EKG/ECG
Determine the HR on EKG
6 Second Method: Count the number of R's in between the 6 second strips and multiply by 10 (6 R's x 10 = 60 bpm). Be sure and check that the strip is 6 seconds - count the boxes Big Box Method: 300 divided by the number of big boxes between the R's (300/5 = 60 BPM)
Sinus Tachycardia
> 100 bpm normal sinus rhythm the sinus node creates an impulse at a faster than normal rate EKG waveform is normal
Implanted Pacemaker: failure to pace
The pacemaker fails to initiate electrical stimulus when it should fire
Ventricular Tachycardia (VT)
150 - 250 bpm normal sinus rhythm, but can be irregular P-wave not visible, buried no PR interval, not measurable QRS complex is wide (like tombstones), distorted, > 0.12 seconds Irregular, coarse waveforms of different shapes. The ventricles are quivering and there is no contraction or cardiac output which may be fatal (no CO = low O2) VT can quickly degenerate into ventricular fibrillation Causes: - MI or ischemia - electrolyte imbalances - Digoxin toxicity - Stimulants: caffeine and methamphetamine Manifestations: - angina - lethargic - anxiety - syncope (fainting or passing out) - palpations Untreated VT can lead to ventricular fibrillation which can lead to DEATH Treatment: treat the cause, Advanced Cardiovascular Life Support (ACLS)
Sinus Bradycardia
< 60 bpm normal sinus rhythm the sinus node creates an impulse at a slower than normal rate EKG waveform is normal Sinus bradycardia and hypotensive: Atropine is the drug of choice for treatment of symptomatic bradycardia. It enhances both sinus node and atrioventricular (AV) node conduction. Atropine must be used cautiously when there is acute coronary ischemia or myocardial infarction because it increases myocardial oxygen consumption.
Lateral wall injury
A lateral (left lateral is understood) wall ischemic event is demonstrated in leads I and aVL. Each of these electrodes has a positive electrode placed laterally on the left arm.
Implanted Pacemaker: failure to capture
A spacer spike is noted but is not followed by a p wave (atrial pacemaker) or a QRS complex (ventricular pacemaker) If pacemaker spikes are present, the pacemaker is firing appropriately, but the lack of resulting QRS complexes indicates that it is not stimulating or 'capturing' the heart. Severe bradycardia or asystole malfunctions: battery, damage, or exit blocked (hyperkalemia)
Atrial Fibrillation
A-Fib Rate is usually over 100 bpm Irregularly irregular rhythm No P-wave, irregular (fibrillary waves) PR interval is visible Irregular R-R intervals QRS complex is narrow and irregular Uncoordinated electrical activity in the atria that causes rapid and disorganized "fibbing" of the muscles in the atrium. The atrial is quivering. Causes: Open heart surgery HF COPD HTN Ischemic Heart Disease Manifestations: all due to low O2 Most commonly asymptomatic Fatigue Malaise Dizzy SOB Tachycardia Anxiety Palpitations Treatment: Cardioversion (NOT defibrillation) - synchronized shock delivered only during the R wave of the QRS complex, lower amounts of joules used, not done with CPR Oxygen, drug therapy (beta blockers, calcium channel block, digoxin, amiodarone, anticoagulant (the atria quiver causes pooling of blood in the heart which increases risk for clots = increased risk for MI, PE, CVA, and DVTs) Amiodarone Coumadin
Anteroseptal wall injury
An anteroseptal injury is demonstrated in the leads facing the precordium (I-VI), with similar changes in aVL. The number of precordial leads involved reflects the extent of anterior wall involvement.
Inferior wall injury
An inferior wall event is demonstrated in leads II, III, and aVF. Each of these electrodes has a positive electrode placed inferiorly on the left foot. Inferior wall injury usually occurs as a consequence of right coronary artery occlusion. Confirmed inferior wall MI is associated with risk for right ventricular failure. Patients at risk should be assessed for: peripheral edema The right side of the heart receives blood from the systemic circulation. Right ventricular failure causes back up of blood entering the right side of the heart from the systemic circulation. Peripheral edema, especially in the feet and ankles, may be observed. jugular venous distention The right side of the heart receives blood from the systemic circulation. Right ventricular failure causes back up of blood entering the right side of the heart from the systemic circulation. Jugular venous distention (JVD) may be observed. shortness of breath The right side of the heart receives blood from the systemic circulation. Right ventricular failure causes back up of blood entering the right side of the heart from the systemic circulation. Shortness of breath, due to an increase in right ventricle preload, may be observed. hypotension Right ventricular failure can cause significant hypotension, because less fluid leaves and circulates from the left side of the heart. The right side of the heart receives blood from the systemic circulation. Right ventricular failure causes back up of blood entering the right side of the heart from the systemic circulation.
After noting that a client in the clinic has an irregularly irregular pulse rhythm at a rate of 88 beats/ minute, the nurse will anticipate further testing for which possible dysrhythmia?
Atrial fibrillation An irregularly irregular rhythm is a classic sign of atrial fibrillation. The irregularity occurs because impulses from multiple atrial sites depolarize the atria in a disorganized fashion.
Supraventricular Tachycardia (SVT)
Atrial tachycardia 151 - 220 bpm normal sinus rhythm P wave is abnormal or hidden PR interval is shortened/normal QRS complex is normal Dysrhythmia starting at an ectopic pacemaker anywhere above the bifurcation of the Bundle of His. Occurs due to the excitation of the atria when there is a 1-way block. The electrical system that controls your heart rhythm is not working properly. This causes your heart to suddenly beat much faster. It can then slow down abruptly. Decreased SV causes decreased CO = low O2 Causes: overexertion emotional stress deep inspiration stimulants (caffeine, tobacco) Manifestations: Hypotension Palpitations Dyspnea Angina Treatment: vagal maneuvers (valsava, carotid massage, coughing) IV adenosine Cardioversion (NOT defibrillation) - synchronized shock delivered only during the R wave of the QRS complex, lower amounts of joules used, not done with CPR
Third Degree AV Heart Block
Complete Heart Block Rhythm is regular P wave is normal PR interval varies QRS complex is normal Atrial rate: 60 -100 bpm Ventricular rate: AV node 40 - 60 bpm, His-Purkinje 20 - 40 bpm Form of AV disassociation, no impulses from the atria are conducted to the ventricles. no atrial impulses are conducted through the AV node to the ventricles. In complete heart block, the atria and ventricles beat independently of each other because the AV node is completely blocked to the sinus impulse and is not conducted to the ventricles. One hallmark of third- degree heart block is that the P waves have no association with the QRS complexes and appear throughout the QRS waveform. Causes: Severe heart disease CAD MI myocarditis cardiomyopathy some systemic diseases (scleroderma) Some drugs (digoxin, Beta blockers, and calcium channel blockers) Usually results in reduced CO with subsequent ischemia, HF, and shock. Syncope or even periods of asystole Treatment: Symptomatic - transcutaneous pacing, dopamine and epinephrine can increase HR and support BP Transvenous pacing Permanent pacemaker - to help support heart rate and cardiac output. Intropin (dopamine) is indicated for hemodynamically-significant hypotension (without hypovolemia). It can be used for hypotension associated with bradycardia while pacing is being set up. When a client develops third degree atrioventricular block with a heart rate of 30 beats/minute, obtain the transcutaneous pacemaker. Transcutaneous pacing is used for emergency treatment of bradycardia, because it is noninvasive and can be rapidly initiated.
Which finding on an electrocardiogram for a client complaining of chest pain indicates possible acute myocardial infarction?
Elevated ST segments are an early typical finding after a myocardial infarction because of the altered repolarization of the heart. The client with chest pressure and ST segment elevation on the electrocardiogram will need emergency treatment for ST segment elevation myocardial infarction (STEMI), including transport to the cardiac catheterization laboratory for percutaneous coronary intervention within 90 minutes, and should be seen first. Q waves do not disappear with myocardial infarction, but large Q waves are seen late in the process of infarction.
Asytole
Flatline: The heart has ceased generating electrical impulses. No rhythm, rate, P-wave, PR interval, QRS complex Causes: MI or ischemia HF Electrolyte imbalances (common hypo/hyperkalemia) Severe acidosis Cardiac tamponade (pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle and the outer covering sac of the heart) Cocaine overdose Treatment: HIGH QUALITY CPR
Premature Atrial Contraction (PAC)
HR varies Rhythm is irregular P wave is visible or hidden PR interval is normal or longer QRS complex is normal Atrial rate: varies Ventricular rate: varies Irregular heart rhythm characterized by atrial contractions occurring before the expected time Causes: Emotional stress Physical fatigue Caffeine, tobacco, or alcohol Hypoxia Electrolyte imbalances hyperthyroidism COPD heart disease CAD Valvular disease Manifestations: "heart skipped a beat" palpitations Treatment: Avoid excessive caffeine or alcohol intake Avoid sypathomimetic drugs (epinephrine, dopamine) Decrease stress Beta blockers if HR is > 100 Occasional PACs (premature atrial contractions) are benign and will not affect cardiac output so the nurse will continue to monitor the client for increased numbers of PACs or other dysrhythmias.
Second Degree Heart Block Type I
Mobitz I or Wenckebach Heart Block Rhythm is irregular P wave is normal PR interval is progressively lengthening QRS complex is normal until blocked Atrial rate is normal Ventricular rate is abnormal (slower) AV conduction time is increasingly prolonged until an atrial impulse is nonconducted and a QRS complex is blocked (missing) Causes: Drugs (Digoxin, Beta Blockers) CAD Other diseases that can slow AV conduction Myocardial ischemia inferior MI Treatment: Symptomatic - Atropine or a temporary pacemaker to increase HR Asymptomatic - transcutaneous pacemaker Because second-degree heart block, type I is usually transient and well tolerated, the nurse's first action would be to assess the client for adequate perfusion by checking parameters such as blood pressure, skin temperature, and alertness. A temporary pacemaker may be needed, but only if the assessment indicates a need to increase heart rate to adequately perfuse the client. Atropine is appropriate if the bradycardia has caused hypotension or decreased alertness, but may not be needed. Notification of the health care provider is appropriate, but the nurse should be able to provide information about blood pressure and other indicators of perfusion to the health care provider.
Second Degree Heart Block Type II
Mobitz II Rhythm is irregular P wave is normal PR interval is normal or prolonged QRS complex is > 0.12 sec Atrial rate is normal Ventricular rate is abnormal A P wave is nonconducted without progressive PR lengthening. Usually happens when there is a block in one of the bundle branches Causes: rheumatic heart disease CAD anterior MI drug toxicity Treatment: transcutaneous pacing, permanent pacemaker (when hypotension and angina are present)
NSTEMI
Non-ST elevation myocardial infarction Non-ST-segment elevation MI (NSTEMI) is initially characterized by chest pain and/or other symptoms of an acute coronary event, and ECG changes that may or may not include slight ST-segment elevation, or ST-segment depression, and/or T-wave inversion. NSTEMI is confirmed when serum cardiac biomarkers elevate (creatine kinase MB and troponins). Usually, with NSTEMI, myocardial damage does not include the entire depth of the myocardial muscle wall
Pulseless Electrical Activity (PEA)
Organized electrical activity is seen on the ECG, but there is no mechanical activity of the ventricles and has no pulse Most common dysrhythmia seen after defibrillation. Prognosis is poor unless the underlying cause is quickly identified and treated Causes: hypovolemia hypoxia metabolic acidosis hyperkalemia hypothermia toxins (drug overdose) cardiac tamponade thrombosis (MI, PE) tension pneumothorax trauma Treatment: Treat the cause, CPR followed by drug therapy (epinephrine) and intubation, ACLS
PR Interval
PR segment is movement of electrical activity from the atria to ventricles (AV node, bundle of his, and Purkinje fiber) Allows the filling on the ventricles The PR interval represents the time it takes for an impulse to completely depolarize the atria and the atrioventricular node and would not be used to assess atrial regularity Normal: 0.12 - 0.20 seconds Measure a PR interval: - one small box = 0.04 seconds - one large box = 0.20 seconds - five large boxes = 1 second
R-R interval
Peak of R wave to peak of next R wave; entire duration of a cardiac action potential are the R-R intervals consistent? - regular or irregular?
QRS complex
QRS complex is ventricle contraction (depolarization) QRS complexes represent ventricular depolarization and would be used to determine ventricular regularity and heart rate. Is every P wave followed by a QRS? - should not be widened or shortened (this may indicate a problem). Widened is often seen is PVCs, electrolyte imbalances, and drug toxicity Normal: 0.06 - 0.12 seconds Measure a QRS complex: - one small box = 0.04 seconds - one large box = 0.20 seconds - five large boxes = 1 second
Premature Ventricular Contractions (PVCs)
Rate depends on the underlying rhythm, varies Rhythm is irregular P-waves are rarely visible but depends on timing of PVC (may be hidden), it is usually lost in the QRS complex PR interval is not measurable QRS complex is wide, distorted, sharp, bizarre, and abnormal during the PVC T wave is generally large Early or premature conduction of a QRS complex. The impulse originates in the ventricles, and it occurs before the next expected ventricular beat. Bigeminy (alternation between a regular heartbeat and extra, skipped heartbeat): every other beat Trigeminy (extra beat): every 3rd beat Quadrigeminy (premature ventricular contraction): every 4th beat R-on-T Phenomenon: PVC arises spontaneously from the depolarization gradient (T-wave) may precipitate V-fib Causes: HF cardiomyopathy electrolyte imbalance MI or ischemia drug toxicity Caffeine, tobacco, alcohol Stress or pain increased workload of the heart (exercise, fever, hypervolemia, HF, and tachycardia) Manifestations: May be asymptomatic feels like your heart skipped a beat, is pounding chest pain Treatment: Treat the cause Beta-blockers Lidocaine Amiodarone Lidocaine is an antidysrhythmic specifically given for treatment of ventricular dysrhythmias. Premature ventricular contractions (PVCs) should decrease with the administration of a lidocaine IV drip. PVCs are common in the first few hours after MI and are usually transient. However, when PVCs occur coupled, in bursts of three of more, are multiform in shape, or more than six occur per minute, treatment with lidocaine is usually initiated. When lidocaine is used post-MI, serum levels are closely followed, since lidocaine clearance is reduced after MI. Lidocaine is not used prophylactically after MI. Recognizing frequent premature ventricular beats is especially important. These beats can precede deterioration into ventricular fibrillation.
Junctional Dysrhythmias
Rate: 40 - 60 bpm (escape), 61 - 100 bpm (accelerated), and 101 - 180bpm (junctional tachycardia) Rhythm is regular P wave is inverted or hidden PR interval is 0.12 seconds QRS complex is normal Start in the AV node to the Bundle of His (AV junction) because the SA node does not fire or the signal is blocked. AV node becomes the pacemaker of the heart Causes: CAD HF cardiomyopathy electrolyte imbalances inferior MI rheumatic heart disease Treatment: Atropine Beta blockers calcium channel blocker Amiodarone (control HR)
First degree AV block
Rate: 60 - 100 bpm Rhythm is regular P wave is normal PR interval is prolonged > 0.20 sec QRS complex is normal Type of AV block in which every impulse is conducted to the ventricles but the time of AV conduction is prolonged Not really a block, more of a delay. In first degree AV block, a P wave precedes every QRS complex, but the PR interval is prolonged. Causes: Increasing age MI CAD rheumatic fever hyperthyroidism electrolyte imbalances (hypokalemia) Vagal stimulation Drugs (Digoxin) NO Treatment Monitor and check labs
Atrial Flutter
Rate: 75 - 150 bpm Rhythm is usually regular P-wave looks like a "sawtooth" configuration shaped flutter waves PR interval are unmeasurable QRS complex are usually normal and upright Similar to A-fib, but the hearts electrical signals spread through the atria. The hearts upper chambers (atria) beat too quickly but at a regular rhythm. Not every atrial impulse is conducted to the ventricles. Causes: coronary artery disease HTN HF valvular disease hyperthyroidism chronic lung disease PE cardiomyopathy Manifestations: May be asymptomatic fatigue/syncope angina SOB low BP palpitations dizziness Treatment: Cardioversion (NOT defibrillation) - synchronized shock delivered only during the R wave of the QRS complex, lower amounts of joules used, not done with CPR Drug therapy (calcium channel blockers, antiarrhythmics, anticoagulant (the atria flutter causes pooling of blood in the heart which increases risk for clots = increased risk for MI, PE, CVA, and DVTs) Beta blockers Amiodarone Ablation Coumadin
STEMI
ST elevation myocardial infarction A heart attack with a completely blocked coronary artery ST-segment elevation MI (STEMI), acute myocardial infarction (MI), usually presents with significant chest pain and/or other symptoms of an acute coronary event, and ST-segment elevation on the presenting ECG. STEMI is confirmed when serum cardiac biomarkers elevate (creatine kinase MB and cardiac troponins) and/or there is evidence of Q waves on ECG. Q waves indicate myocardial cell death is present. Q waves can persist on an ECG for months to years after an MI. With STEMI, myocardial damage is significant. The entire depth of the myocardial muscle wall has been affected. Will require rapid treatment with thrombolytic medications or percutaneous intervention to achieve reperfusion.
EKG waveform
The P wave is atrial contraction (depolarization) PR segment is movement of electrical activity from the atria to ventricles · AV node, bundle of his, and Purkinje fiber QRS complex is ventricle contraction (depolarization) QT Interval is the time it takes for ventricles to depolarize and repolarize (to contract and relax) ST segment is time between ventricular depolarization and repolarization (ventricular contraction and emptying) T wave is ventricle relaxing (repolarization) TP interval is ventricle relaxing and filling Memory trick: depolarization think DEcompressing Memory trick: repolarization think RElaxing, REpolarizing, and REfilling with blood
P Wave
The P wave is atrial contraction (depolarization) The P wave represents atrial depolarization and a nurse would use P waves to determine atrial rate and rhythm. Identify and examine the P wave - should be present and upright - comes before QRS complex - One P-wave for every QRS 2.5 mm 0.11 sec
ST segment
The ST-segment of an electrocardiogram (ECG) waveform reflects the heart's ability to repolarize (prepare for the next contraction). ST segment is time between ventricular depolarization and repolarization (ventricular contraction and emptying) ST-segment variations from baseline occur when the myocardium is ischemic or there is myocardial tissue injury. With myocardial ischemia there may be ST-segment depression. Myocardial tissue injury or infarction is generally characterized by ST-segment elevation. Flattened or depressed T waves indicate hypokalemia.
Implanted Pacemaker: failure to sense
The pacemaker does not sense the patients own cardiac rhythm and initiates an electrical impulse Failure to sense would occur if pacemaker spikes continue to be seen even though the client's rate is above the preset pacemaker level. Misfires can lead to V-Fib Fails to recognize atrial and ventricular contractions malfunctions: battery, sensitivity too high
Ventricular Fibrillation (VF)
V-Fib Rate is unknown, not measurable Rhythm is chaotic and irregular P wave, PR interval, and QRS complex are not visible or measurable Ventricular fibrillation reflects a rapid, feeble twitching/quivering of the ventricles; it has an irregular sawtooth configuration with unidentifiable PR intervals and QRS complexes. Rapid, disorganized pattern of electrical activity in the ventricle in which electrical impulses arise from may different foci. Ventricular fibrillation (VF) commonly precedes and occurs with cardiac arrest. VF is characterized by rapid, ineffective ventricular vibrations. The sinoatrial (SA) node, which normally initiates the heartbeat, does not act as the steady pacemaker. The fibrillating ventricles are unable to contract and pump blood. Coarse VF, characterized by large erratic waveforms, usually indicates recent onset of VF. Fine VF, characterized by a less erratic waveform that is close to the baseline, usually indicates that some time has passed since the onset of VF. Ventricular fibrillation is a life-threatening dysrhythmia characterized by a chaotic rhythm and rate, and pulselessness. Multiple, uncoordinated ectopic foci cause the ventricles to fibrillate. Cardiac output is absent. Causes: Cardiac injury Medication toxicity Electrolyte imbalances Untreated VT Manifestations: Loss of consciousness may not have a pulse or BP Respirations may stop Cardiac Arrest - No cardiac output = no blood or oxygen to the body Treatment: treat the cause, Advanced Cardiovascular Life Support (ACLS) Memory trick: Defib the Vfib AED, higher amounts of joules used, CPR Give O2, drug therapy (epinephrine [vasodilation], amiodarone, lidocaine, magnesium), possibly intubate
Pacemaker: malfunctions
With loss of battery power, the nurse would observe that no spikes occurred even when the client's rate dropped. If pacer wires were displaced, no pacemaker spikes would be observed even if the client rate dropped below the preset pacemaker rate. Sensitivity could be too high
Electrocardiogram (EKG/ECG)
recording of the electrical changes that occur in the myocardium during a cardiac cycle In a patient presenting with clinical signs of acute MI, candidacy for reperfusion is primarily determined by 12-lead ECG. An ECG that demonstrates persistent significant ST-segment elevation (greater than 2 mm above the baseline in two contiguous precordial leads and 1 mm in two limb leads) is diagnostic for myocardial injury that would benefit from reperfusion of the injured area. Whether primary percutaneous coronary intervention (PCI) is used or reperfusion is accomplished with fibrinolysis, the earlier treatment is initiated, the better the chance of successful reperfusion.
