashion so it looks upside down) •SA node has failed to fire, or impulse has been blocked at the AV node AV node becomes pacer—retrograde transmission of an impulse to atria -prim. pooped out SO now AV node is the pace maker of the heart AV node usually moves in a backward fashion and produces abnormal P waves. Abnormal P wave; (INVERTED P wave) normal QRS associated with CAD HF electrolyte imbalances MI’S cardiomyopathy rheumatic heart disease drugs Nicotine caffeine amphetamines can cause J.D. Junctional escape rhythm-Serves as a safety mechanism—do not suppress Sa node has not been effected sa node isn't doing its job so now av node is the pacemaker Esc. rhythm should not be suppressed- bc it is doing the job of the AV If rhythms are rapid, may result in a reduction of CO Accelerated junct rhythm- is do to the sympathetic stimulation to improve the CO -trying to create enough blood is to the sympathetic stimulation to improve the CO -trying to create enough blood Treat if the patient is symptomatic Atropine for escape rhythm Correct cause- stop stim or drug Drugs to reduce rate if tachycardia(beta, CCB) First degree Heart Block (Note normal PR 0.12-0.20) $$ looks like normal sinus BUT WATCH PR=longer than 0.20) •1st deg AV block every impulse is conducted to the ventricles but the time of the AV conduction is prolonged. Consistent, exactly the same length , it is just prolonged(slow getting to the ventricles) Associated with disease -MI -CAD -rheumatic fever -hyperthyroidism -electrolyte imbalances especially low potassium(hypokalemia) -vagal stim (bc your slowing down to much) RX TX: digoxin beta blcrs CCB flecainide (Antiarrhythmic) It can treat and prevent serious irregular heartbeats (arrhythmias). •ECG Appearance: -PRI greater than .20 Typically not serious but can be a sign of a higher AV block usually Asymptomatic-they are contracting fine TX: -No treatment Monitor for changes in heart rhythm Pemature Ventricular Contractions (PVC) -not harmful in pt with normal heart ###Shock and not synch =R on T phen sending them in to V-tach and event V-fib an extra stimulus, premature or early occurrence of QRS complex PVC is wide and distorted in shape compared to normal QRS conduction BC not following normal cond it is distorted bc it is coming from a diff location) PVC’s that arise from different focusses app. differ. in shape from each other and are called multi focal!. Unifocal all look the same. V. B- (ventricular Bigemony) when every other beat is a pvc ventricular bigeminy V. T- (ventricular tachycardia)when every other 3rd beat is a pvc= ventricular trigeminy couplet.-two group consecutive together PVC is R on t phenomenon occurs when PVC falls on the T wave V Tach is multiple PVCs Sustained V-tach deadly rhythm Associated with stimulant: Alcohol Caffeine Nicotine Epi Digoxin electrolyte imbalances: hypoxia Fever Exercise emotional distress disease: MI Mitral valve prolapse HF Cardiomyopathy CAD DIS: -MI, mitral valve prolapse, HF, cardiomyopathy, CAD •ECG Appearance: -Early QRS beats •Hemodynamic Effects & Nursing Implications: -Pt. may be asymptomatic -Possible may have: HR will lead to V-tach → V-fib → Cardiac Arrest if not treated •Treatment: Correct cause Hypoxia- O2 Electrolyte imbal- Replace electrolytes Asses pt hemodynamic status to det if TX is needed RX: Beta blockers Amiodarone Antidysrhythmic (convert and get PVC BACK IN ORDER) Not harmful with normal heart but CO reduction, angina, and HF in the diseased heart Assess apical-radial pulse deficit because PVC and CAD, acute MI indicate ventricular irritability, assess the patient's physiological response. Irritable its going its premature it is not following our normal pathway asses pt physiological RESP APICAL RADIAL PULSE make sure to see if they are symptomatic What is the CO ? If couplet probably not going to see a lot of difference VT= look poor Ventricular Tachycardia (VT) (WIDE a bunch of PVC’s ) 150-250 bpm •**3 or more PVC's in a row** dysrhythmia can be seen in patients with no sign of heart disease. A Lot of PVC’s, a run of 3 or more PVCs defines the tach Ventricular rate is 150-250 bpm regular or irregular AV dissociation could be present NO P WAVES because they are covered up, EKG will take the strongest electrical impulse over the time QRS is distorted in appearance and wide, so greater than 0.12 sec in duration Ectopic foci take over as pacemaker Monomorphic( do they all look the same? (coming=from one location) polymorphic(do they all look different?(coming from diff locations), Sustained= considered V-tach longer than 30 sec. Nonsustained= less than b30 sec. Extra stimulus in our ventricles development of v tach is an ominous sign Considered life-threatening because of decreased CO and the possibility of deterioration to ventricular fibrillation= LETHAL DYSTHYMIA Associated with heart disease, electrolyte imbalances, drugs ( toxicity), CNS disorder Can be stable (patient has a pulse) unstable (pulseless) Sustained VT = last longer than 30 sec. causes a severe decrease in CO bc < ventricular diastolic filling times( HARDLY ANY BLOOD GOING T O THE BODY) -Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest the episode may reoccur if prophylactic treatment is not started, need to fix the cause. $$Can go from sustained/ unsustained V-TACH and then to normal rhythm they are still be at risk to go back into the deadly rhythm bc we didn’t fix the cause. $$$$Precipitating causes must be identified and treated Hypoxia Electrolytes Ischemia – cath lab open blockage Ventricular Fibrillation (VF) (looks like a ribbon)- No distinguished p waves QRS ANYTHING NOTHING TO SYNCH TO (SEARCH SEARCH SEARCH) never ok to send jolt $$(NOT TX RAPIDLY YOUR PT. WILL DIE) D fib for V-fib and pulseless V-tach THE ONLY ONES YOU D_FIB FOR •**Ventricle continually firing; only electrical, no contractions** severe derangement of heart rhythm characterized on an EKG by irregular waveforms of varying shapes and amplitudes firing of multiple ectopic sites in the ventricle (A LOT FIRING) HOT GARBAGE No cardiac output Not a sustainable rate Heart rte not meas. Rhythm irreg and chaotic P waves aren’t visible PR interval- aren’t meas QRS – aren’t meas Associated with: MI Ischemia disease states: HF cardiomyopathy procedures- cardiac pacing or cardiac catheterization procedure Unresponsive(no CO), pulseless(no), and apneic Treat with immediate CPR and ACLS Defibrillation Drug therapy (epinephrine, vasopressin) NO DELAY IN USING DEFIB ONCE AVAILABLE Idioventricular Rhythm •*Heart is dying, slowly stopping, periodic QRS wave* •ECG Appearance: -Slow wide QRS complexes •Hemodynamic Effects & Nursing Implications: -Faint pulse or none •Treatment: -Check DNR status -Check pt: Call code -CPR -Epi / vasopressin -Do not shock! Asystole (must assess in more than 1 lead)- can occasionally see a p wave!--DEAD -lethal dysrhythmia that req immediate TX. Look at rhythm in more leads than one ( are they for sure ASTOLE, change to lead 2 etc) MAIN LEAD ONE FOR TESTING •**Nothing, No HR, No Pulse, No CO, No Electrical Activity** Represents total absence of ventricular electrical activity No ventricular contraction Patient unresponsive, pulseless, apneic Must assess in more than one lead •ECG Appearance: -Straight lining -Periodic QRS; electrical activity slowing, no contractions occurring in the heart Usually result of advanced cardiac disease, severe conduction disturbance, or end-stage HF generally, the patient has an stage heart disease or has a prolonged arrest so been in vfib and could not be resuscitated Treat with immediate 1.CPR (cant shock bc we can't defibrillate this.) ACLS measures Epinephrine and/or vasopressin Intubation Poor prognosis CPR to try to circulate Epi try to get the heart rate back. If you get a rhythm back, THEN DEFIB synchronized cardioversion-electrical shock timed to avoid cardiac repolarization (represented by the T wave on EKG) MAINTAIN PT. AIRWAY critical Procedure similar to defibrillation except sync button turned ON If patient stable, sedate prior( versed or fentanyl) Teach pt what to expect if it’s a planned procedure. Medication Will be uncomfortable Burn marks from pads HAIRY person clip before Initial energy lower 50-100 joules (biphasic) 100 joules (monophasic) bigger punch one way $$$$ If patient becomes pulseless, or rhythm turns to v-fib turn off sync button and defibrillate Synchronized Cardioversion TX's ( Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG Synch on the R wave) is the electrical management of choice for atrial fibrillation ( with a pulse), supraventricular tachycardia (SVT)(with a pulse) and ventricular tachycardia (with a pulse) PAC (Premature Atrial Contraction)atrium to soon ( a beat too soon) HEALTHY HEART OK DONT TREAT) ( pt with dis heart issue monitor is it just a PAC or V-tach? V-tach needs follow up •contract origin in ectopic focus in the atrium in =location other than SA node $$ p wave looks weird not fitting in it is coming from a differ location **Single abnormal beat that originates in the ventricle** $$ SA node going but has a friend in there that shouldn't be sending his own stimulus$$ travels across atria by abnormal pathway creating distorted P wave -may be stopped delayed or consulted normally at the AV Manifest: -heart skips a beat _ palpitations normal heart (healthy heart DONT TX it's OK) -caffeine, emotional stress, fatigue, tobacco, alcohol Also: -hypoxia, elect imbal DIS: -hyperthyroidism, COPD, CAD, valvular disease HEALTHY heart= isolated PAC are ok Causes: -stress, fatigue, caf, tobac, alcho, hypoxia, elect imbal, dises states HEART dis pt. watch for more serious dysrth-supraventricular tachy TX; withhold from stimulant RX : bet blcker used to < PAC's