Cardiac Alterations
PR interval
(0.12-0.20 sec) Represents AV conduction time
Premature Atrial contractions (PACs): Cause
1. In a normal heart - Emotional stress, physical fatigue, caffeine, tobacco, alcohol 2. Hypoxia 3. Electrolyte imbalances 4. Disease states such as hyperthyroidism, COPD, CAD, valvular disease.
Ventricular Tachycardia
1. Irritable focus generating impulse is located within the ventricles 2. Causes...think back to the slide on causes of irritable foci within ventricles... 3. Rate <150-250
Rapid Estimation
1. Look at distance between R waves - 300,150,100,75,60,50 2. Less than 3 boxes = tachy 3. Greater than 6 boxes = brady
Leads (Electrodes)
1. Look at electrical activity from different angles 2. There is always a positive (or sensing) electrode which looks toward a negative electrode
AV Block: 1st Degree causes
1. MI, CAD, rheumatic fever, hyperthyroidism, electrolyte imbalances (hypokalemia), vagal stimulation. 2. Drugs such as digoxin, Beta blockers, calcium channel blockers, and flecainide.
AV Block: 1st Degree Patient Assessment
1. Patients are asymptomatic 2. May consider causative factors that can be changed. 3. Usually benign, but if associated with an acute MI it can lead to higher degree blocks - monitor for any new change
Premature Beats
1. Premature beats can originate from the atrial, AV junction, or the ventricles 2. The result of an irritable foci spontaneously firing a single stimuli 3. Occurring earlier than expected 4. The corresponding pulse may be weaker than normal (due to reduced filling time, or may not be felt at all causing an apical-radial pulse deficit) 5. 12 leads is best to figure out source
Lead Placement
1. Proper placements is critical 2. Arm leads should be below shoulder joint and parallel 3. Foot/leg leads should be below hip joints 4. With bedside monitoring keep limb leads wide - think camera, lose perspective if you are too close 5. Lead 2 is the preferred lead. P, QRS and T are seen well 6. View from right upper chest to left lower trunk.
P-Wave
Atrial depolarization (0.06-0.12 sec)
Ventricular Tachycardia: Treatment
Follow Tachycardia Algorithm Treat with Amiodarone
Supraventricular Tachycardia (SVT): Tx
Follow the Tachycardia Algorithm Administer Adenosine
Premature Ventricular complex/contraction (PVCs): Cause
Hypoxia #1 CAUSE
AV Block: 1st Degree
Lengthens the delay between atrial and ventricular depolarization by slowing AV node conduction
EKG interpretation
Step 1: What is the rate? Does the atrial rate = the ventricle rate? Step 2: Is the rhythm regular or irregular? (check R-R interval) Step 3: Is there a P wave before every QRS complex? None? Multiple? Do they all look alike? Lead 2, is the best to see this Step 4: Is the PR interval normal? Consistent? Step 5: QRS complexes wide or narrow? Normal configuration? Q-waves present? Step 6: Are the ST segments normal (above or below baseline)? Can recognize potential ischemia Step 7: Is there a T wave after every QRS complex Is it depressed? Peaked? In the same direction as the P wave? Step 8: QT interval normal?
Natural Pacemaker: Overdrive suppression
The higher frequency of SA nodal firing suppresses other pacemaker sites
T-Wave
Ventricular repolarization
Sinus tachycardia EKG
What is the rate? Greater than 100 (101-200) Rhythm? Regular Are there QRS complexes? Yes Are there p-waves? Yes, normal shape Is there a p wave for every QRS? Yes PR interval: normal, 0.12-.02 Are QRS complexes wide or narrow? Narrow, <0.12
QT interval
1. (0.34-0.43 sec) 2. Represents ventricular systole 3. Used to reflect ventricular repolarization time 4. QT interval is mostly repolarization 5. prolonged QT can be dangerous - can be prolonged due to medications 6. Generally considered normal if less than half of RR interval at normal rates
QRS Complex
1. (<0.12, or 0.06 0.1 sec) 2. Ventricular depolarization 3. Atrial repolarization is buried with in QRS complex 4. A downward deflection occurring before an upward deflection (first downward deflection) is a Q wave 5. First upward deflection is an R wave 6. A downward wave preceded by an upward wave is called an S wave. 7. QRS complex is taking longer than it should = something is wrong with the ventricular depolarization
Leads
1. 3 leads (usually used for cardiac telemetry monitoring) - Limb leads (give us 6 views) 2. 5 lead: Limb leads plus one chest lead 3. 6 chest leads: V1 - V6 - Looks at horizontal plan - Electrodes are positive - Each chest lead is oriented through the AV node and projects through the patient's back (negative) - Comprehensive picture of the heart 4. 12 lead: Limb leads plus 6 chest leads leads
Six Second Strip
1. 5 large boxes = 1 sec 2. 15 large boxes = 3 sec 3. 30 large boxes = 6 sec 4. # beats in 6 sec x 10 = beats in a minute
PVC: Treatment
1. Administer oxygen 2. Further treatment depends on hemodynamic stability 3. May need drug therapy such as beta blockers or an antidysrhythmic like procainamide or amiodarone.
Atrial and Junctional irritability due to...
1. Adrenaline (epinephrine) released from adrenal glands 2. Increased sympathetic stimulation 3. Presence of caffeine, amphetamines, cocaine, or other Beta1 receptor stimulants 4. Hyperthyroidism 5. Stretch 6. And to some extent, low oxygen
2nd Degree AV Block Wenckebach (Type 1): Causes
1. Associated with parasympathetic excess or drugs that mimic or induce parasympathetic effects - Beta blockers - Digoxin 2. May be associated with CAD and other diseases that can slow AV conduction - Usually the result of myocardial ischemia or inferior MI - Usually transient and well tolerated as long as the rate is not too slow
Third degree AV block (complete): patient assessment
1. Associated with severe heart disease including CAD, MI, myocarditis, cardiomyopathy 2. Can be caused by some drugs such as digoxin, Beta blockers, and Calcium channel blockers 3. Severe reduction in cardiac output leading to ischemia, HF, and shock.
Sinus Bradycardia: Tx
1. Asymptomatic, just monitor 2. Symptomatic treat with 0.5mg Atropine - inhibits the parasympathetic nervous system, letting the sympathetic nervous system to take over 3. Follow Bradycardia algorithm
Natural Pacemaker: Automaticity Foci
1. Backup pacemakers 2. if SA node is firing 60-100, the automaticity foci do not fire 3. Atria (60-80): intrinsic rate 4. AV junction (40-60) 5. Ventricles (20-40): last chance automaticity foci
Second Degree Mobitz (Type II)
1. Block occurs below the AV node in the Purkinje fiber bundles (His Bundle or Bundle Branches) 2. Totally blocks a number of atrial impulses before conducting one to the ventricles. 3. Can be 2:1, 3:1, or higher... 4. The higher the ratio, the more dangerous the block.
AV Blocks
1. Blocks slow or prevent (or sometimes both) the conduction of depolarization 2. They can occur in the SA node, AV node, or in the larger divisions of the ventricular conduction system
Third degree AV block (complete)
1. Complete block of atrial impulses to the ventricles 2. Atria are stimulated and contract regularly 3. Can be junctional or ventriculal
PACs: Treatment
1. Depends on symptoms - Withdrawal source of stimulation - Beta blockers may decrease PACs
Natural Pacemaker: SA Node
1. Heart's dominant pacemaker - rhythms generated from SA node are called 'sinus' rhythms 2. Inherent (or intrinsic) rate of 60-100 impulses per minute
Sinus Tachycardia: Treatment
1. Identify and treat underlying cause 2. Usually a normal compensatory response with something going on in the body Ex. Dehydration = increase HR = treat with fluids Febrile patient = increase HR = treat with antipyretic
Paroxysmal Supraventricular Tachycardia: Causes
1. In a normal heart is can result from: overexertion, emotional stress, stimulants like caffeine, tobacco 2. Rheumatic heart disease: heart valves become damaged. The valves most affected by rheumatic fever, in order, are the mitral, aortic, tricuspid, and pulmonary valves. In most cases, the mitral valve is involved with 1 or more of the other 3. 3. CAD 4. Cor pulmonale: abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels 5. Digitalis toxicity
Adenosine
1. Initial dose = 6 mg IV push, followed by 20mL NS bolus 2. Followed by a 20 mL flush, after 1-2 of first dose 3. Second dose of 12 mg may be given if needed 4. GIVEN RAPDILY 5. slows cardiac conduction particularly affecting conduction through the AV node
Ischemia and Infarct
1. Injury is a progression of ischemia that is potentially reversible but may evolve to infarct 2. ST elevation can indicate injury or infarct - Significant if it is at least 1 mm above baseline in at least 2 contiguous leads 3. T wave inversion can be present related to an MI and may persist for months and then resolve ST depression = ischemia ST elevation = MI
EKG Changes with ACS (acute coronary syndrome)
1. Ischemia, injury and infarct cause EKG changes 2. Leads facing the area of injury demonstrate the changes 3. Leads facing the opposite area may show reciprocal, or opposite, EKG changes
PACs: Patient assessment
1. Isolated PACs are generally not significant in people with healthy hearts - Patients may report palpitations or sense that heart "skipped a beat" 2. Frequent PACs in someone with heart disease may indicate, or start, a more serious dysrhythmia
Ventricular Irritability due to...
1. Low oxygen (hypoxia or ischemia) = #1 cause of ventricular irritability - Airway obstruction - Absence of air - Air with poor oxygen content - Minimal blood oxygenation in the lungs - Reduced cardiac output - Poor or absent coronary blood supply 2. Hypokalemia 3. Pathology - Mitral valve prolapse - Stretch - Myocarditis
Atrial Fibrillation: Treatment
1. Main GOAL: rate control and preventing thromboembolism 2. Prevention of thromboembolism - Antithrombotic therapy: need to do risk stratification for both stroke and bleeding to inform decision making and drugs 3. Rate Control: - Beta blockers and calcium channel blockers commonly used - digoxin and amiodarone 4. Rhythm control: Most often used for new onset a-fib; younger patients; patients who remain symptomatic despite rate control or who are intolerant of rate control medication. - Conversion of rhythm (cardioversion) with antiarrhythmics, electrical cardioversion, ablation, or a combination. - Cardioversion requires assessment/prevention of thromboembolism if duration of A-fib is > 48 hours 5. Follow tachycardia algorithm
Secondary Pacemakers
1. May fire - In response to receiving impulses at a rate below their own intrinsic rate (termed 'escape' beats) - When irritable can cause them to spontaneously fire producing 'premature' beats, or suddenly pace very fast resulting in various dysrhythmias
Sinus bradycardia causes
1. Most often caused by parasympathetic excess 2. May be normal in aerobically trained athletes or during sleep 3. Valsalva maneuver (bearing down to poo), Vagal stimulation, Hypothermia 4. Certain medications (beta-blockers, calcium channel blockers)
Third degree AV block (complete): treatment
1. Need temporary pacemaker if symptomatic 2. Will need a permanent pacemaker as soon as possible 3. Follow bradycardia algorithm
Repolarization
1. Occurs immediately following depolarization 2. After depolarization, cells must return to their resting state (negatively charged interior) so they are ready to respond to the next impulse 3. This is accomplished by movement of potassium (K+) ions out of the cell.
Normal Conduction: AV Node
1. Only conduction pathway between atria and ventricles 2. Slows conduction to allow ventricular filling 3. Triggered by slow moving Ca++ ions
PAC EKG
1. PACs will cause the overall rhythm to be irregular 2. They will occur sooner than the next beat would be expected 3. P wave will be abnormal (shape and size will be different than a p-wave from the SA node because the path of depolarization through the atria is different is coming from a different origin) 4. PR interval may vary from other beats but should be WNL 5. QRS following is usually normal
PVC: EKG
1. PVCs will cause the overall rhythm to be irregular 2. QRS will occur sooner than the next beat would be expected 3. There will be NO P-WAVE 4. QRS will be wide and distorted in shape (shape and size will be different than a QRS following the normal conduction pathway because the path of depolarization through the ventricle is different)
Paroxysmal Tachycardias
1. Paroxysmal means "sudden" 2. Can be atrial, junctional, or ventricular 3. Atrial and junctional tachycardias are often hard to distinguish from each other, so they are often simply termed Supraventricular tachycardias 4. Rate is 150-250 5. Coming from somewhere above the ventricles
Atrial Fibrillation: patient assessment
1. Reduced cardiac output (due to loss of atrial kick and/or rapid ventricular rate) 2. Hypotension, dyspnea, angina, changes in LOC, heart failure Increased myocardial oxygen consumption/demand (with increased V rate) 3. Thrombus formation in atria due to blood stasis 4. Increased risk of stroke (A-fib accounts for as many as 17% of all strokes, Lewis, p. 766) 5. Other symptoms - Patient may feel palpitations/"heart racing"
Dysrhythmias
1. Result from disorders of impulse formation, conduction of impulses, or both. 2. Determining the cause (or possible causes) of the dysrhythmia is a priority. 3. First thing to do if a patient has dysthymias, is check the patient (ABCs, O2, LOC, check leads) 4. EKG responds to movement, producing an artifact (false reading) ex. patient brushing teeth and moving around the room
Sinus bradycardia EKG
1. Rhythm? Regular Are there QRS complexes? Yes 2. Are there p-waves? Yes, normal shape 3. Is there a p wave for every QRS? Yes 4. PR interval: normal, 0.12-0.2 5. Are QRS complexes wide or narrow? Narrow, <0.12 ** between R waves we would have 5 boxes at least (bc bradycardia)
Normal Conduction: Atrial Conduction System
1. SA node: starts depolarization 2. Cell to cell depolarization triggered by fast moving Na+ ions 3. Impulse travels through internodal pathways
ST Segment
1. Should be flat and at baseline 2. the beginning of repolarization 3. Repolarization is accomplished by K+ leaving the cells
Normal Sinus EKG
1. Starts in SA node 2. Rate between 60-100 3. Follows normal conduction pathway 4. Rhythm? Regular 5. Are there QRS complexes? Yes 6. Are there p-waves? Yes 7. Is there a p wave for every QRS? Yes 8. PR interval: normal, 0.12-0.2 9. Are QRS complexes wide or narrow? Narrow, <0.12
Sinus Tachycardia
1. Starts in the SA node 2. Rate greater than 100 3. Follows normal conduction pathway
Sinus bradycardia
1. Starts in the SA node 2. Rate less than 60 3. Follows normal conduction pathway
Atrial Fibrillation
1. Total disorganization of atrial electrical activity 2. Multiple irritable atrial foci all firing at rapid rates - loss of overdrive suppression 3. No single impulse completely depolarizes both atria (No P-Wave), wavy baseline 4. Results in loss of atrial contraction, atria merely twitch rapidly 5. Only those foci near the AV node are able to stimulate the AV node, resulting in an irregular ventricular response 6. May be paroxysmal or persisten
Electrocardiogram
1. Tracing of the heart's electrical activity 2. Gives us info about the heart's rate and rhythm* 3. Gives info about heart's function and structure
Normal Conduction: Ventricular Conduction System
1. Triggered by fast moving Na+ ions 2. His bundle 3. Right and left bundle branches 4. Terminal Purkinje Fibers - Depolarize the ventricular myocardium
Ischemia: EKG
1. Typical EKG changes seen with ischemia include ST depression and/or T-wave inversion - ST segment depression is significant if it is at least 1 mm below baseline in at least 2 contiguous leads - Represents inadequate supply of blood/oxygen - Changes will resolve when adequate blood flow/oxygen are restored. 2. Because of reciprocal changes, check opposite leads for possible elevation that was overlooked.
Second Degree Mobitz (Type II): Patient Assessment
1. Typically associated with rheumatic heart disease, CAD, anterior MI, and drug toxicity 2. Often progresses to a third-degree block and is associated with a poor prognosis 3. Slow ventricular rates can reduce cardiac output and cause myocardial ischemia
PVC Types
1. Unifocal PVCs: all originate from same irritable foci (will all have the same size/shape) 2. Multifocal PVCs: originate from different irritable foci (will have a different size/shape) 3. Two PVCs in a row is a couplet 4. Three or more consecutive PVCs is considered ventricular tachycardia - count the number of PVCs and call it a "run of # PVCs" 5. 6 or more is considered pathological (we are concerned and indication that something is not right)
Atrial Fibrillation: Causes
1. Usually occurs in patient with underlying heart disease CAD, valvular disease, cardiomyopathy, HF, hypertensive heart disease, and pericarditis 2. Can develop acutely with thyrotoxicosis (too much thyroid in the body), alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery
Ventricular Tachycardia: patient assessment
1. What are we worried about? - Considered a life-threatening dysrhythmia - Ability of complex to produce a pulse (need to distinguish v-tach with a pulse from pulseless V-tach) - Reduced cardiac output - rate is usually too fast for the heart to function effectively (not perfusing correctly) - Increased myocardial oxygen consumption/demand - Potential for worsening dysrhythmia (pulseless V-tach or V-fib) 2. What will that look like? Hypotension Dyspnea/pulmonary edema Angina Changes in LOC (confusion, dizziness, syncope) Cardiac arrest
PVCs: Patient Assessment
1. What are we worried about? - Indications of ventricular irritability (early warning system for hypoxia - don't ignore) - Potential for decreased cardiac output - Potential for worsening dysrhythmias (continued/worsening irritability, or R on T phenomenon), to many ventricular beats can land on T wave and disrupt the repolarization, this can cause ventricular tachycardia 2. Are the unifocal or multifocal 3. Assess apical-radial pulse rate for a pulse deficit: PVCs may or may not generate a sufficient ventricular contraction to results in a peripheral pulse - Can have a non-perfusing PVC (when you cant feel the pulse, when a PVC occurs) 4. Numerous multifocal PVCs in a patient with infarction are VERY dangerous! 5. Multifocal PVCs may indicate severe myocardial hypoxia 6. In a healthy heart, isolated PVCs are not usually harmful 7. Multifocal increase concern - any one of those foci could suddenly start firing at a rapid rate
Supraventricular tachycardia: Patient assessment
1. What are we worried about? - Reduced filling time - Reduced cardiac output - Increased myocardial oxygen consumption/demand 2. What will that look like? - Hypotension - Dyspnea - Angina - Changes in LOC (confusion, dizziness, syncope) - Patients may also feel palpitations
Sinus bradycardia: Patient Assessment
1. What are we worried about? Reduced cardiac output 2. What will that look like? Hypotension Dyspnea Angina Changes in LOC (confusion, dizziness, syncope)
Sinus Tachycardia: patient assessment
1. What are we worried about? Reduced cardiac output decreased time to fill Increased myocardial oxygen consumption/demand 2. What will that look like? Hypotension Dyspnea Angina Changes in LOC (confusion, dizziness, syncope) Patients may also feel their heart racing
Ventricular Tachycardia: EKG
1. What is the rate? 150-250 2. Rhythm? Regular 3. Are there QRS complexes? Yes 4. Are there p-waves? not visible 5. Are QRS complexes wide or narrow? Wide 6. Looks like a rapid series of PVCs (which is what it is)
Supraventricular tachycardia: EKG
1. What is the rate? 150-250 2. Rhythm? Regular 3. Are there qrs complexes? Yes 4. Are there p-waves? Usually cannot be seen (may not be present, or may be buried in preceding t-wave) 5. Are the qrs complexes wide or narrow? Narrow (unless abnormally conducted through ventricles) 6. Occurs out of the blue, rhythm is consistent
Atrial Fibrillation: EKG
1. What is the rate? Atrial rate is impossible to determine (said to be 350-450). Ventricular rate varies. 2. Rhythm? Irregularly, irregular 3. Are there QRS complexes? Yes 4. Are there p-waves? No, often appears as a wavy baseline 5. PR interval: NA 6. Are QRS complexes wide or narrow? Usually narrow, <0.12
Sinus Tachycardia: Causes
1. usually the result of sympathetic stimulation of the SA node 2. can also be caused by parasympathetic (vagal) inhibition 3. Exercise, fever, anxiety, fear, pain. 4. hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, 5. HF, MI, hyperthyroidism 6. Drugs/Medications
Second Degree Mobitz (Type II): Treatment
1. will usually need a temporary pacemaker if symptomatic, followed by a permanent pacemaker
2nd Degree AV Block Wenckebach (Type 1)
Block occurs at the AV node
2nd Degree AV Block Wenckebach (Type 1): Treatment
Follow Bradycaridia algorithm
AV Block: 1st Degree EKG
Rate: usually normal Rhythm: regular Are there p-waves? Yes, normal shape Is there a p wave for every QRS? Yes Is every p wave followed by a QRS? Yes PR interval: LENGTHENED, > 0.20 Are QRS complexes wide or narrow? Narrow, <0.12
Second Degree Mobitz (Type II): EKG
What is the rate? Atrial rate is normal, ventricular rate is more likely to be slow Rhythm? Atrial rate is regular, ventricular rate may be regular if pattern is consistent Are there QRS complexes? Yes Are there p-waves? Yes Is there a p-wave for every QRS? Yes Is every p-wave followed by a QRS? No, lone P-waves PR interval: consistent with conducted beats (may be normal or prolonged) Are QRS complexes wide or narrow? Usually wide, > 0.12
2nd Degree AV Block Wenckebach (Type 1): EKG
What is the rate? Atrial rate is normal, ventricular rate may be slow due to non-conducted, or blocked, impulses. Rhythm? Atrial rate is regular, ventricular rate is irregular Are there QRS complexes? Yes Are there p-waves? Yes Is there a p-wave for every QRS? Yes Is every p-wave followed by a QRS? No PR interval: gradually lengthens, until one p wave does not produce a QRS Are QRS complexes wide or narrow? Usually narrow, <0.12
Third degree AV block (complete): EKG
What is the rate? Atrial rate is usually sinus (60-100), ventricular rate is slow (how slow depends upon where the escape rhythm is being generated. Rhythm? Atrial rate is regular, ventricular rate is regular but the two rates are unrelated. Are there QRS complexes? Yes Are there p-waves? Yes Is there a p-wave for every QRS? No Is every p-wave followed by a QRS? No PR interval: variable with no relationship between p waves and qrs Are QRS complexes wide or narrow? Normal or wide depending on source of ventricular depolarization
