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Cardiovascular
PPT 1 for Cardio
| Term | Definition |
|---|---|
| Pacemaker cells | Spontaneously create action potential; primary are located in the SA node of the heart. Generate impulse at 60-100 times a minute |
| Sympathetic nervous system | Increases firing rate of the SA node. Increases heart rate (norepi and epi release) |
| Parasympathetic nervous system | Decreases firing rate of the SA node. Decreases heart rate. (acetylcholine release) |
| One full contraction of the heart | 1. Action potential created by SA node 2. reaches AV (delayed for filling in ventricles) 3. Bundle of His 4. Bundle Branches (right and left) 5. Purkinje fibers into ventricles |
| Order of Placing Leads | V1, V2, V4, V3, V5 and V6 (in that order) |
| What is needed to place a 12 lead? | Site needs to be clean, dry, free from oils and lotions. Do not place leads over pacemaker or devices. Check expiration date on electrode package |
| P wave | Depolarization of the right atria; latter part of P wave represents depolarization of the left atrium. |
| Q wave | depolarization of interventricular septum. Deflects downward because septum depolarizes left to right |
| R wave | Early ventricular depolarization; reflects signal spreading through largest part of the heart. |
| S wave | final ventricular depolarization. Deflects downward as depolarization moves from bottom of ventricles, upward via Purkinje fibers |
| T wave | Ventricular repolarization begins at apex causing this wave |
| 5 steps to analyzing rhythms | Regularity, rate, P wave morphology, PR interval, QRS complex duration and morphology |
| Regularity | Measure from the tip of one R wave to the next. Considered regular or constant when the distance apart is the same or varies only by 1 1/2 small boxes. |
| Rate | Measure from R-to-R wave to determine ventricular rate, measuring from P-to-P wave to determine atrial rate. Count \number of small boxes between the waves. Divide by 1500 to calculate rate of normal rhythm. For irregular, count cardiac complexes x10 |
| P wave morphology | Are they present? Is there one for every QRS complex? Are they discernable. should be upright, rounded |
| PR interval | Represents the time from atrial depolarization to ventricular depolarization. Measure from the beginning of the P wave to the beginning of the QRS complex (3-5 small boxes). Look at whole strip |
| 1st degree AV block analyzed | Rate is normal, rhythm: regularity of underlying rhythm, P wave is same as underlying rhythm, PR is prolonged (>0.20), QRS normal. "IF R IS FAR FROM P - YOU HAVE 1ST DEGREE". Usually benign, patients are asymptomatic. NO TREATMENT |
| 1st degree AV block causes | older age, myocardial infarction, coronary artery disease, hyperthyroidism, electrolyte imbalance, drugs (digoxin, beta blockers, calcium channel blockers) |
| QRS complex | is there one for every P wave? Measure from beginning of Q to end of S. (0.04-0.10 seconds). Widened may be indicative of bundle branch block, electrolyte imbalance and/or drug toxicity |
| Afib patho | Most common arrythmia; caused by erratic electrical activity in the atria. Overwhelms the AV node, irregular rapid HR. |
| Afib symptoms | chest pain, palpitations, dizziness, lightheadedness, syncope, diaphoresis, reduced exercise tolerance, anxiety, shortness of breath, weakness, fatigue, some pts will be asymptomatic |
| Afib analyzed | Rhythm is irregularly irregular; atria at 350-400 BPM, ventricular rate is variable slower than atria. P wave is not detectable. Less than 100 bpm is controlled, over is uncontrolled (Afib with RVR) |
| Afib assessment | LOC, palpable pulse, HR and BP, 12 lead, underlying causes |
| Afib causes | surgery/cardiac procedures, acute MI, HTN, obesity, severe mitral valve dx, thyrotoxicosis, pericarditis, CAD, diabetes, CKD, COPD, cardiomyopathy |
| Afib treatment | Rate control: calcium channel blockers, beta blockers (slows HR, decreases workload/O2 demand), Rhythm control: amiodarone, cardioversion (must hold digoxin 48 hours prior), oxygen for cardiac output |
| Complications from Afib | thromboembolic risk (blood pools in atria = increased risk of stroke), heart failure, decreased cardiac output (compensatory tachycardia) |
| Left sided HF | Fluid in lungs (drowning) |
| Right sided HF | Fluid in veins (swelling) |
| Normal sinus rhythm | 60-100 bpm, regular rhythm, P wave precedes every QRS, PR interval is consistent. Normal rhythm originates in the SA node |
| Sinus bradycardia analyzed | Rate is less than 60; Regular rhythm with normal P wave and QRS. |
| Sinus bradycardia nursing interventions | Notify dr (even if this is baseline for pt), obtain 12 lead, assess for: LOC, palpable pulses and BP; |
| Causes of sinus bradycardia | Hypoxia, electrolyte imbalance, may occur during sleep, hypothermia, well trained athletes, med toxicity of digoxin of CCB overdose |
| Sinus bradycardia symptoms | Often asymptomatic; can have dizziness, anxiety, syncope, chest pain, hypotension, SOB, diaphoresis |
| Treatment of sinus bradycardia | Assess and treat cause; oxygen, atropine 0.5 mg IV push (increases SA node stimulus), pacemaker |
| Sinus tachycardia analyzed | 100-180 bpm; regular rhythm, normal P wave, PR interval and QRS is normal. |
| Sinus tachycardia causes | fever, anemia, hypotension, hypovolemia, PE, MI, infection, electrolyte imbalance, stimulants, pain/stress |
| Sinus tachycardia symptoms | can be asymptomatic; dizziness, lightheadedness, syncope, SOB, diaphoresis, anxiety, hypotension, palpitations |
| Sinus tachycardia treatment | Under 150: observe for decompensation, treat cause. Above 150: vagal maneuvers, carotid massage, beta blockers (atenolol, metoprolol, carvedilol, sotalol), defib pads may be needed |
| Supraventricular tachycardia analyzed | Regular, vent rate 150-250 bpm, not discernable P wave, PRI not measurable, QRS is normal but narrow; LIFE THREATENING. Will cause death if not treated |
| Paroxysmal SVT | Intermittent SVT that has sudden onset and resolves quickly |
| Causes of SVT | hypovolemia, hypoxia, acidosis, hypo or hyperkalemia, toxins, MI, PE, hypoglycemia, hypothermia, cardiac tamponade |
| Treatment of SVT | based on symptoms and underlying rhythm (sinus tach, atrial tach, afib RVR, aflutter RVR) |
| Atrial flutter analyzed | Rate is wide range of BPM, rhythm is usually regular, P wave is sawtooth pattern, PR interval is not measurable, QRS is normal. Same rhythm as afib but P wave is visible (sawtooth is distinction). Increased risk of blood clots |
| Aflutter causes | coronary artery disease, hypertension, mitral valve disorders, pulmonary embolism, hyperthyroidism, cardiomyopathy, drugs (digoxin, epi, quinidine). |
| Aflutter meds and treatment | Treatment: radiofrequency catheter ablation, cardioversion in unstable patient. Meds: calcium channel blockers, beta blockers, antidysrhythmias, anticoags (warfarin) |
| Premature atrial contractions (PACs) | Normal sinus rhythm. Pacemaker cell fires earlier than expected. Causes include hypoxia, stimulants (caffeine, infection, digoxin toxicity), CAD. Treatment is to monitor frequency and address or eliminate cause |
| Premature Ventricular Contractions (PVCs) | Normal sinus rhythm. Wide and bizarre QRS, signal fires earlier than expected in ventricles. Causes are hypoxia, stimulants, CAD, MI, cardiomyopathy, electrolyte imbalances, HTN, recreational drug use. Treatment: treat cause and assess LOC/Pulses/VS |
| PVCs symptoms | dizziness, lightheadedness, syncope, SOB, diaphoresis, anxiety, palpitations, hypotension |
| V tach analyzed | Atria are not measurable and ventricles are usually regular, rate is 150-250 bpm, P wave is absent and PRI is unmeasurable, QRS is wide and bizarre. Occurs when ventricular ectopic focus fires repeatedly. LIFE THREATENING, LEADS TO DEATH. |
| Causes of vtach | MI, CAD, electrolyte imbalance, cardiomyopathy, drug toxicity, CNS disorders, hypovolemia, acidosis, hypoglycemia, hypoxia, hypothermia, cardiac tamponade, PE |
| Stable patient presenting with vtach | Has a pulse. Will have symptoms of dizziness, lightheadedness, syncope, diaphoresis, anxiety, palpitations, hypotension, SOB. Treatment is to treat cause with vagal maneuvers, antiarrhythmic meds, and cardioversion. |
| Unstable patient presenting with vtach | No pulse, unresponsive, no BP. Treat cause with CPR, defib, epi, vasopressin, antiarrhythmic meds |
| Ventricular fibrillation analyzed | No rate, irregular and chaotic rhythm, absent P wave, PRI interval and QRS. No contraction with quivering ventricles. NO cardiac output and can be fatal with no treatment. |
| Symptoms of Vfib | unconscious, pulseless, no BP, apneic |
| Treatment of Vfib | Immediate CPR, treat causes, O2, ACLS (advanced cardiovascular life support) with defib |
| Medications given for Vfib | epi, amiodarone, vasopressin, antiarrhythmics |
| Synchronized cardioversion | A synchronized circuit in the defib delivers a shock on the R wave; lower dose of energy and switch must be ON. Can be used for vtach with pulse, aflutter and afib |
| Defibrillation | asynchronous, high dose of energy delivered. switch must be OFF and can be used for vfib, pulseless vtach. |
| Idioventricular rhythm analyzed | SA and AV nodes fail; atria rhythm is not measurable but vent is normal, usually less than 40 bpm but can be up to 100 in accelerated idioventricular rhythm (AIVR). P wave is absent and PRI not measurable. WRS is uniform but wide/bizarre |
| Causes of idioventricular rhythm | MI, post cardiac arrest, drug toxicities, electrolyte imbalance, myocarditis, cardiomyopathy, congenital heart disease |
| Symptoms of idioventricular rhythm | dizziness, lightheadedness, syncope, SOB, diaphoresis, anxiety, palpitations, hypotension and decreased LOC |
| Management of idioventricular rhythm | treat the underlying cause; assess VS, LOC, pulses. PREPARE PATIENT FOR PACING. Continuous ECG monitoring |
| Asystole | FATAL; no measurable electrical activity. Check more than one lead. Symptoms include unresponsiveness, no pulse, no BP. Treat with CPR, causes and give epi! |
| 2nd degree AV block I (Wenckebach) analyzed | irregular rate less than 60 bpm, irregular rhythm. PRI gets longer until QRS is dropped, then resets and starts over. "LONGER LONGER LONGER DROP, NOW YOU HAVE WENCHEBACK". Not all atrial impulses get through AV node to ventricles |
| Treatment of Wenchebach | symptomatic: atropine, temporary pacemaker. Asymptomatic: transcutaneous pacemaker on standby (watch VS, 12 lead and put on O2) |
| Causes of Wenchebach | drugs, CAD, myocardial ischemia, AV node ischemia |
| 2nd degree AV block II (Mobitz 2) analyzed | rate is slower, rhythm is irregular, more P waves present with a prolonged PR interval. Widened QRS. "IF SOME PS DONT GET THROUGH YOU HAVE MOBITZ 2." A serious type of block with symptoms of poor perfusion |
| Causes of Mobitz 2 | Rheumatic fever, CAD, MI, drug toxicity. |
| Treatment of Mobitz 2 | Temporary pacemaker, permanent pacemaker if pt becomes symptomatic (angina and hypotension) |
| 3rd degree AV block analyzed | Atrial rate is 60-100, vent is less than 40 bpm. Irregular rhythm with normal P wave (no connection to QRS with PR interval as inconsistent.) QRS is normal or widened. "IF Ps AND Qs DONT AGREE, YOU HAVE A 3RD DEGREE," aka complete heart block |
| Causes of 3rd degree block | CAD, MI, myocarditis, scleroderma, digoxin, beta and calcium channel blockers. Risk of ischemia, HF, shock, asystole and DEATH |
| Treatment of 3rd degree block | Permanent pacemaker ASAP; transcutaneous pacemaker until this can be done. Dopamine, epi, increased HR until pacemaker pacing starts |
| Transcutaneous pacemaker | Pads on skin, external pacing. Pacer spike before the QRS. Sedation is often needed and done pretty quickly |
| Transvenous pacemaker | Wire is inserted into the right ventricle, connected to external pacemaker. Packer spike before QRS |
| Transthoracic pacemaker | surgically placed wire in atrium or ventricle that is external. Spike before P wave or before QRS |
| Atrial pacing | wire is placed in atrium and it spikes before P wave |
| Ventricular pacing | Wire is placed in the ventricle and it spikes before QRS wave |
| Biventricular pacing | wires are placed in both ventricles, double spikes before QRS. Another is the dual chamber pacing with wires in both the atria and ventricles with a spike before P wave and QRS |
| Assessment for dysrhythmias | 12 lead, determine rhythm, is pt symptomatic? check VS for decreased CO/HR, compensatory (SOB, tachypnea), SNS response (diaphoresis), chest pain, poor perfusion, edema, GI s/s (N/V) |
| Nursing actions for dysrhythmias | administer antiarrhythmic meds, perform ECG, be prepared for CPR/defib and emergency meds; document |
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