Week 2: Intro to EKG/Cardiac Arrhythmias
Ventricular paced rhythm
Show up as spikes (pacemaker spikes) 1 spike = (depending where but in this pic) is indicating the pacemaker is initiating impulse prior to each ventricular beat We know its a ventricular pace maker because the spike is just before QRS complex
PR interval QRS interval ST segment T wave QT interval Times for PR, QRS, QT interval?
PR Interval: -P-Wave is the beginning of atrial depolarization -The PR interval is measured from the beginning of the P wave to beginning of QRS complex -Normal PR interval = 0.12 to 0.20 second QRS Interval: -Ventricular depolarization -Normal - 0.06 to 0.12 second ST Segment: -Look for depression or elevation (want it to be flat?) -ST elevation: myocardial injury* (myocardial infarction) -ST depression: reciprocal changes, digoxin, and ischemia -Above or below baseline = can indicate ischemic changes for the pt T Wave: -Ventricular repolarization* -Follows a QRS complex -Bigger than a P wave* -No greater than five small boxes high -Inversion (upside down) indicates ischemia to myocardium (standard leads) QT Interval: -Beginning of QRS complex to end of T wave -Range = 0.32 to 0.50 second -Varies with heart rate (men shorter length, women longer length) -Gender differences (men's measurements are typically shorter) -Mathematical formula is use to correct for variations in heart rate (QTc) (formula corrected or calculated to give an average) -Prolonged QT interval can lead to life-threatening dysrhythmias! -0.50 seconds... need to monitor the patient closely and track QT Normal sinus rhythm -Originates in the SA node -Regular rhythm -Rate 60-100 BPM, normal P wave before QRS (most nurses like lead II) Normal Values to Know**: PR interval - 0.12 - 0.20 QRS interval - 0.06 - 0.12 QT interval - varies with gender and heart rate; requires a mathematical correction factor to measure. (0.32 - 0.50) QTc - Correcting for HR extremes, improves measurement reliability.
PR interval? (time)* QRS interval? (time)* QT interval? (time) U wave? (what does it indicate)
PR interval* = 0.12-0.2 seconds (important for heart blocks) QRS *= 0.06- .12 sec QT interval* = depends upon HR and sex (ventricular depolarization to end of venticular repolarization) U wave = sometimes see, could be abnormality in electrolytes/ischemia. Small ones we don't really have to worry about?
What does hyperkalemia look like on an EKG?
Peaked T waves! K+ can be up to 6/7
SA Node (Sinoatrial) Dysrhythmias Sinus Arrhythmia
-Normal sinus rhythm -Rate varies with respirations -- from engagement of the sympathetic nervous system as you breathe in (HR increases) and parasympathetic as you breathe out (HR decreases) Inspire = HR increases Expire = HR decreases -Indication of autonomic nervous system function (is functioning well) -Rarely affects hemodynamic status (normal for children < 12) AKA Respiratory Sinus Arrhythmia Book: Sinus arrhythmia* (resp): cyclical change in HR associated with respiration. The HR slightly increases during inspiration and slightly slows during exhalation because of changes in vagal tone. ECG shows alternating patterns of faster/slower HR that changes with the resp cycle. Rate: atrial/ventricular beats between 60-100 BPM Regularity: rhythm is cyclically irregular, slowing with exhalation and increasing with inhalation Interval measurements: normal Shape/sequence: normal Patient response: tolerated well Causes: N/A Care/treatment: No treatment required
Ventricular Dysrhythmias Ventricular Tachycardia (V-tach, VT) What are the two types?
-Rapid, life-threatening dysrhythmia Three or more PVCs in a row Fast rate (>100 beats/min) Initiated by ventricles Two types: Monomorphic - unifocal beats (arising from one place in the ventricle) Polymorphic - multifocal beats (arising from many places in the ventricle cells) -- not identical Book: Ventricular tachycardia (VT)*: is a rapid, life-threatening dysrhythmia originating from a single ectopic focus in the ventricles. It is characterized by at least 3 PVCs in a row*. VT occurs at a rate > 100 BPM and as high as 250 BPM. Depolarization of the ventricles is abnormal and produces a widened QRS complex. The patient may or may not have a pulse. The P waves are usually absent, if they are present, they have no association with the QRS complex (they may appear to be randomly scattered throughout the rhythm but they are fired at a consistent rate from the sinus node - AV dissociation - another clue its VT.) Occasionally a P wave will "capture" the ventricle because of timing of atrial depolarization interrupting VT - this capture beat is also a clue to VT. -Torsades de pointes (twisting about the point) is a type of VT caused by a prolonged QT interval often caused by a magnesium deficiency*. It is characterized by both positive and negative complexes and moves above and below the isoelectric line. Can be caused by an increase in QT/QTc intervals. Rate: HR 110-250 BPM Regularity: regular unless capture beats occur and momentarily interrupt the VT Interval measurements: No PR interval, the QRS complex is greater than 0.12 seconds and often wider than 0.16 seconds Shape and sequence: QRS complex is consistent in shape but appears wide and bizarre. Patient response: If enough CO is generated by the VT, a pulse and BP are present. If CO is imparied, the patient has s/s of low cO and may experience cardiac arrest Causes: Hypoxemia, acid-base imbalance, exacerbation of HF, ischemic heart disease, hypokalemia, hypomagnesemia, GT prolongation and more. Care and treatment: determine whether pt has a pulse. If no pulse = BLS measures (defibrillation,) if pulse is present and BP is stable, treat with IV amiodarone or lidocaine. Cardioversion if they are hemodynamically unstable.
Cardiac cycle
1) Atrial diastole 2) Early atrial systole 3) Atrial systole, atrial kick 4) Early ventricular systole 5) Ventricular systole 6) Early atrial diastole
Cardiac Conduction Pathway 1) SA node* 2) AV node* 3) ? 4) ? 5) Purkinje fibers* BPM for stared?
1) SA node (beats at 60-100 bpm) -Depolarization begins -Atrial contraction (expels blood out of atrium into ventricles or atrial kick! -Impulse is usually initiated in the SA node, the eclectic signal stimulates the atrial muscle (atrial systole) that causes the atria to contract simultaneousl;y and eject their blood volume into the ventricles (called atrial kick) -Atrial kick = contributes about 30% more blood into the caridac output of the ventricles -SA → AV node -Electrical pathways from the SA node to AV node - called intranodal 2) AV node (beats at 40-60 bpm) -Delays impulse to ventricles; allows for filling (of ventricles) -Back-up pacemaker if SA node is not working* -AV node = where junctional rhythms arise. No normal P wave (like seen in sinus rhythm) 3) Bundle of His 4) Left and right bundle branches; fascicles 5) Purkinje fibers (15-40 bpm) -If you have a huge MI that damages both the SA node and AV node... The purkinje fibers can generate their own heart beat... Even though it's slow it can help
12 lead EKG How many electrodes? How many views?
10 electrodes (6 chest/precordial (V1-V6), 4 standard limb leads (I, II, III) (air, AvL, AvF) **The 6 precordial leads offer 6 views **The 3 hip/shoulder (standard leads) offer 6 views (because they are augmented/double up) (Also a 4th grounding lead)
ST elevation must appear in ____ continuous leads? Large ST elevations are referred to as __________?
2 Large ST elevations also referred to as "tombstone Ts" Get person to cath lab ASAP
12-Lead ECG What are the leads? (2 types) Impulses towards/away from electrode show what? V1-V6 are placed where? Which are unipolar? bipolar?
3 standard limb leads (I, II, III) (frontal plane) (bipolar) -3 augmented (voltage, different voltage to see waves better) limb leads (AvR, AvL, AvF) (look more towards center of heart) (look more towards center of heart from the limbs) (frontal view, vertically) 6 precordial (chest) leads (V1-V6) (horizontal plane of chest) Impulses toward electrode = Positive QRS complex on ECG Impulses away from electrode = Negative QRS complex on ECG aVR = from heart to right arm aVF = from heart to left foot aVL = from heart to left arm I- RA to LA (right arm to left arm) II - RA- LL (right arm to left leg) III - LA- LL (left arm to left leg) Precordial leads (chest leads); unipolar and placed over the heart V1: 4th intercostal space, right sternal border V2: 4th intercostal space, left sternal border V3: halfway between V2 and V4 V4: 5th intercostal space, left midclavicular line V5: 5th intercostal space, left anterior axillary line V6: 5th intercostal space, left midaxillary line RL (right leg) = grounding lead also called the reference lead... Helps us more accurately read the rest of the configuration 12 lead ECG but only 10 electrodes because some leads share an electrode (standard leads)
A narrow QRS complex (<0.12 seconds) indicates _____________ A wide QRS complex (>0.12 seconds) indicates ___________
A narrow QRS complex (< 0.12 seconds) indicates a supraventricular origin (above the ventricles) = Atria A wide QRS complex (≥ 0.12 seconds) indicates a ventricular origin
Atrial Dysrhythmias Supra-ventricular tachycardia Paroxysmal atrial tachycardia (PAT)?
Any tach arrhythmia that originates above the ventricles (supra), in the atrium outside the sinus node Paroxysmal Atrial Tachycardia (PAT): Example of one type of SVT Paroxysmal - Sudden; Occurs without warning Heart rate 150 to 250 beats/min HR > 150 = most likely to be supra ventricular* Regular rhythm P waves (if present) may merge in T waves QRS complex width is normal (0.06 - 0.012 sec) Hemodynamic effects vary **Not treated unless symptomatic (ends on its own)
Atrial Dysrhythmias Atrial Fibrillation with rapid ventricular response (RVR) How to calculate BPM on a 10 second strip?
Atrial Fibrillation where the ventricles are contracting rapidly. PR Interval = Unable to measure QRS Complex = .04-.12 secs QT = Unable to measure Irregular Rhythm Ventricular Rate >150 10 sec strip = multiply the number of beats by 6 to estimate BPM If there's 29 peaks multiply by 6 = 174 BPM
What do the following cause (PQRST)? -Atrial depolarization -Atrial repolarization -Ventriciular depolarization -Venticular repolarization PR segment, ST segment, J point? U wave?
Atrial depolarization: P wave Atrial repolarization: Tp wave (burried under QRS -- cant see it) Ventriciular depolarization: QRS complex Venticular repolarization: T wave PR segment = end of P wave to start of Q wave ST segment = end of S wave to start of T wave? J point* = junction of end of QRS and beginning of ST. Marking the end of depolarization and beginning of repolarization. U wave = slightly abnormally but usually don't treat
What is electrical automaticity? What are you checking for when checking a pulse?
Automaticity = Cardiac muscle can generate its own electrical activity Special group of cells generate the automatic impulse (where electricity is generated in the heart - keeps the heart beating, Pacemaker cells (nodal cells) Electrical activity + mechanical activity = Heart beat What are you checking? (When checking a pulse): -Pressure of blood flow on the artery (mechanical/muscular function of the heart) not the electrical activity. We can have electrical activity without having mechanical activity* (V-fib?)
Basic dysrhythmias are grouped by which anatomic areas? (3) What additional 2 areas?
Basic Dysrhythmias Grouped by anatomic areas: 1) SA node 2) Atria 3) Ventricles Additional abnormal rhythms: -AV node (junctional rhythms) -AV blocks **Anything that arises from the SA node will have a P wave!!
Permanent pacemakers? What can they pace? What do they treat? Dual pacemaker?
Can pace atria, ventricles, or dual chamber (both atria and ventricle) They are inserted transvenously Can be used for heart blocks, symptomatic bradycardia Teachers notes: demand pacemaker, or permanent pacemaker. Can tell with pacer spikes on EKG**. Dual chamber will pace atria and ventricle. The Permanent pacemaker: can pace atria, ventricles, or dual chamber Inserted transvenously -Used for heart blocks, symptomatic brady cardia
Cardiac action potential
Cardiac action potential: consists of phases called depolarization, repolarization and resting/polarized state of the cell. Resting (polarized) state of the cell = inside the cell is predominantly negative (-) and the outside is positively charged (+). There's a higher concentration of Sodium (Na) outside the cell causing the outside to be positive (+) and the inside of the cell to be more negative (-) with higher levels of Potassium (K) Voltage during the resting period is - 90 mV of the interior cardiac muscle cell (+30 during depolarization aka contraction?) Voltage of the pacemaker cells in the SA and AV nodes is - 65 mV Stimulation of Cardiac muscle cells via electrical impulse = changes the permeability of myocardial cell membranes Sodium (Na) ions rush INTO the cell and Potassium (K) ions rush out of the cell. This causes a more positively charged cell interior. The first phase of the action potential occurs when the cell membrane reaches - 65 mV (threshold) - sodium rushes into the cell; the cell interior quickly reaches + 30 mV resulting in depolarization Following this is the plateau phase (calcium enters the cell) The next phase is the resting state with a polarity of - 90 mV again
Ventricular Dysrhythmias Ventricular Fibrillation (V-Fib, VF) Treatment?
Chaotic pattern No discernible P, Q, R, S, or T waves (V-tach has QRS complex)* Coarse vs fine: -More electricity (coarse) fine (less electricity and harder to recover from) **Worse than V-tach No cardiac output Life threatening: **Immediate emergency defibrillation Book: Ventricular fibrillation (VF)*: is a chaotic rhythm that is characterized by a quivering of the ventricles which results in total loss of cardiac output and pulse - It is a life threatening emergency (leads to asystole.) VF produces a wavy baseline without a PQRST complex. Rate: HR not discernible Regularity: not discernible Interval measurements: no waveforms Shape and sequence: the baseline is wavy and chaotic with no PQRST complexes Patient response: the patient is in cardiac arrest Causes: VF can be caused by ischemic and valvular heart disease, electrolyte imbalances, and QT prolongation Care and treatment: begin BLS immediately and ACLS interventions
Normal cardiac function Depolarization leads to _____ Repolarization leads to ______ Sodium / potassium at rest? -Resting membrane potential? -Which cells are outside/inside the cell at rest? At depolarization? -What is Ca+ responsible for?
Depolarization -> Leads to contraction* (D → C) At rest -> Na+ outside cell; K+ inside the cell Change cell permeability (Na enters, K leave cells, Ca slowly entering cell as heart contracting) Repolarization begins -> Leads to resting and filling of ventricles -Resting membrane potential = - 90 mV (inside the cell is more negative than the outside) -Main cells found outside the cell at rest are sodium (Na+) and chloride (Cl-) The action potential (depolarization) causes the opening of sodium channels that allow Na+ to flow into the cell Potassium channels open, K+ leaves the cell causing repolarization Calcium (Ca+) is responsible for the plateau phase of the action potential*
Electrical activity versus muscular contraction? Depolarization --> Repolarization -->
Depolarization leads to Contraction Repolarization leads to Relaxation ECG is evidence of electrical activity*, not mechanical contraction (no pulse = no muscular contraction) In other words, electrical activity can take place without muscle contraction. **You can have electrical activity on the monitor without muscular activity taking place
Dual paced rhythm
Dual paced rhythm shows a pacemaker initiates impulse prior to each atrial and ventricular beat. (will see two different spikes on EKG) Atrial pacemaker spikes occur where the P wave is, QRS pacemaker spike occur before QRS complex
Atrial Dysrhythmias Premature Atrial Contractions (PACs)
Early beats initiated in the atrium For pt in NSR, it is a beat that arrives too early (interrupting regularity of the rhythm) P waves and PR interval may vary Non-compensatory pause**: Is the time interval on an ECG after a PAC that has the capacity to enter a sinus node and rest it's timing. Because PACs reset the sinus pacemaker, the next sinus beat will not appear when it should have P wave may be found in T wave Beats arrive early P wave is buried in the T wave -A few random ones are not a big deal* -Treat when the patient becomes symptomatic -Coffee, stress, little sleep can all cause PACs Book: Dysrhythmias of the Atria: Normally the SA node is the dominant pacemaker that initiates heart rhythm, however, cells outside the SA node within the atria can create an ectopic focus that can cause dysrhythmia. An ectopic focus is an abnormal beat or rhythm that occurs outside the normal conduction system (atrial dysrhythmias arise in the atrial tissue.) Premature atrial contractions (PAC)*: is a single ectopic beat arising from atrial tissue (NOT THE SINUS NODE.) The PAC occurs earlier than the next normal beat and interrupts the regularity of the underlying rhythm. The P wave of the PAC has a different shape than the sinus P wave because it arises from a different area in the atria. It may follow the T wave preceding a normal beat. Following the PAC, a pause occurs and the underlying rhythm typically resumes. The pause is noncompensatory (meaning the P wave following the pause does not occur on time**) PACS are common and show an irritable area in the atria. Nonconducted PACS are beats that create an early P wave but are not followed by a QRS complex. The ventricles are unable to depolarize in response to early stimulus because they are not fully repolarized (this creates a pause, the P wave occurs either in or after the T wave.) Rate: matches the underlying rhythm Regularity: PAC interrupts the regularity of the underlying beat (so irregular) - PAC is followed by a non-compensatory pause. Interval measurements: PAC may have different PR interval than normal sinus beat (usually shorter) Shape/sequence: P wave with PAC is a different shape than sinus P wave. The T wave preceding the beat may be distorted if the P wave of the PAC lies within it Patient response: PAC's are usually well tolerated (patients may complain of palpitations) Causes: stimulants like caffeine, tobacco, myocardial hypertrophy/dilation, ischemia, lung disease, hypokalemia, hypomagnesemia may cause PACS. May also be a normal variant. Care/treatment: No treatment indicated for PACS
Atrial Dysrhythmias Atrial Flutter (A-flutter) HR? Caused by? Goals? How to calculate atrium rate?
Ectopic foci in atria (outside the sinus node), heart disease Classic "sawtooth" pattern in leads II, III, and aVF (narrow QRS) Atrial rate fast and regular with AV block (blockage to internodal pathway) Patients present with heart rate of 250 to 350 beats/min Degree of conduction varies; may be 1:2, 1:3, 1:4, etc (1 QRS per 4 flutter beats = conduction ratio of 1:4) -- First flutter may be really small but we still count it (might be buried in QRS) Can be caused by a number of disorders, including heart failure, obesity, obstructive sleep apnea, sinus node dysfunction, pericarditis, pulmonary disease, and pulmonary embolism. The incidence increases markedly with age, ranging from 5 per 100,000 person years under age 50, to 587 per 100,000 person years over age 80. Goals: -Control of the ventricular rate -Revert to and maintain normal sinus rhythm (NSR) -Prevention of systemic embolization For patients who require immediate rate slowing, and for whom cardioversion (and the restoration of sinus rhythm) is not chosen, first line medications for treatment are diltiazem (calcium channel blocker) or esmolol (beta blocker). In this case, you will find 9 R-waves in the 6-second strip or 90 beats per minute. *One QRS per 4 flutter beats Conduction ratio = 1:4 Calculate the atrium by taking how many flutter beats and multiplying by the BPM ... 110 BPM x a conduction ratio of 3 flutter waves = 330 BPM for the atria Book: Atrial Flutter*: arises from a single irritable focus in the atria. The atrial focus is an extremely rapid and irregular rate (240-320 BPM.) An ECG with a rate faster than 340 BPM = type II flutter. The P waves are called flutter waves because of their sawtooth appearance. The number of flutter waves to each QRS complex is called the conduction ratio. Flutter waves occur through the QRS complex and the T wave and often alter their appearance Rate: Atrial rate between 240-320 beats/min but is typically 300 BPM (ventricular rate is determined by the conduction ratio of the flutter waves) Regularity: flutter waves are regular, but the QRS complex and T waves may be irregular depending on the conduction ration Interval measurements: No PR interval is present, QRS and QT intervals normal unless distorted by flutter eave Shape/sequence: P waves consistent in shape and look like teeth on saw tooth blade. QRS waves altered in shape by flutter waves Patient response: usually asymptomatic unless atrial flutter results in tachycardia called rapid ventricular response (RVR) - Atrial flutter with RVR occurs when the atrial impulses cause a ventricular response greater than 100 Bpm Causes: Lung disease, ischemic heart disease, hyperthyroidism, hypoxemia (low o2 in blood), heart failure, alcoholism Care/treatment: alteration in atrial blood flow can lead to blood stasis and cause clots. Patients with atrial flutter usually receive chronic antithrombotic therapy. Rate controlled with medications that block the AV node.
Atrial Dysrhythmias Atrial Fibrillation
Erratic impulse formation in atria No discernible P wave (hallmark ECG sign) Irregular ventricular rate (hallmark ECG sign) Aberrant (abnormal) ventricular conduction can occur Results in loss of atrial kick (last bit of atrium squeezing to expel blood down into the ventricles) High risk for stroke or pulmonary emboli (because the blood pools without the atrial kick*) - need to be on anticoagulation* Rate is irregular P waves are indistinct or absent; not uniform Book: Atrial fibrillation*: most common dysrhythmia observed in clinical practice. It arises from multiple ectopic foci in the atria causing chaotic quivering of the atria and ineffectual atrial contractions (looks like squiggly line.) The AV node is bombarded with hundreds of atrial impulses and conducts them in an unpredictable manner to the ventricles. The atrial rate may be as high as 700 and no P waves can be identified. Causes extremely irregular ventricular response (irregularly irregular) - also causes loss of atrial kick*. If too many impulses conduct to the ventricles, atrial fibrillation with RVR (irregular Heart beat) can compromise CO. When atrial fibrillation occurs sporadically, it's called paroxysmal atrial fibrillation. -One complication of atrial fibrillation is thromboembolism from the blood that collects in the atria (it's agitated by fibrillation and normal clotting is accelerated.) Small thrombi called mural thrombi begin to form along the walls of the atria - the clots can dislodge and cause PE or stroke. Rate: Atrial rate is uncountable (too fast?); ventricular rate may vary widely Regularity: ventricular response is irregularly irregular. Interval measurements: PR interval is absent. QRS complex and QT interval are normal in duration unless a bundle branch block is present Shape/sequence: No recognizable P waves present, the isoelectric line is wavy, QRS complex is consistent in shape unless aberrantly conducted, followed by T wave Patient response: pt may or may not be aware of atrial fibrillation, if ventricular response is rapid, the patient may show signs of decreased CO or worsening HF symptoms Causes: Ischemic heart disease, valvular heart disease, hyperthyroidism, lung disease, HF, aging. Care/treatment: anticoagulants* (they are at risk for throwing a clot), ventricular rate is controlled by giving AV nodal blocking agents, emergent cardioversion is considered if tachycardia is associated with hemodynamic instability.
What are atrial dysrhythmias? Causes? Width of the QRS?
Impulses are initiated from upper portion of the heart Ectopic and escape beats arise within the atrium (outside the SA node) May be regular or irregular rhythm We know it's coming from the Atrium if the Width of QRS complex is WNL (0.06-0.12 sec) Causes: -Stress/sleep/nicotine (Anything that can trigger fight/flight) -Electrolyte -Imbalances (hypokalemia, hypomagnesemia) -Hypoxia (sleep apnea) -Cardiac muscle injury -Digitalis toxicity (overdose of digoxin) -Hypothermia -Hyperthyroidism -Alcohol -Pericarditis -Heart disease, other chronic diseases (diabetes, COPD) **Many of these diseases can lead to ventricular dysrhythmias
Ventricular dysrhythmias What are they? Common causes?
Impulses initiated from lower portion of the heart Ectopic and escape beats within the ventricles When depolarization occurs, electricity does not follow normal nodal pathways - goes on a detour - leading to abnormally wide, bizarre QRS complex (starts in the ventricles and goes the wrong way) Often irregular, but can appear regular (particularly at high heart rates) Width of the QRS complex is wide (>0.12 sec) Common causes: -Myocardial ischemia, injury, and infarction -Low potassium or magnesium -Hypoxia -Acid-base imbalances - can stimulate ventricular ectopy (associated with respiratory acidosis) Book: Ventricular dysrhythmias arise from ectopic foci (pacemakers outside the SA node) in the ventricles. The QRS complex is widened (> 0.12 seconds, often > 0.16 seconds) and has a bizarre shape. Most ventricular dysrhythmias have no apparent P waves. If a P wave is present, it is usually seen on the T wave of the following beat or has no relationship to the QRS complex and is dissociated from the ventricular rhythm. Ventricular dysrhythmias can be life threatening
Interpretation of rhythms 4 main steps?
Interpretation of Rhythms -Develop a systematic approach Four main steps: 1) Rhythmicity (is it regular or irregular?) 2) Rate (How many beats in 6 seconds?) 3) Waveform (Are there p, q, r, s, and t waves for every beat? Is the configuration uniform?) 4) Intervals (Elevated? Depressed? How wide?)
Lead II shows which plane? Lead V1 shows which plane? Leads I, II, III show ______ plane, V leads show ______ planes
Lead II = frontal plane* Lead V1 (chest lead) = Horizontal plane* You can think of "leads" as views. Leads I, II, lll (standard leads) "see" waveforms from the view of the frontal or coronal plane The V leads ""see" waveforms from the view of the horizontal or transverse plane **Leads V1 and III are the standard recommendations
Using calipers for measuring
Measuring R to R If no calipers, measure with piece of paper
Ventricular Dysrhythmias Asystole (Ventricular standstill)
No PQRST waveforms Assess in two leads. Why? (to make sure leads aren't loose! Assess pt first) No cardiac output Death Always confirm asystole in at least 2 leads! Book: Asystole*: characterized by complete cessation of electrical activity. A flat baseline is seen without any evidence of PQRST waveforms. A pulse is absent and there is no CO; cardiac arrest has occurred. Asystole often occurs following ventricular fibrillation* or ventricular escape rhythm. During cardiac arrest situations, if asystole occurs when another rhythm has been monitored, a check of two leads should occur to confirm asystole. Rate: heart rate is absent Regularity: heart rhythm is absent Interval measurements: no PQRST waveforms Shape and sequence: flat line on the monitor Patient response: patient is in cardiac arrest (dead, heart stopped) Causes: Asystole usually follows another dysrhythmia such as V-fib or ventricular escape rhythm Care and treatment: initiate BLS and ACLS protocols.
Normal sinus rhythm
Normal Sinus Rhythm (NSR)*: reflects normal conduction of the sinus impulse through the atria and ventricles; ANY deviation from sinus rhythm is a dysrhythmia NSR is initiated by an impulse in the sinus node → conductive fibers of the atria → AV node → slight pause → ventricles causing depolarization and resultant cardiac contraction in a timely and organized manner. Rate: atrial and ventricular rates are the same (60-100 BPM) Regularity: rhythm is regular Interval measurements: PR interval is 0.12-0.20 seconds, QRS is 0.06-0.10 seconds Shape and sequence: P and QRS waves are consistent in shame, P wave precedes every QRS complex which is followed by a T wave Hemodynamic effect: patient is hemodynamically stable
What is PQRST? Pathological Q wave?
P = Atrial depolarization (contraction of atria) QRS = Ventricular depolarization (contraction of ventricles) T = Ventricular repolarization (back to resting state, relaxation of ventricles) -R wave = always positive (going up) -Q and S wave = always negative (going down) -Q's are the FIRST deflections (going down) -S's are the deflection after an R wave (down) One cardiac cycle = has to have PQRST (to be in normal sinus rhythm) Very deep/defected Q wave (pathological Q wave) = myocardial infarction *PQRST = equidistant R->R intervals = sinus rhythm
What are the 4 phases of the cardiac action potential (ventricles)? Phase 0-4 mV for resting, threshold and depolarization?
Phase 0 (Rapid upstroke): Primarily Na+ channel opening -Sodium flows in the cell, potassium flows out Phase 1 (early rapid repolarization): Inactivation of Na+ current, opening of K+ channels Phase 2 (plateau phase): Balance between K+ and Ca++ currents Phase 3 (final rapid repolarization): Activation of Ca++ channels Phase 4 (right before? diastolic depolarization) Balance between Na + and K + currents Prior to depolarization: Na outside cell; K inside the cell (0 mV outside the cell, -90 mV inside the cell)(more negative outside with Na, more positive inside with the K) - BEFORE depolarization. Once depolarization occurs, they switch (rapid upstroke - contraction of ventricles) Phase 0: With the change in cell membrane permeability potassium and sodium channels open. Potassium will flow out of the cardiac myocyte, sodium will flow in. Depolarization - generating the QRS complex and contraction of the ventricles Phase 1: Na+ flow ceases leaving the cell as current of Na+ channels become inactive; K+ channels remain open (early repolarization) Phase 2: A balance between the currents of K+ and Ca++ is achieved (called the plateau phase) Phase 3: Activation of Ca++ channels (final rapid repolarization; readies for depolarization). The repolarization phase occurs because the Ca2+ channels gradually inactivate the K+ channels inhibiting any outward K+ current. Ca++ slowly enters cells - Repolarization -> activates myofilaments that will produce contraction (phase 3) Phase 4: Repolarized myocardium - Returning to the baseline (resting myocardium) - Resting (Phase 4): Sodium is outside of the cell and potassium is inside the cell. The electric charge outside the cell is positive (approximately 0 mV) and the electrical charge inside the cell is negative (as low as -90 mV). Depolarization will begin again with the change in cell wall permeability. - 90 mV = resting membrane potential - 65 mV = threshold (more channels open up allowing sodium to rush into cell) + 30 mV = results in depolarization Depolarization -Na outside cell; K inside the cell -Change cell permeability -Na enters cells; K leaves cells -Ca slowly enters cells -ATP needed to move electrolytes back to resting state Repolarization begins
Prolonged QT interval (> 0.5 seconds) can cause _________ Arrhythmia vs Dysrhythmia
Prolonged QT interval ( > 0.5 seconds) can cause Torsades de Pointes* Arrhythmia = abnormal/irregular rhythm (alteration in heartbeat) Dysrhythmia: bad or ill rhythm or simply an irregular rhythm (can be used interchangeably)
Cardiac conduction pathway Normal cardiac rhythm is __________ Where is the AV node located?
SA (right atrium) → AV (junction between R/L heart/upper/lower chambers) → bundle of his → R/L bundle branches → purkinje fibers Abnormal rhythms happen because the electrical rhythms happen abnormally (not starting in the SA/AV nodes) Normal cardiac cycle = equidistant apart. Normal sinus rhythm has PQRST waves with equal distance between each R wave. The AV node is between the RA/LA and upper/lower chambers of the heart
14 Rhythms to Know 1)Sinus node 2) Atria 3) Ventricles
SINUS NODE -Normal Sinus Rhythm -Sinus Tachycardia -Sinus Bradycardia -Sinus Arrhythmia -Sinus Pause/Arrest ATRIA -PACs -PAT or PSVT -A-Flutter -A-Fibrillation VENTRICLES -PVCs -Unifocal -Multifocal -V-Tach -Torsades de Pointes -V-Fib -Asystole
SA Node (Sinoatrial) Dysrhythmias Pause or Sinus Arrest Causes? Rhythm?
Sinus node fails to initiate impulse Causes: vagal reaction, heart disease, and drugs that slow heart rate Heart rate can be normal or slow Irregular rhythm **No QRS for 3 or more seconds*** Can decrease cardiac output Not usually a problem if it happens once... If happens frequently, maybe heart disease 15 boxes = 3 seconds Book: Sinus pauses*: occur when the SA node either fails to generate an impulse (sinus arrest) or the impulse is blocked and does not exit from the SA node (sinus exit block.) The result from the SA not firing is a pause without any electrical activity. Sinus arrest: failure of the SA node to generate an impulse is called sinus arrest. The arrest results from lack of impulse from the SA node. -The sinus beat following the arrest is NOT on time because the sinus node has been reset and the next sinus impulse begins a new rhythm** -The result is that no atrial or ventricular depolarization occurs for one heart beat or more* -If the pause is long enough, the AV node or ventricular backup pacemaker may fire, resulting in escape beats (junctional escape/ventricular escape beats) -Typically the SA node resumes normal generation of impulses following the pause
SA Node (Sinoatrial) Dysrhythmias Sinus Tachycardia Causes? Assess for what?
Sinus rhythm with a rate of 100 to 150 beats/min Causes: stimulants, exercise, fever, and alterations in fluid status (fluid deficit -- dehydrated) Assess for symptoms of low cardiac output (what pt reports, dizzy, lightheaded, weak) -There's a full cardiac cycle with each beat (PQRST) -Regular 12 beats in 6 seconds = 120 bpm (pic) Book: Sinus tachycardia*: HR > 100 BPM, results when the SA node fires faster than 100 beats/min. Sinus tachy is a normal response of sympathetic nervous system and normal in children under 6 years old* Rate: both atrial/ventricular rates are greater than 100 beats/min (can be as high as 180 BPM) Regularity: onset is gradual rather than abrupt, sinus tachy is regular or essentially regular Interval measurements: PR interval is 0.12-0.20 seconds, QRS is 0.06 -0.10 seconds Shape/sequence: P and QRS waves are consistent in shape, P waves come before QRS followed by T wave Patient response: the fast HR can cause a decrease in CO because of shorter filling time for the ventricles* Causes: Hyperthyroidism, hypovolemia, HF, anemia, exercise, use of stimulants, fever, sympathetic response to fear/pain/anxiety Care/treatment: The dysrhythmia itself is not treated, but the cause is identified and treated (give pain meds for pain, antipyretics for fever)
SA Node (Sinoatrial) Dysrhythmias Sinus Bradycardia Causes?
Sinus rhythm with rate less than 60 Causes: vagal (bearing down with BM), drugs (beta blocker), ischemia, ICP, and athletes (normal) Produce various hemodynamic responses (light headed, low BP, etc) -Full cardiac cycle with each beat -Regular 5 beats in 6 seconds = 50 bpm What does it mean to have symptomatic bradycardia? -- -Symptoms: Pt feeling weak, lightheaded, faint, cold, dizzy -Signs: vital signs, prolonged cap refill, pallor Book: Sinus bradycardia*: HR < 60 BPM. Normal heart rhythm for athletes or may occur during sleep. Usually is asymptomatic but can cause instability if it results in a decrease of CO. (assess pt for s/s of instability) Rate: both atrial and ventricular rates are < 60 BPM Regularity: rhythm is regular/essentially regular Interval measurements: normal but QT may be prolonged (from slowed HR) Shape/sequence: Normal P, QRS followed by T wave Patient response: may cause decrease in CO resulting in hypotension and decreased organ perfusion* Causes: Vasovagal response; medications like digoxin or AV nodal blocking agents (calcium channel blockers, beta blockers,) myocardial infarction, normal for athlete, increased ICP, hypoxemia, hypothermia Care/treatment: Assess for hemodynamic instability; if pt is symptomatic, interventions like atropine, transcutaneous pacing, dopamine, epinephrine can be given. (atropine is avoided for hypothermia.)
EKG boxes Small box ___ sec Large box ___ sec 5 large boxes = ___ sec 10 large boxes = ___ sec 15 large boxes = ___ sec mV of one large box?
Small box = 0.04 sec Large box = 0.2 sec (has 25 small boxes in it) 5 large boxes = 1 sec 10 large boxes = 2 sec 15 large boxes = 3 sec Height: -Large box = 0.5 millivolts (mV) -2 large boxes = 1 mV Horizontal axis = time, Vertical axis = amplitude Book: -The horizontal axis on an ECG paper measures time, the vertical axis measures voltage or amplitude. -Larger boxes contain 5 smoller boxes horizontally and vertically for a total of 25 small boxes per large box. 1 small box = 0.04 sec (40 ms) 1 large box = 0.2 sec The vertical hash marks on the ECG occur every 15 large boxes, between these marks is 3 seconds. (Normal strip shows 6-second interval) (30 large boxes = 6 seconds) (10 large boxes = 2 sec) The measurement of time on the ECG tracing represents the speed of depolarization and repolarization in the atria and ventricles and is printed at 25 mm/sec Each small box = 0.1mV in amplitude Low voltage and small waveforms are expected from the small muscle mass of the atria (PR interval), large-voltage and large waveforms are expected from the larger muscle mass of the ventricles (QRS)
What are the key electrolytes of normal cardiac function?
Sodium (Na+) Potassium (K+) Calcium (+) Magnesium is also an important electrolyte for cardiac function* (But there is not a specific Mg channel like for Na, K, Ca)
Waveforms and Intervals P wave PR interval QRS complex QRS interval T wave ST segment QT interval U Wave
The ECG tracing shows P, QRS, T waves that rise from the isoelectric line (flat line) P wave: represents atrial depolarization** -Normally does not exceed 3 boxes (3mm) in height. -The P wave indicates that the SA node initiated the impulse that depolarized the atrium (Atrial depolarization) -Changes in the shape or the intrinsic or baseline P wave can indicate the impulse atose from a site in the atria other than the SA node* PR Interval: -From the beginning of the P wave to the next deflection from baseline. -The PR interval measures the time it takes for the electrical impulse to depolarize the atria, travel to the AV node, and dwell there briefly before entering the bundle of His. -Normal PR interval = 0.12 - 0.2 seconds (3-5 small boxes wide) -Longer than normal means the speed of conduction is delayed to the AV node, shorter than normal means the speed of conduction is abnormally fast. QRS complex: represents ventricular depolarization** -*Atrial repolarization also occurs simultaneously to ventricular depolarization, but since the ventricles have a larger muscle mass, we see it better on the ECG (as QRS) -The classic QRS complex begins with a negative or downward deflection from the isoelectric line immediately after the PR interval (Q wave) -The Q wave may or may not be present before the R wave. If the first deflection from the isoelectric line is positive or upright, the waveform is called the R wave (tallest point) -The S wave is a negative waveform that follows the R wave (S wave deflects below the isoelectric line.) -Some patients have a second positive waveform in their QRS complex called the R prime -Pathological Q wave: (bad) has a width of 0.04 seconds and a depth greater than one fourth of the height of the R wave; represents myocardial infarctions and myocardial muscle death. QRS interval: is measured from where it leaves the isoelectric line of the PR interval to the end of the QRS complex. The waveform that initiates the QRS complex (whether it is Q or R wave) marks the beginning of the interval. -Normal width of the QRS complex is 0.06-0.10 seconds (1.5-2.5 small boxes.) A delay over 0.10 seconds can signify delay in conduction through the ventricles. T wave: represents ventricular repolarization** -In contrast to P waves which are usually symmetrical, T waves are usually asymmetrical. -Changes in T wave amplitude or direction can indicate electrical disturbances from electrolyte imbalances or from myocardial injury. -Hyperkalemia can cause tall, peaked T waves -Ischemia can cause flattened or inverted (upside down) T wave -**P waves come before the QRS, T waves follow the QRS. T waves normally have greater width and amplitude than the P because the ventricles are larger and produce a larger wave form than the P (Atria) ST segment: connects the QRS complex to the T wave and is usually a flat, isoelectric line. -The point where the QRS complex ends and the ST segment begins is called the J (junction) point -**To identify ST elevation, use the isoelectric portion of the PR segment as a reference for baseline. -Displacement in the ST segment can indicate myocardial ischemia or injury. QT interval: is measured from the beginning of the QRS complex to the end of the T wave. (total time taken for ventricular depolarization and repolarization**.) -QT interval becomes longer with slower HR and shortens with faster HR -Risk of lethal heart rhythm called torsades de pointes occurs if QTc is prolonged greater than 0.50 seconds. U wave: final waveform, follows T wave, represents repolarization of a small segment of the ventricles or delayed repolarization. -U wave is usually small and less than 2mm in heighter -Larger U waves can indicate hypokalemia, cardiomyopathy and digoxin toxicity Depolarization = corresponds with contraction of the heart muscle Repolarization = return of the ions to their previous resting state
Einthoven's Triangle
The triangle around the heart formed by the bipolar limb leads Standard Limb Leads* Lead 1 = Right arm (-) to left arm (+) Lead 2 = Right arm (-) to left leg (+) Lead 3 = left leg (+) to left arm (+) (left arm is more neg, look at next pic) **Going towards → most positive electrode = defects upwards on ECG paper (more neg → more positive) Standard leads: The heart is the negative pole for all augmented leads. The sensor on the skin is the positive pole.
Ventricular Dysrhythmias Monomorphic V-tach Polymorphic Ventricular Tachycardia (example? Treatment?
Types of V-tach Monomorphic beats: -Series of unifocal beats -HR estimate (first pic) = 220 BPM Polymorphic V-tach: Multifocal beats (arising from many ventricle cells) ex: R on T, Torsades de pointes Increased risk with long QT interval Potentially lethal Treatment: Magnesium* (reduced irritability of heart, relaxes heart) DO NOT defibrillate for polymorphic V-tach
V leads view what?
V leads (precordial leads) are placed on the chest Heart is negative (-) and the electrodes are positive (+) It views the heart from six positions in a transverse plane (towards the heart) Putting electrodes on shoulders/hip gives a lot less artifact (static) on ECG (RA, LA, RL, LL) V1/V2 = reflect downward V3 = starts to reflect more upward V4-V6 = reflect upward
Ventricular Dysrhythmias (PVCs) Ventricular couplet? When are PVCs dangerous? R on T?
Ventricular Couplet: -Two PVCs occur following three normal QRS complexes -The PVCs have the same morphology -This is a universal couplet When Are PVCs Dangerous?: -When they become frequent -Multifocal (more concerning than unifocal) because this means there is more than one area in the heart, specifically the lower chambers of the ventricles, that are irritable and generating abnormal beats, AKA ECTOPIC beats (Two or more beats in a row) Three or more beats in a row = Run of V-Tach R on T -PVC falls into the vulnerable period of the T wave -The ventricle attempts to contract at the same time it is attempting to relax -Ventricular tachycardia or fibrillation can result (PVC --> leads to more lethal dysrhythmia)
Ventricular Dysrhythmias Premature Ventricular Contractions (PVCs) What is a defining characteristic? Run of V-tach? PVC patterns?
Wide and bizarre beats Usually followed by a complete compensatory pause because the sinus node timing is not interrupted Compensatory Pause: Characteristic of a ventricular ectopic beat which fails to conduct retrogradely to the atria, hence leaving the sinus node undisturbed, i.e. the heart misses contraction of the atria; No p-wave to trigger a contraction of the atria. Atrial (PACs) = non compensatory Ventricle (PVCs) = compensatory pause because the ventricle beats are a little longer No p-wave = no atrial contraction. One sinus P wave isn't able to reach the ventricles because they are still refractory from the PVC The following sinus impulse occurs on time based on the sinus rate. This ability to "reset" and resume the normal heart rate has been hypothesized to be protective of the heart. However, not all PVCs are followed by a pause. If a PVC occurs early enough - especially if the heart rate is slow - the PVC may appear sandwiched in between two normal beats. In a complete compensatory pause occurs when the sum of the coupling interval and the compensatory pause is equal to twice the sinus cycle length Run of V-Tach = 3 or more beats in a row Patterns: -Couplets (Two PVCs with same morphology -- look alike) -Runs of Ventricular Tachycardia (V-Tach) -Bigeminy (every other beat is a ventricular premature beat) -Trigeminy (every third beat is a PVC) -Unifocal versus multifocal: -Unifolical = coming from one place in the ventricles (look alike)* -Multifocal = coming from multiple cells in heart (look different)* - more dangerous Book: Premature ventricular contractions (PVC)*: PVC's are early beats that interrupt the underlying rhythm. They can arise from single ectopic focus or multiple foci within the ventricles. -A single ectopic focus produces PVC waveforms that look alike (called unifocal PVCs.) Waveforms that arise from multiple foci are not identical and called multifocal PVCs. PVCs may occur in predictable patterns (every other beat, every third beat, etc.) Two PVCs in a row is called a pair, 3 or more is called nonsustained VT.The peak of the T wave through the downslope of the T wave is considered the vulnerable period, which coincides with partial repolarization of the ventricles. Rate: matches the underlying rhythm Regularity: rhythm is interrupted by the premature beat Interval measurements: there is no PR interval, and the QRS complex is greater than 0.12 seconds* Shape and sequence: QRS complex is wide and bizarre looking* Patient response: pt may have palpitations and may become symptomatic if PVCs occur frequently. Causes: hypoxemia (blood,) ischemic heart disease, hypokalemia, hypomagnesemia, acid-base imbalances, and increased catecholamine levels Care and treatment: treat if PVCs increasing in frequency (sometimes occur in health people and do not require treatment)
Who invented the electrocardiogram?
Willem Einthoven Invented the electrocardiogram 1903 Einthoven's String Galvanometer 1st ECG ECG or EKG? (Means the same thing, the K is cardiac in dutch/german)
