ECG Summary ECG Result
Description
Nornal Sinus Rhythm
Rate
Rhythm
P wave Normal Upright and uniform
PR Interval Normal (0.120.20 seconds)
QRS Complex Normal (0.06-0.10 seconds)
Normal 60-100 bpm
Regular
Sinus Arrhythmia
- SA node discharges irregularly
60 -100 bpm Inc. w/ inspiratio n, dec. w/ expiratio n
Irregular , varies with respirati on
Normal
Normal
Normal
Sinus Bradycardia
-Normal in atheletes during sleep - Not pathological -At rest usually asymptomatic -Physical sign
Below 60 bpm
Regular
Normal
Normal
Normal
Intervention
- Only treat if s/s are developed -Oxygen is always appropriate
Sinus Tachycardia
- May be caused by
Fast
Regular
Normal
Normal
Normal
Intervention sequence: Atropine 0.5 to 1 mg IV if vagal mechanism Transcutaenous pacing if available If S&S are sever, consider catecholamine infusions: o Dopamine 5 to 20 ug/kg/min o Epinephrine 2 to 10 ug/min o Isoproterenol 2 to 10 ug/min Treat only the causes of the
exercise, anxiety, fever, hypoxemia, hypovolemia or cardiac failure - Not pathological, Physical sign
ECG Result
Atrial Flutter
Atrial Fibrillation
>100bp m
Atrial Arrhythmias (P waves differ in apperance from sinus P wave; After the dropped beat, cycles continue on time) Description Rate Rhythm P wave PR QRS Interval Complex -Atrial focus captures Atrial: Irregular - no true Variable Usually the heart rhythm and 250-350 but P wave normal, but discharges impulses at bpm; more - flutter may appear a rate bet. 200regular waves widened if 400x/min Ventricul than in "saw flutter -"saw tooth" pattern ar: atrial tooth waves are -A-flutter may be the slow or fibrillatio pattern" buried in first indication of fast n QRS cardiac disease -Causes: Atrial stretching, MI, CHF, elevated atrial pressure, hyperthyroidism, pericarditis - A fib is a dysrhythmia Atrial: "Irregula - no true None Normal that is caused by a 350 or rly P wave, rapid & chaotic firing by greater irregular chaotic atrial impulses caused bpm; " atrial by a multitude of (too activity ectopic foci rapid to - Causes: CHF, cor count) pulmonale, CHD, pericarditis, pulmonary Ventricul
tachycardia. NEVER countershock. Treat only if the client is at risk/experiencing symptoms of MI or myocardial damage B-blockers; verapamil Tachycardia is more life threatening to a patient with MI
Intervention Treatment: digitalis preparations (enhances the block of AV node thus slows down atrial rate); quinidine (controls ectopic foci); calcium channel blockers (for dysrhythmias); Propanolol (B adrenergic blocker); amnioderol; electrical cardioversion (giving small doses of electric current) Emergency drugs:
V - Verapamil I - Inderal D - Diltiazem
Treatment (same sa Atrial Flutter) Diltiazem, Ca channel blocker (decreases work load & O2 demand), beta blocker Amiodarone (B blocker; class III antidysrhythmic; prolongs repolarization during ventricular dysrhythmia) Digoxin (for purposes of reverting irregular rhythm to sinus rhythm) Cardioversion (giving of small electrical impulses (100 – 200
emboli, hyperthyroidism -s/s: DOE, SOB, Acute Pulmonary Edema
ar: slow or fast
joules) For an impaired heart: Heparin or other anticoagulants (but do NOT give to patients with hemorrhagic stroke) Quinidine (purpose: suppresses ectopic foci)
Emergency drugs:
V - Verapamil I - Inderal D - Diltiazem
Atrial Tachycardia
Causes: common in elderly patients with COPD
150-250 bpm
Regular
Normal but differ in shape from sinus P wave
May be short in rapid waves (<0.12 s)
PR Interval Usually not possible to measure
ECG Result
Description
Rate
Rhythm
P wave
Paroxysmal Supraventricular Tachycardia (PSVT)
- Pathophysiology: Reentry phenomenon: impulses arise & recycle repeatedly in the AV node because of areas of unidirectional block in the Purkinje fibers - S&S: Palpitations felt by pt. at the paroxysmal onset; becomes anxious, uncomfortable, Exercise tolerance low with very high rates, Symptoms of unstable tachycardia may occur -Etiology:
150 250 bpm
Regular
Frequen tly buried in precedi ng T waves and difficult to see "not identifiable"
Normal but can be aberrant at times
QRS Complex Normal but may be wide if abnormally conducted through ventricles
Treatment: Usually no treatment b/c underlying cause cannot be resolved Usually refractory to any treatment Emergency drugs: A - Adenosine
Intervention
Treatment: Just try to treat the cause / Preserved heart function: o B blocker o Calcium channel blocker o Digoxin o DC cardioversion o Parenteral antiarrhythmic: procainamide, amiodarone Impaired heart function: o DC cardioversion o Digoxin o Amiodarone
Factors that provoke the paroxysm: caffeine, hypoxia, cigarettes, stress, anxiety, sleep deprivation, numerous medications Also increased frequency of PSVT in unhealthy patients with CAD, COPD, CHF
o
Diltiazem
Junctional Arrhythmias ECG Result
Junctional Rhythm
Description (Junctional Arrhythmias) -The atria and SA node do not perform their normal pacemaking functions. A junctional escape
Rate
Rhythm
P wave
40 - 60 bpm
Regular
Absent, inverted , buried or retrogra
PR Interval None, short or retrograd e
QRS Complex Normal
Intervention
Treatment: If specific dx is unknown, attempt therapeutic/diagnostic maneuver with vagal stimulation, adenosine, THEN Preserved heart function:
de
rhythm begins.
Accelerated Junctional Rhythm
61 -100 bpm
Regular
Absent, inverted , buried or retrogra de
None, short or retrograd e
Normal
Junctional Tachycardia
-s/s of decreased cardiac output may be seen in response to the rapid rate
101 180 bpm
Regular
Absent, inverted , buried or retrogra de
None, short or retrograd e
Normal
Junctional Escape Beat
-an escape complex comes later than the next expected sinus complex
Depends on rate of underlyin g rhythm
Irregular wheneve r an escape beat occurs
None, short or retrograd e
Normal
Premature Junctional Contraction (PJC)
-enhanced automaticity in the AV junction produces PJC
Depends on rate of underlyin g rhythm
Irregular wheneve r a PJC occurs
Absent, inverted , buried or retrogra de in the escape beat Absent, inverted , buried or retrogra de in the PJC
None, short or retrograd e
Normal
-before deciding that the isolated PJC may be significant, consider the cause
Ventricular Arrhythmias
B blocker, Ca channel blocker, amiodarone o No DC cardioversion! If impaired heart function: o Amiodarone o No DC cardioversion! o
- Monitor the patient for clinical improvement, not just ECG
ECG Result
Description
Rate
Rhythm
P wave
Ventricular Fibrilation
Two types: •Fine – dili kaau distorted ang imong rhythm or imong firing of impulses •Coarse – the firing of impulses are either chaotic or disorganized
Too rapid to count
Chaotic
None
Condition where patient goes into a complete arrest Characterized by random & chaotic discharging of impulses within the ventricles at rates that exceed 300BPM Produces clinical death & must be reversed immediately S&S •Pulse disappears with onset of VF •Collapse, unconscious •Agonal breaths --- apnea in <5 min •Onset of reversible death Causes •Acute MI; deteriorating ventricular rhythms; acidosis; electrolyte disturbances
PR Interval None
QRS Complex None
Intervention
Indeterminate
Treatment Early defib is essential Agents given to prolong period reversible death – oxygen, CPR, intubation, epinephrine, vasopressin Agents given to prevent refib after a shock causes defib – lidocaine, amiodarone, procainamide, B blockers Agents given to adjust metabolic milieu – sodium bicarbonate, magnesium Priority management – electrical defib; ideal current: 200-400 watts/sec Successful defib will stop the heart and allowing it to restart; once restarted, it will be controlled by the normal sinus pace Emergency Drug E - Epinephrine V - Vasopressin A - Amiodarone L - Lidocaine (the same emergency drug in Pulseless V-tach)
ECG Result
Description
Rate
Rhythm
P wave
PR Interval
QRS Complex
Ventricular Tachycardia (Monophormic)
Impulse conduction is slowed around areas of ventricular injury, infarct or ischemia These areas also serve as source of ectopic impulses (irritable foci) These areas of injury can cause the impulse to take a circular course, leading to the reentry phenomenon and rapid repetitive depolarizations Can be asymptomatic Majority of times, symptoms of dec. cardiac output are seen (orthostatic hypotension, syncope, exercise limitations, etc.) Untreated & sustained will deteriorate to unstable V-Tach, often VF Areas serve as the source of ectopic impulses (irritable foci); irritable foci occur in multiple areas of the ventricles, thus “polymorphic” These areas of injury can cause impulses to
100-250 bpm
Regular
None (not associat ed with QRS)
None
Wide (> 0.10sec), bizarre appearance
Ventricular Tachycardia (Polymorphic)
Intervention
100-250 bpm
Regular or irregular
None (not associat ed with QRS)
None
Wide (> 0.10sec), bizarre appearance
Treatment Parenteral medications: any one o B blockers o Lidocaine (if pt. is unconscious, do not give lidocaine; immediately defib instead) o Amiodarone o Procainamide o Sotalol Impaired heart o Amiodarone o Lidocaine then discontinue cardioversion (to abolish all cardiac rhythms and allow normal pacemaker the opportunity to restart) if persists Endocardial resection, removal of aneurysm, aneurysmectomy, antitachycardia pacemakers – if unresponsive to drugs
Emergency Drugs A - Adenosine A - Amiodarone L - Lidocaine P - Procainamide drip
take a circular course, leading to the reentry phenomenon and rapid repetitive depolarizations Manifestations
ECG Result
Torsades de pointes
Pulseless Electrical Activity
Rare: asymptomatic polymorphic VT Majority of times: symptoms of dec. CO are seen (orthostatic hypotension, syncope, exercise limitations) Tends toward rapid deterioration to pulseless VT or VF
Description
Rate
Rhythm
P wave
“spindle-node” pattern Consequence of quinidine therapy Signs Majority of times, patients have symptoms of dec. CO Asymptomatic torsades, sustained torsades, or “stable” torsades is uncommon Tends towards sudden deterioration to pulseless VT or VF Prolonged Q-T interval (>0.6sec)
200 250 bpm
Irregular ventricul ar rhythm
None
-Equivalent to asystole
Rhythm displays organized electrical activity (not VF/pulseless VT)
PR Interval None
QRS Complex Display classic Wide (>0.10sec), bizarre appearance
Intervention Treatment Treat ischemia Correct electrolytes if abnormal Then therapies (any one): Magnesium Overdrive pacing (ventricular pacing to override the ventricular rate & capture the rhythm) Isoproterenol (pharmacologic overdrive pacing) [shortens QT interval] Phenytoin Lidocaine
Treatment Per PEA algorithm Primary CABD (basic CPR) C (IV epinephrine, AtSo4 if electrical activity <60 complexes per minute)
ECG Result
Asystole
Description
Seldom as organized as normal sinus rhythm Manifestations o Collapse; unconscious o Agonal respirations or apnea o No pulse detectable by arterial palpation (thus could still be as high as 5060mmHg; in such cases termed pseudo PEA)
Manifestations Early stages: may see agonal respirations (labored); unconscious; unresponsive; no pulse; no blood pressure; cardiac arrest
Secondary AB (adv. Airway and ventilation) D (identify and treat reversible causes) Key: identify & treat a reversible cause of the PEA
Common Etiology: Mnemonic of 5 H’s and 5 T’s aids recall: Hypovolemia Hypoxia H+ ion – acidosis pneumothorax Hyper/hypoK+ Hypothermia Tablets (drug OD, ingestions) Tamponade Cardiac tension Thrombosis (ACS) Thrombosis, pulmonary embolism
Rate
Rhythm
P wave
None
None
None
PR Interval None
QRS Intervention Complex Do not defibrillate None
Treatment o Always check for DNR status o Primary CABD survey (basic CPR) o Secondary CABD survey (ACLS)
Emergency Drug E - Epinephrine Atrioventricular (AV) Blocks
ECG Result
1st degree AV Block
Description
Impulse conduction is
Rate
Rhythm
P wave
Depends
Regular
Normal
PR Interval Prolonge
QRS Complex Normal
Intervention
Rarely indicated
slowed (partial block) at the AV node by a fixed amount Closer to being a physical sign than an abnormal arrhythmia
on the rate of the underlyin g rhythm
d (> 0.20 sec)
Usually AV block is benign, but if associated with an acute MI, it may lead to further AV defects.
2nd degree AV Block - Mobitz I (Wenkebach)
2nd degree AV Block - Mobitz II (Non-Wenkebach)
Site of pathology: AV node AV node blood supply comes from branches of the right coronary artery Impulse conduction is increasingly slowed at the AV node causing increasing PR interval Until one sinus impulse is completely blocked and a QRS complex fails to follow Due to bradycardia o Symptoms: chest pain, SOB, dec. level of consciousness o Signs: hypotension,
(narrow, <0.10sec in absence of intraventric ular conduction defect)
Depends on the rate of the underlyin g rhythm
Irregular
Normal
Progressively longer until one P wave is blocked and QRS is blocked
Normal
Atrial rate (usually 60–100 bpm); faster
Atrial regular and ventricul ar irregular
Normal (upright and uniform) ; more P waves
Normal or prolonge d but constant
Usually wide (_0.10 sec)
Treat only if patient has significant signs or symptoms due to the bradycardia Oxygen is always appropriate Intervention sequence for bradycardia o Atropine 0.5-1 mg IV if vagal mechanism o Transcutaenous pacing if available If SS are severe, consider catecholamine infusions o Dopamine 5 to 20 ug/kg/min o Epinephrine 2 to 10 ug/min o Isoproterenol 2 to 10 ug/min Treatment o Atropine 0.5 to 1MG IV if vagal mechanism o Transcutaneous pacing o If SS are severe Dopamine Epinephrine Isoproterenol Intervention for bradycardia d/t type II 2nd/3rd degree <3 block: o Prepare for transvenous pacer o Atropine seldom effective for infranodal block o Use transcutaneous pacing if available as a bridge to transvenous pacing (verify patient tolerance and mechanical capture. Use sedation and
shock, pulmonary congestion, CHF, angina, MI
3rd degree AV Block
Injury or damage to the cardiac conduction system so that no impulses pass between atria and ventricles (complete) This can occur at several different anatomical areas: o AV node (high/supra/jun ctional nodal block) o Bundle of his o Bundle branch (lownodal/infranoda l block) No relationship between atrial activity & ventricular activity Both chambers are discharging impulses
than ventricul ar rate
Atrial: 60–100 bpm; ventricul ar: 40–60 bpm if escape focus is junctiona l, <40 bpm if escape focus is ventricul ar
than QRS complex es
Usually regular, but atria and ventricle s act independently
Normal (upright and uniform) ; may be superimposed on QRS complex es or T waves
Varies greatly (NO relations hip bet. P wave and R wave)
Normal if ventricles are activated by junctional escape focus; wide if escape focus is ventricular
Sever TCP o o o
analgesic as needed) SS and unresponsive to Dopamine Epinephrine Isoproterenol
Intervention for bradycardia (view 2nd degree)
